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Review for 10.1186/1471-2407-1-16
|
Reviewed - bmc_cancer
|
Reviewer's□report
□Alterations□of□E-cadherin□and□b-catenin□in□gastric□cancer Title:
Authors:
Chen□Huiping□( [email protected] )
Sigrun□Kristjansdottir□( [email protected] )
Jon□G□Jonasson□( [email protected] )
Jonas□Magnusson□( [email protected] )
Valgardur□Egilsson□( [email protected] )
Sigurdur□Ingvarsson□( [email protected] )
□4□ □4□Oct□2001 Version: Date:
□Dr□Raffaele□Baffa Reviewer:
□A□paper□of□limited□interest Level□of□interest:
□Reject□because□scientifically□unsound Advice□on□publication:
In□this□manuscript□Dr.□Huiping□and□colleagues□studied□the□alterations□of□E-cadherin□and□b-catenin□in□50□
primary□adenocarcinomas□of□the□stomach□using□different□approaches.□E-cadherin□is□a□major□
calcium-dependent□homophilic□cell□adhesion□molecule□in□normal□epithelial□cells.□Its□intracellular□domain□
binds□directly□to□b-catenin□which,□along□with□alpha□catenin,□links□E-cadherin□to□the□actin□cytoskeleton.□ Reduced□expression□of□the□E-cadherin-catenin□complex□represents□one□of□the□molecular□events□ involved□in□dysfunction□of□the□cell-cell□adhesion□system,□triggering□cancer□invasion□and□metastasis.□The□
authors□performed□an□LOH□analysis□at□the□E-cadherin□locus□and□screened□for□mutations□of□the□entire□
E-cadherin□gene□as□well□as□exon□3□of□the□b-catenin□genes.□They□analyzed□50□gastric□carcinomas□as□wellas□many□other□solid□tumors.□The□authors□also□performed□RT-PCR□analysis□for□presence□of□the□ E-cadherin□abnormal□transcripts,□and□immunoistochemistry□analysis□for□both□E-cadherin□and□b-catenin□
protein□expression.□Results□of□this□study□include□75%□allelic□loss□at□16q22.1,□a□missense□mutation□of□the
E-cadherin□gene□(A592T)□detected□in□three□primary□tumors□as□well□as□in□normal□individuals,□detection□of□
aberrant□E-cadherin□transcripts□in□seven□cases,□altered□E-cadherin□and□b-catenin□expression□in□many□
cases,□and□association□between□E-cadherin□and□b-catenin□expression□as□well□as□between□reduced□
E-cahderin□and□diffuse□histotype.□In□general□this□is□a□well□written□paper□that□could□have□potential□clinical□
significance.□However,□the□long□list□of□data□reported□represent□only□an□interesting□adjunct□to□reports□ previously□published.□For□instance,□inherited□mutations□in□the□E-cadherin□gene□have□been□described□in□ familial□gastric□cancer,□a□missense□mutation□in□exon□12,□codon□592□(A592T)□was□also□found,□and□LOH□
at□16q22□and□reduced□E-cadherin□and□b-catenin□expression□have□also□been□described.□Despite□being□
technically□sound□this□study□does□not□provide□new□insights□in□the□understanding□of□how□the□ E-cadherin-catenin□complex□may□play□a□role□in□the□alteration□of□cell-cell□adhesion□or□in□the□development□ and□progression□of□gastric□cancer.□
The□following□specific□comments□should□be□addressed:□
1.□Analysis□of□microsatellite□instability□is□not□inherent□to□this□study□and□should□be□removed.□
2.□Please□indicate□if□you□obtained□the□patient's□informed□consent.□
Competing□interests:
None□declared.
|
Reviewer's□report
□Alterations□of□E-cadherin□and□b-catenin□in□gastric□cancer Title:
Authors:
Chen□Huiping□( [email protected] )
Sigrun□Kristjansdottir□( [email protected] )
Jon□G□Jonasson□( [email protected] )
Jonas□Magnusson□( [email protected] )
Valgardur□Egilsson□( [email protected] )
Sigurdur□Ingvarsson□( [email protected] )
□4□ □4□Oct□2001 Version: Date:
□Dr□Raffaele□Baffa Reviewer:
□A□paper□of□limited□interest Level□of□interest:
□Reject□because□scientifically□unsound Advice□on□publication:
In□this□manuscript□Dr.□Huiping□and□colleagues□studied□the□alterations□of□E-cadherin□and□b-catenin□in□50□
primary□adenocarcinomas□of□the□stomach□using□different□approaches.□E-cadherin□is□a□major□
calcium-dependent□homophilic□cell□adhesion□molecule□in□normal□epithelial□cells.□Its□intracellular□domain□
binds□directly□to□b-catenin□which,□along□with□alpha□catenin,□links□E-cadherin□to□the□actin□cytoskeleton.□ Reduced□expression□of□the□E-cadherin-catenin□complex□represents□one□of□the□molecular□events□ involved□in□dysfunction□of□the□cell-cell□adhesion□system,□triggering□cancer□invasion□and□metastasis.□The□
authors□performed□an□LOH□analysis□at□the□E-cadherin□locus□and□screened□for□mutations□of□the□entire□
E-cadherin□gene□as□well□as□exon□3□of□the□b-catenin□genes.□They□analyzed□50□gastric□carcinomas□as□wellas□many□other□solid□tumors.□The□authors□also□performed□RT-PCR□analysis□for□presence□of□the□ E-cadherin□abnormal□transcripts,□and□immunoistochemistry□analysis□for□both□E-cadherin□and□b-catenin□
protein□expression.□Results□of□this□study□include□75%□allelic□loss□at□16q22.1,□a□missense□mutation□of□the
E-cadherin□gene□(A592T)□detected□in□three□primary□tumors□as□well□as□in□normal□individuals,□detection□of□
aberrant□E-cadherin□transcripts□in□seven□cases,□altered□E-cadherin□and□b-catenin□expression□in□many□
cases,□and□association□between□E-cadherin□and□b-catenin□expression□as□well□as□between□reduced□
E-cahderin□and□diffuse□histotype.□In□general□this□is□a□well□written□paper□that□could□have□potential□clinical□
significance.□However,□the□long□list□of□data□reported□represent□only□an□interesting□adjunct□to□reports□ previously□published.□For□instance,□inherited□mutations□in□the□E-cadherin□gene□have□been□described□in□ familial□gastric□cancer,□a□missense□mutation□in□exon□12,□codon□592□(A592T)□was□also□found,□and□LOH□
at□16q22□and□reduced□E-cadherin□and□b-catenin□expression□have□also□been□described.□Despite□being□
technically□sound□this□study□does□not□provide□new□insights□in□the□understanding□of□how□the□ E-cadherin-catenin□complex□may□play□a□role□in□the□alteration□of□cell-cell□adhesion□or□in□the□development□ and□progression□of□gastric□cancer.□
The□following□specific□comments□should□be□addressed:□
1.□Analysis□of□microsatellite□instability□is□not□inherent□to□this□study□and□should□be□removed.□
2.□Please□indicate□if□you□obtained□the□patient's□informed□consent.□
Competing□interests:
None□declared.
|
BMC
|
12885_2001_16_ReviewerReport_V4_R1.pdf
|
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"content": "Reviewer's□report \n□Alterations□of□E-cadherin□and□b-catenin□in□gastric□cancer Title: \nAuthors: \nChen□Huiping□( [email protected] )\nSigrun□Kristjansdottir□( [email protected] )\nJon□G□Jonasson□( [email protected] )\nJonas□Magnusson□( [email protected] )\nValgardur□Egilsson□( [email protected] )\nSigurdur□Ingvarsson□( [email protected] )\n□4□ □4□Oct□2001 Version: Date: \n□Dr□Raffaele□Baffa Reviewer: \n□A□paper□of□limited□interest Level□of□interest: \n□Reject□because□scientifically□unsound Advice□on□publication: \nIn□this□manuscript□Dr.□Huiping□and□colleagues□studied□the□alterations□of□E-cadherin□and□b-catenin□in□50□ \nprimary□adenocarcinomas□of□the□stomach□using□different□approaches.□E-cadherin□is□a□major□ \ncalcium-dependent□homophilic□cell□adhesion□molecule□in□normal□epithelial□cells.□Its□intracellular□domain□ \nbinds□directly□to□b-catenin□which,□along□with□alpha□catenin,□links□E-cadherin□to□the□actin□cytoskeleton.□ Reduced□expression□of□the□E-cadherin-catenin□complex□represents□one□of□the□molecular□events□ involved□in□dysfunction□of□the□cell-cell□adhesion□system,□triggering□cancer□invasion□and□metastasis.□The□ \nauthors□performed□an□LOH□analysis□at□the□E-cadherin□locus□and□screened□for□mutations□of□the□entire□ \nE-cadherin□gene□as□well□as□exon□3□of□the□b-catenin□genes.□They□analyzed□50□gastric□carcinomas□as□wellas□many□other□solid□tumors.□The□authors□also□performed□RT-PCR□analysis□for□presence□of□the□ E-cadherin□abnormal□transcripts,□and□immunoistochemistry□analysis□for□both□E-cadherin□and□b-catenin□ \nprotein□expression.□Results□of□this□study□include□75%□allelic□loss□at□16q22.1,□a□missense□mutation□of□the \nE-cadherin□gene□(A592T)□detected□in□three□primary□tumors□as□well□as□in□normal□individuals,□detection□of□ \naberrant□E-cadherin□transcripts□in□seven□cases,□altered□E-cadherin□and□b-catenin□expression□in□many□ \ncases,□and□association□between□E-cadherin□and□b-catenin□expression□as□well□as□between□reduced□ \nE-cahderin□and□diffuse□histotype.□In□general□this□is□a□well□written□paper□that□could□have□potential□clinical□ \nsignificance.□However,□the□long□list□of□data□reported□represent□only□an□interesting□adjunct□to□reports□ previously□published.□For□instance,□inherited□mutations□in□the□E-cadherin□gene□have□been□described□in□ familial□gastric□cancer,□a□missense□mutation□in□exon□12,□codon□592□(A592T)□was□also□found,□and□LOH□ \nat□16q22□and□reduced□E-cadherin□and□b-catenin□expression□have□also□been□described.□Despite□being□ \ntechnically□sound□this□study□does□not□provide□new□insights□in□the□understanding□of□how□the□ E-cadherin-catenin□complex□may□play□a□role□in□the□alteration□of□cell-cell□adhesion□or□in□the□development□ and□progression□of□gastric□cancer.□ \nThe□following□specific□comments□should□be□addressed:□ \n1.□Analysis□of□microsatellite□instability□is□not□inherent□to□this□study□and□should□be□removed.□ \n2.□Please□indicate□if□you□obtained□the□patient's□informed□consent.□ \nCompeting□interests: \nNone□declared. ",
"role": "assistant"
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0
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Review for 10.1186/1471-2407-1-14
|
Reviewed - bmc_cancer
|
Reviewer's report
Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:
Fat Intake
Authors:
Shigeyuki S Nakaji ([email protected] )
Takashi T Umeda ([email protected] )
Tadashi T Shimoyama ([email protected] )
Juichi J Sakamoto ([email protected] )
Shuji S Katsura ([email protected] )
Kazuo K Sugawara ([email protected] )
David D Baxter ([email protected] )
1 7 Jun 2001 Version: Date:
Dr Richard Le Leu Reviewer:
A paper of considerable general medical or scientific interest Level of interest:
Accept after revision, which I do not need to see Advice on publication:
An interesting paper which has examined the effect of dietary factors in Japanese people who consume
relatively low levels of fat.
Agree that a limitation of the study is the short time frame (10 years), as it is well known that colorectal
cancer has a long latency period.
Minor points:
Page 5 (line 7) spelling error "lead" should be replaced with "led"
In tables "SMR" should be defined in the footnote. In table 2 intake of dietary fiber, energy, protein, fat
and carbohydrate should be defined ie. g/day.
Would have been interesting to discriminate between the fat intakes, as omega-3 fats may have a
protective effect against colorectal carcinogenesis. Both protein and carbohydrate levels were measured, however why weren't any of these included in
correlations.
Starch intake has been shown to be associated with colorectal cancer (Cassidy et al. 1994: Brit. J Clin Nutr. 69, 119-125. It might be worth the authors examining starch correlations.
Major points:
Methods:
There is no mention about how the nutrients Vitamin A and Vitamin C were elucidated. Why not also
include folic acid, as this nutrient is very topical.
In Table 3 the correlation coefficients are adequately defined for in the colon, however only fat is defined
for the rectum. All Nutrients and food groups should be displayed for the rectum even if they are
non-significant.
This also applies to dietary fiber correlations for both the colon and rectum. Don't just display significant
correlations.
Competing interests:
None declared.
|
Reviewer's report
Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:
Fat Intake
Authors:
Shigeyuki S Nakaji ([email protected] )
Takashi T Umeda ([email protected] )
Tadashi T Shimoyama ([email protected] )
Juichi J Sakamoto ([email protected] )
Shuji S Katsura ([email protected] )
Kazuo K Sugawara ([email protected] )
David D Baxter ([email protected] )
1 7 Jun 2001 Version: Date:
Dr Richard Le Leu Reviewer:
A paper of considerable general medical or scientific interest Level of interest:
Accept after revision, which I do not need to see Advice on publication:
An interesting paper which has examined the effect of dietary factors in Japanese people who consume
relatively low levels of fat.
Agree that a limitation of the study is the short time frame (10 years), as it is well known that colorectal
cancer has a long latency period.
Minor points:
Page 5 (line 7) spelling error "lead" should be replaced with "led"
In tables "SMR" should be defined in the footnote. In table 2 intake of dietary fiber, energy, protein, fat
and carbohydrate should be defined ie. g/day.
Would have been interesting to discriminate between the fat intakes, as omega-3 fats may have a
protective effect against colorectal carcinogenesis. Both protein and carbohydrate levels were measured, however why weren't any of these included in
correlations.
Starch intake has been shown to be associated with colorectal cancer (Cassidy et al. 1994: Brit. J Clin Nutr. 69, 119-125. It might be worth the authors examining starch correlations.
Major points:
Methods:
There is no mention about how the nutrients Vitamin A and Vitamin C were elucidated. Why not also
include folic acid, as this nutrient is very topical.
In Table 3 the correlation coefficients are adequately defined for in the colon, however only fat is defined
for the rectum. All Nutrients and food groups should be displayed for the rectum even if they are
non-significant.
This also applies to dietary fiber correlations for both the colon and rectum. Don't just display significant
correlations.
Competing interests:
None declared.
|
BMC
|
12885_2001_14_ReviewerReport_V1_R1.pdf
|
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"content": "Please review this paper.",
"role": "user"
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{
"content": "Reviewer's report\n Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:\nFat Intake\nAuthors:\nShigeyuki S Nakaji ([email protected] )\nTakashi T Umeda ([email protected] )\nTadashi T Shimoyama ([email protected] )\nJuichi J Sakamoto ([email protected] )\nShuji S Katsura ([email protected] )\nKazuo K Sugawara ([email protected] )\nDavid D Baxter ([email protected] )\n 1 7 Jun 2001 Version: Date:\n Dr Richard Le Leu Reviewer:\n A paper of considerable general medical or scientific interest Level of interest:\n Accept after revision, which I do not need to see Advice on publication:\nAn interesting paper which has examined the effect of dietary factors in Japanese people who consume \nrelatively low levels of fat. \nAgree that a limitation of the study is the short time frame (10 years), as it is well known that colorectal \ncancer has a long latency period. \nMinor points: \nPage 5 (line 7) spelling error \"lead\" should be replaced with \"led\" \nIn tables \"SMR\" should be defined in the footnote. In table 2 intake of dietary fiber, energy, protein, fat \nand carbohydrate should be defined ie. g/day. \nWould have been interesting to discriminate between the fat intakes, as omega-3 fats may have a \nprotective effect against colorectal carcinogenesis. Both protein and carbohydrate levels were measured, however why weren't any of these included in \ncorrelations. \nStarch intake has been shown to be associated with colorectal cancer (Cassidy et al. 1994: Brit. J Clin Nutr. 69, 119-125. It might be worth the authors examining starch correlations. \nMajor points: \nMethods: \nThere is no mention about how the nutrients Vitamin A and Vitamin C were elucidated. Why not also \ninclude folic acid, as this nutrient is very topical. \nIn Table 3 the correlation coefficients are adequately defined for in the colon, however only fat is defined\nfor the rectum. All Nutrients and food groups should be displayed for the rectum even if they are \nnon-significant. \nThis also applies to dietary fiber correlations for both the colon and rectum. Don't just display significant \ncorrelations. \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-14
|
Reviewed - bmc_cancer
|
Reviewer's report
Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:
Fat Intake
Authors:
Shigeyuki S Nakaji ([email protected] )
Takashi T Umeda ([email protected] )
Tadashi T Shimoyama ([email protected] )
Juichi J Sakamoto ([email protected] )
Shuji S Katsura ([email protected] )
Kazuo K Sugawara ([email protected] )
David D Baxter ([email protected] )
1 29 Jun 2001 Version: Date:
Prof Lynnette Robin Ferguson Reviewer:
A paper of limited interest Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
This paper follows from an American report
that suggested no protective effect of dietary fibre against colorectal cancer in a sizable study cohort of health professionals. Although it has a large amount of data, it simply uses a geographic comparison to associate dietary fibre intake with deaths from colon and rectal cancers between 1995 and 1997 in
the
23 target prefectures. The authors conclude that dietary fiber showed no preventive effect in these Japanese people.
The methodology is adequate and the number of subjects included strengthens the study. However,
such an approach is notoriusly insensitive to effects, since different prefectures would differ in more ways than
just their dietary fibre content. Thus, while the paper is generally adequate, I belive that the claims of
significance of the study should be played down somewhat. The title impies that they have directly
measured the effects of dietary fiber on these cancers, while in fact the authors can only demonstrate a
correlation.
Additionally, the English requires some improvement
Specific points:
I was disappointed that the authors have not recognised the enormous controversy that the Fuchs
paper
generated. Several reasons have beeen given, especially in the correspondence in the same jounral over following months. Would these same criticisms be applicable to the authors own study?
I don't belive that the prosky method is generally accepted for dietary fiber analysis. There would be
virtue
in having other analyses and breaking down the dietary fibre into different types.
Competing interests:
None declared.
|
Reviewer's report
Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:
Fat Intake
Authors:
Shigeyuki S Nakaji ([email protected] )
Takashi T Umeda ([email protected] )
Tadashi T Shimoyama ([email protected] )
Juichi J Sakamoto ([email protected] )
Shuji S Katsura ([email protected] )
Kazuo K Sugawara ([email protected] )
David D Baxter ([email protected] )
1 29 Jun 2001 Version: Date:
Prof Lynnette Robin Ferguson Reviewer:
A paper of limited interest Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
This paper follows from an American report
that suggested no protective effect of dietary fibre against colorectal cancer in a sizable study cohort of health professionals. Although it has a large amount of data, it simply uses a geographic comparison to associate dietary fibre intake with deaths from colon and rectal cancers between 1995 and 1997 in
the
23 target prefectures. The authors conclude that dietary fiber showed no preventive effect in these Japanese people.
The methodology is adequate and the number of subjects included strengthens the study. However,
such an approach is notoriusly insensitive to effects, since different prefectures would differ in more ways than
just their dietary fibre content. Thus, while the paper is generally adequate, I belive that the claims of
significance of the study should be played down somewhat. The title impies that they have directly
measured the effects of dietary fiber on these cancers, while in fact the authors can only demonstrate a
correlation.
Additionally, the English requires some improvement
Specific points:
I was disappointed that the authors have not recognised the enormous controversy that the Fuchs
paper
generated. Several reasons have beeen given, especially in the correspondence in the same jounral over following months. Would these same criticisms be applicable to the authors own study?
I don't belive that the prosky method is generally accepted for dietary fiber analysis. There would be
virtue
in having other analyses and breaking down the dietary fibre into different types.
Competing interests:
None declared.
|
BMC
|
12885_2001_14_ReviewerReport_V1_R2.pdf
|
{
"criticism": 3,
"example": 0,
"importance_and_relevance": 1,
"materials_and_methods": 6,
"praise": 2,
"presentation_and_reporting": 1,
"results_and_discussion": 1,
"suggestion_and_solution": 3,
"total": 13
}
|
{
"criticism": 0.23076923076923078,
"example": 0,
"importance_and_relevance": 0.07692307692307693,
"materials_and_methods": 0.46153846153846156,
"praise": 0.15384615384615385,
"presentation_and_reporting": 0.07692307692307693,
"results_and_discussion": 0.07692307692307693,
"suggestion_and_solution": 0.23076923076923078
}
| 1.307692
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Dietary Fiber Showed no Preventive Effect from Colon and Rectal Cancers in Japanese with Low Title:\nFat Intake\nAuthors:\nShigeyuki S Nakaji ([email protected] )\nTakashi T Umeda ([email protected] )\nTadashi T Shimoyama ([email protected] )\nJuichi J Sakamoto ([email protected] )\nShuji S Katsura ([email protected] )\nKazuo K Sugawara ([email protected] )\nDavid D Baxter ([email protected] )\n 1 29 Jun 2001 Version: Date:\n Prof Lynnette Robin Ferguson Reviewer:\n A paper of limited interest Level of interest:\n Unable to decide on acceptance or rejection until I see revised version Advice on publication:\nThis paper follows from an American report \nthat suggested no protective effect of dietary fibre against colorectal cancer in a sizable study cohort of health professionals. Although it has a large amount of data, it simply uses a geographic comparison to associate dietary fibre intake with deaths from colon and rectal cancers between 1995 and 1997 in \nthe \n23 target prefectures. The authors conclude that dietary fiber showed no preventive effect in these Japanese people. \nThe methodology is adequate and the number of subjects included strengthens the study. However, \nsuch an approach is notoriusly insensitive to effects, since different prefectures would differ in more ways than \njust their dietary fibre content. Thus, while the paper is generally adequate, I belive that the claims of \nsignificance of the study should be played down somewhat. The title impies that they have directly \nmeasured the effects of dietary fiber on these cancers, while in fact the authors can only demonstrate a \ncorrelation. \nAdditionally, the English requires some improvement \nSpecific points: \nI was disappointed that the authors have not recognised the enormous controversy that the Fuchs \npaper \ngenerated. Several reasons have beeen given, especially in the correspondence in the same jounral over following months. Would these same criticisms be applicable to the authors own study? \nI don't belive that the prosky method is generally accepted for dietary fiber analysis. There would be \nvirtue \nin having other analyses and breaking down the dietary fibre into different types.\nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-15
|
Reviewed - bmc_cancer
|
Reviewer's report
Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:
Authors:
Matthew Pavao ([email protected] )
Yue-Hua Huang ([email protected] )
Laurie J Hafer ([email protected] )
Robert B Moreland ([email protected] )
Abdulmaged M Traish ([email protected] )
1 3 Aug 2001 Version: Date:
Dr Michael Fasco Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
This is a potentially interesting series of experiments to determine the mechanism whereby
nmt55/p54nrb is apparently under-expressed in a subset estrogen receptor positive (ER+) breast
tumors. nmt55/p54nrb participates in pre-mRNA splicing and may serve as a potential tumor marker for
hormone/antiestrogen responsiveness since it is absent in estrogen receptor negative (ER-) tumors as
well as the subset of ER+ tumors. An aberrant form of nmt55/p54nrb is identified using separate
antibodies that have epitopes in the N- and C-terminal and center regions of nmt55/p54nrb. The
approach of using antibodies with different epitopes arose from prior experiments that showed no
obvious correlation between nmt55/p54nrb mRNA and protein levels, suggesting that a
post-transcriptional change had occurred in at least some ER+ tumors.
Unfortunately, portions of this work and manuscript were apparently prepared in haste.
Major Criticisms:
1. The cornerstone of this work is the differential antibody reactivity shown in Figure 6, but it poorly
presently and very inadequately explained.
Do the authors really believe that all the proteins in this Figure have the same molecular weight? On page 11 they state that a possible cause for the differential antibody recognition could be proteolytic degradation, but immediately dismiss the notion because "the estimated molecular weight of 55 kD is
unaltered in these variants". From Figure 6, it would certainly appear that the antibody positive protein in
lane 9 is of lower molecular weight than the others, and those in lanes 6 through 8 may be lower than
the nmt55/p54nrb in MCF-7 cells. Moreover, the tumor nmt55/p54nrb detected by antibodies NMT-4 and
NMT-5 is much different in shape than in the MCF-7 cells, which could be due to the presence of
multiple forms. Some mixing experiments would resolve these questions. Also some of the questions
raised as to why antibody NMT-4 does not react with nmt55/p54nrb in tumors 8 and 9 (such as a point mutation) could be readily answered by PCR and sequencing of the region of interest. A splice variant could also be the reason, and its presence is readily detected by PCR..
2. The inability of NMT-4 to detect nmt55/p54nrb in tumors 8 and 9 is not entirely convincing. Antibodies
do not have the same detection limits on Western blots so it is possible that the absence of reactive
protein could be apparent and due to a sensitivity difference. nmt55/p54nrb in MCF-7 cells could be
loaded at various concentrations, surrounding the estimated nmt55/p54nrb concentration in the tumor protein, and then detected with each antibody to eliminate sensitivity difference as a cause.
Minor Criticisms:
1. Abstract. Beginning assumes too much prior knowledge on the part of the reader. For example, in
background says nmt55/p54nrb expression decreased in a subset of tumors. Later find out that subset
is from ER+ tumors, but also decreased in ER- tumors.
2. Page 2 Result - 1st sentence. Why only ER-? Conclusion not justified from 1st part of sentence.
3. Page 4. Last Sentence. in large (ER+ ?) and/ or ER-. Again conclusion not warranted from sentence
as written.
4. Figure 3B. Mislabeled or backwards. NH2 and C-terminals of translated protein are 5' and 3'
respectively.
Competing interests:
None declared.
|
Reviewer's report
Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:
Authors:
Matthew Pavao ([email protected] )
Yue-Hua Huang ([email protected] )
Laurie J Hafer ([email protected] )
Robert B Moreland ([email protected] )
Abdulmaged M Traish ([email protected] )
1 3 Aug 2001 Version: Date:
Dr Michael Fasco Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
This is a potentially interesting series of experiments to determine the mechanism whereby
nmt55/p54nrb is apparently under-expressed in a subset estrogen receptor positive (ER+) breast
tumors. nmt55/p54nrb participates in pre-mRNA splicing and may serve as a potential tumor marker for
hormone/antiestrogen responsiveness since it is absent in estrogen receptor negative (ER-) tumors as
well as the subset of ER+ tumors. An aberrant form of nmt55/p54nrb is identified using separate
antibodies that have epitopes in the N- and C-terminal and center regions of nmt55/p54nrb. The
approach of using antibodies with different epitopes arose from prior experiments that showed no
obvious correlation between nmt55/p54nrb mRNA and protein levels, suggesting that a
post-transcriptional change had occurred in at least some ER+ tumors.
Unfortunately, portions of this work and manuscript were apparently prepared in haste.
Major Criticisms:
1. The cornerstone of this work is the differential antibody reactivity shown in Figure 6, but it poorly
presently and very inadequately explained.
Do the authors really believe that all the proteins in this Figure have the same molecular weight? On page 11 they state that a possible cause for the differential antibody recognition could be proteolytic degradation, but immediately dismiss the notion because "the estimated molecular weight of 55 kD is
unaltered in these variants". From Figure 6, it would certainly appear that the antibody positive protein in
lane 9 is of lower molecular weight than the others, and those in lanes 6 through 8 may be lower than
the nmt55/p54nrb in MCF-7 cells. Moreover, the tumor nmt55/p54nrb detected by antibodies NMT-4 and
NMT-5 is much different in shape than in the MCF-7 cells, which could be due to the presence of
multiple forms. Some mixing experiments would resolve these questions. Also some of the questions
raised as to why antibody NMT-4 does not react with nmt55/p54nrb in tumors 8 and 9 (such as a point mutation) could be readily answered by PCR and sequencing of the region of interest. A splice variant could also be the reason, and its presence is readily detected by PCR..
2. The inability of NMT-4 to detect nmt55/p54nrb in tumors 8 and 9 is not entirely convincing. Antibodies
do not have the same detection limits on Western blots so it is possible that the absence of reactive
protein could be apparent and due to a sensitivity difference. nmt55/p54nrb in MCF-7 cells could be
loaded at various concentrations, surrounding the estimated nmt55/p54nrb concentration in the tumor protein, and then detected with each antibody to eliminate sensitivity difference as a cause.
Minor Criticisms:
1. Abstract. Beginning assumes too much prior knowledge on the part of the reader. For example, in
background says nmt55/p54nrb expression decreased in a subset of tumors. Later find out that subset
is from ER+ tumors, but also decreased in ER- tumors.
2. Page 2 Result - 1st sentence. Why only ER-? Conclusion not justified from 1st part of sentence.
3. Page 4. Last Sentence. in large (ER+ ?) and/ or ER-. Again conclusion not warranted from sentence
as written.
4. Figure 3B. Mislabeled or backwards. NH2 and C-terminals of translated protein are 5' and 3'
respectively.
Competing interests:
None declared.
|
BMC
|
12885_2001_15_ReviewerReport_V1_R1.pdf
|
{
"criticism": 10,
"example": 7,
"importance_and_relevance": 1,
"materials_and_methods": 14,
"praise": 1,
"presentation_and_reporting": 6,
"results_and_discussion": 3,
"suggestion_and_solution": 3,
"total": 38
}
|
{
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"example": 0.18421052631578946,
"importance_and_relevance": 0.02631578947368421,
"materials_and_methods": 0.3684210526315789,
"praise": 0.02631578947368421,
"presentation_and_reporting": 0.15789473684210525,
"results_and_discussion": 0.07894736842105263,
"suggestion_and_solution": 0.07894736842105263
}
| 1.184211
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:\nAuthors:\nMatthew Pavao ([email protected] )\nYue-Hua Huang ([email protected] )\nLaurie J Hafer ([email protected] )\nRobert B Moreland ([email protected] )\nAbdulmaged M Traish ([email protected] )\n 1 3 Aug 2001 Version: Date:\n Dr Michael Fasco Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Unable to decide on acceptance or rejection until I see revised version Advice on publication:\nThis is a potentially interesting series of experiments to determine the mechanism whereby \nnmt55/p54nrb is apparently under-expressed in a subset estrogen receptor positive (ER+) breast \ntumors. nmt55/p54nrb participates in pre-mRNA splicing and may serve as a potential tumor marker for \nhormone/antiestrogen responsiveness since it is absent in estrogen receptor negative (ER-) tumors as \nwell as the subset of ER+ tumors. An aberrant form of nmt55/p54nrb is identified using separate \nantibodies that have epitopes in the N- and C-terminal and center regions of nmt55/p54nrb. The \napproach of using antibodies with different epitopes arose from prior experiments that showed no \nobvious correlation between nmt55/p54nrb mRNA and protein levels, suggesting that a \npost-transcriptional change had occurred in at least some ER+ tumors. \nUnfortunately, portions of this work and manuscript were apparently prepared in haste. \nMajor Criticisms: \n1. The cornerstone of this work is the differential antibody reactivity shown in Figure 6, but it poorly \npresently and very inadequately explained. \nDo the authors really believe that all the proteins in this Figure have the same molecular weight? On page 11 they state that a possible cause for the differential antibody recognition could be proteolytic degradation, but immediately dismiss the notion because \"the estimated molecular weight of 55 kD is \nunaltered in these variants\". From Figure 6, it would certainly appear that the antibody positive protein in\nlane 9 is of lower molecular weight than the others, and those in lanes 6 through 8 may be lower than \nthe nmt55/p54nrb in MCF-7 cells. Moreover, the tumor nmt55/p54nrb detected by antibodies NMT-4 and\nNMT-5 is much different in shape than in the MCF-7 cells, which could be due to the presence of \nmultiple forms. Some mixing experiments would resolve these questions. Also some of the questions \nraised as to why antibody NMT-4 does not react with nmt55/p54nrb in tumors 8 and 9 (such as a point mutation) could be readily answered by PCR and sequencing of the region of interest. A splice variant could also be the reason, and its presence is readily detected by PCR.. \n2. The inability of NMT-4 to detect nmt55/p54nrb in tumors 8 and 9 is not entirely convincing. Antibodies\ndo not have the same detection limits on Western blots so it is possible that the absence of reactive \nprotein could be apparent and due to a sensitivity difference. nmt55/p54nrb in MCF-7 cells could be \nloaded at various concentrations, surrounding the estimated nmt55/p54nrb concentration in the tumor protein, and then detected with each antibody to eliminate sensitivity difference as a cause. \nMinor Criticisms: \n1. Abstract. Beginning assumes too much prior knowledge on the part of the reader. For example, in \nbackground says nmt55/p54nrb expression decreased in a subset of tumors. Later find out that subset \nis from ER+ tumors, but also decreased in ER- tumors. \n2. Page 2 Result - 1st sentence. Why only ER-? Conclusion not justified from 1st part of sentence. \n3. Page 4. Last Sentence. in large (ER+ ?) and/ or ER-. Again conclusion not warranted from sentence \nas written. \n4. Figure 3B. Mislabeled or backwards. NH2 and C-terminals of translated protein are 5' and 3' \nrespectively. \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-15
|
Reviewed - bmc_cancer
|
Reviewer's report
Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:
Authors:
Matthew Pavao ([email protected] )
Yue-Hua Huang ([email protected] )
Laurie J Hafer ([email protected] )
Robert B Moreland ([email protected] )
Abdulmaged M Traish ([email protected] )
1 16 Aug 2001 Version: Date:
Dr R Sutherland Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
The authors have previously identified a 55kDa nuclear RNA binding protein
(nmt55/p54nrb), the expression of which is decreased in ER-negative breast cancer. In the present study they evaluate mRNA and protein expression in
a series of primary breast cancers. Northern blots and ribonuclease
protection assays demonstrated that nmt/p54nrb mRNA is expressed independent of ER status and that the decrease in protein levels in ER-negative tumors was thus not mediated at the mRNA level. The
development of domain specific polyclonal antibodies NMT-4 (amino terminus)
and NMT-5 (mid region) together with the NMT-1 monoclonal antibody to the carboxy terminus facilitated an analysis of protein expression in ~40 breast cancers. ER-positive tumors had detectable expression; only ~60% of
which were positive when the N-terminal antibody was employed. When this
study was extended to immunohistochemical analysis a similar pattern of
expression was observed i.e. several nmt/p54nrb positive tumors were not detected with the NMT-4 antibody supporting the presence of N-terminal
truncated isoforms.
These data provide further insight into the expression of a protein with a
potential role as a marker of breast cancer phenotype. In order to confirm
these preliminary findings a more extensive study on a large cohort of
patients with accompanying detailed clinicopathologic data including significant follow-up will be required. Until these data and further information on the function and regulation of this gene product are
available the full implication of the current dataset remain unknown and
thus several aspects of the Discussion are highly speculative e.g. relationships with known prognostic factors and its role in cell growth.
The manuscript could be improved by:
1. Providing more detail on the number and characteristics of the breast
cancers understudy i.e. primary or metastatic, total number of tumours
analysed by the different methodologies, clinicopathological parameters of
the group and are they representative of the population from which they
were collected
2. Shortening of the Discussion.
Competing interests:
None declared.
|
Reviewer's report
Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:
Authors:
Matthew Pavao ([email protected] )
Yue-Hua Huang ([email protected] )
Laurie J Hafer ([email protected] )
Robert B Moreland ([email protected] )
Abdulmaged M Traish ([email protected] )
1 16 Aug 2001 Version: Date:
Dr R Sutherland Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
The authors have previously identified a 55kDa nuclear RNA binding protein
(nmt55/p54nrb), the expression of which is decreased in ER-negative breast cancer. In the present study they evaluate mRNA and protein expression in
a series of primary breast cancers. Northern blots and ribonuclease
protection assays demonstrated that nmt/p54nrb mRNA is expressed independent of ER status and that the decrease in protein levels in ER-negative tumors was thus not mediated at the mRNA level. The
development of domain specific polyclonal antibodies NMT-4 (amino terminus)
and NMT-5 (mid region) together with the NMT-1 monoclonal antibody to the carboxy terminus facilitated an analysis of protein expression in ~40 breast cancers. ER-positive tumors had detectable expression; only ~60% of
which were positive when the N-terminal antibody was employed. When this
study was extended to immunohistochemical analysis a similar pattern of
expression was observed i.e. several nmt/p54nrb positive tumors were not detected with the NMT-4 antibody supporting the presence of N-terminal
truncated isoforms.
These data provide further insight into the expression of a protein with a
potential role as a marker of breast cancer phenotype. In order to confirm
these preliminary findings a more extensive study on a large cohort of
patients with accompanying detailed clinicopathologic data including significant follow-up will be required. Until these data and further information on the function and regulation of this gene product are
available the full implication of the current dataset remain unknown and
thus several aspects of the Discussion are highly speculative e.g. relationships with known prognostic factors and its role in cell growth.
The manuscript could be improved by:
1. Providing more detail on the number and characteristics of the breast
cancers understudy i.e. primary or metastatic, total number of tumours
analysed by the different methodologies, clinicopathological parameters of
the group and are they representative of the population from which they
were collected
2. Shortening of the Discussion.
Competing interests:
None declared.
|
BMC
|
12885_2001_15_ReviewerReport_V1_R2.pdf
|
{
"criticism": 1,
"example": 0,
"importance_and_relevance": 2,
"materials_and_methods": 9,
"praise": 2,
"presentation_and_reporting": 1,
"results_and_discussion": 3,
"suggestion_and_solution": 4,
"total": 17
}
|
{
"criticism": 0.058823529411764705,
"example": 0,
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"materials_and_methods": 0.5294117647058824,
"praise": 0.11764705882352941,
"presentation_and_reporting": 0.058823529411764705,
"results_and_discussion": 0.17647058823529413,
"suggestion_and_solution": 0.23529411764705882
}
| 1.294118
| 0
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Immunodetection of nmt55/p54nrb Isoforms in Human Breast Cancer. Title:\nAuthors:\nMatthew Pavao ([email protected] )\nYue-Hua Huang ([email protected] )\nLaurie J Hafer ([email protected] )\nRobert B Moreland ([email protected] )\nAbdulmaged M Traish ([email protected] )\n 1 16 Aug 2001 Version: Date:\n Dr R Sutherland Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Accept after revision, which I do not need to see Advice on publication:\nThe authors have previously identified a 55kDa nuclear RNA binding protein \n(nmt55/p54nrb), the expression of which is decreased in ER-negative breast cancer. In the present study they evaluate mRNA and protein expression in \na series of primary breast cancers. Northern blots and ribonuclease \nprotection assays demonstrated that nmt/p54nrb mRNA is expressed independent of ER status and that the decrease in protein levels in ER-negative tumors was thus not mediated at the mRNA level. The \ndevelopment of domain specific polyclonal antibodies NMT-4 (amino terminus) \nand NMT-5 (mid region) together with the NMT-1 monoclonal antibody to the carboxy terminus facilitated an analysis of protein expression in ~40 breast cancers. ER-positive tumors had detectable expression; only ~60% of \nwhich were positive when the N-terminal antibody was employed. When this \nstudy was extended to immunohistochemical analysis a similar pattern of \nexpression was observed i.e. several nmt/p54nrb positive tumors were not detected with the NMT-4 antibody supporting the presence of N-terminal \ntruncated isoforms. \nThese data provide further insight into the expression of a protein with a \npotential role as a marker of breast cancer phenotype. In order to confirm \nthese preliminary findings a more extensive study on a large cohort of \npatients with accompanying detailed clinicopathologic data including significant follow-up will be required. Until these data and further information on the function and regulation of this gene product are \navailable the full implication of the current dataset remain unknown and \nthus several aspects of the Discussion are highly speculative e.g. relationships with known prognostic factors and its role in cell growth. \nThe manuscript could be improved by: \n1. Providing more detail on the number and characteristics of the breast \ncancers understudy i.e. primary or metastatic, total number of tumours \nanalysed by the different methodologies, clinicopathological parameters of \nthe group and are they representative of the population from which they \nwere collected \n2. Shortening of the Discussion. \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-13
|
Reviewed - bmc_cancer
|
Reviewer's□report
□Comparison□of□two□methods□based□on□cross-sectional□data□for□correcting□corpus□uterine□cancer□ Title:
incidence□and□probabilities
Authors:
Ray□M□Merrill□( [email protected] )
Joseph□L□Lyon□( [email protected] )
Charles□Wiggins□( [email protected] )
□2□ □8□Aug□2001 Version: Date:
□Dr□Michael□Murphy Reviewer:
□A□paper□of□limited□interest Level□of□interest:
□Accept□without□revision Advice□on□publication:
This□paper□compares□two□methods□of□expressing□the□burden□of□corpus□uterine□cancer□in□relation□to□the□
true□population□at□risk□(ie□in□particular,□excluding□women□without□a□uterus□because□of□hysterectomy).□The
authors□have□reported□on□this□general□topic□before□and□this□study□presents□a□further□minor□development□
of□their□method.□I□have□few□criticisms□of□their□paper□except□that□I□am□not□convinced□of□the□practical□value□
or□the□theoretical□desirability□of□excluding□women□who□have□already□been□diagnosed□with□uterine□cancer□
from□the□denominator,□irrespective□of□whether□they□had□a□hysterectomy.□
As□the□authors□point□out,□similar□methods□can□be□used□to□estimate□the□true□population□at□risk□of□other□
cancers□of□the□female□genital□tract,□such□as□cervix.□I□believe□that□this□application□is□particularly□important□
when□assessing□the□effects□of□screening□programmes□on□timetrends□in□the□occurrence□of□disease□(as□
we□have□recently□done□for□Britain□:□Redburn□and□Murphy□in□Br□J□Obstet□&□Gynaecology□
2001;108:388-95).□
The□use□of□operation□rate□data□to□calculate□cumulative□lifetime□risk□of□being□without□an□organ□has□quite□a□
long□history,□and□is□not□confined□to□hysterectomy.□The□Oxford□Record□Linkage□Study□reported□on□e.g.□the
chance□of□losing□your□gallbladder□or□appendix□nearly□40□years□ago.□Although□few□operations□are□as□
common□(in□the□USA□or□elsewhere)□as□hysterectomy,□the□use□of□the□methods□proposed□by□the□authors□
for□calculating□other□types□of□organ□removal□cumulatively□should□be□valid□and□potentially□also□of□interest.□
Mike□Murphy□
Competing□interests:
None□declared.
|
Reviewer's□report
□Comparison□of□two□methods□based□on□cross-sectional□data□for□correcting□corpus□uterine□cancer□ Title:
incidence□and□probabilities
Authors:
Ray□M□Merrill□( [email protected] )
Joseph□L□Lyon□( [email protected] )
Charles□Wiggins□( [email protected] )
□2□ □8□Aug□2001 Version: Date:
□Dr□Michael□Murphy Reviewer:
□A□paper□of□limited□interest Level□of□interest:
□Accept□without□revision Advice□on□publication:
This□paper□compares□two□methods□of□expressing□the□burden□of□corpus□uterine□cancer□in□relation□to□the□
true□population□at□risk□(ie□in□particular,□excluding□women□without□a□uterus□because□of□hysterectomy).□The
authors□have□reported□on□this□general□topic□before□and□this□study□presents□a□further□minor□development□
of□their□method.□I□have□few□criticisms□of□their□paper□except□that□I□am□not□convinced□of□the□practical□value□
or□the□theoretical□desirability□of□excluding□women□who□have□already□been□diagnosed□with□uterine□cancer□
from□the□denominator,□irrespective□of□whether□they□had□a□hysterectomy.□
As□the□authors□point□out,□similar□methods□can□be□used□to□estimate□the□true□population□at□risk□of□other□
cancers□of□the□female□genital□tract,□such□as□cervix.□I□believe□that□this□application□is□particularly□important□
when□assessing□the□effects□of□screening□programmes□on□timetrends□in□the□occurrence□of□disease□(as□
we□have□recently□done□for□Britain□:□Redburn□and□Murphy□in□Br□J□Obstet□&□Gynaecology□
2001;108:388-95).□
The□use□of□operation□rate□data□to□calculate□cumulative□lifetime□risk□of□being□without□an□organ□has□quite□a□
long□history,□and□is□not□confined□to□hysterectomy.□The□Oxford□Record□Linkage□Study□reported□on□e.g.□the
chance□of□losing□your□gallbladder□or□appendix□nearly□40□years□ago.□Although□few□operations□are□as□
common□(in□the□USA□or□elsewhere)□as□hysterectomy,□the□use□of□the□methods□proposed□by□the□authors□
for□calculating□other□types□of□organ□removal□cumulatively□should□be□valid□and□potentially□also□of□interest.□
Mike□Murphy□
Competing□interests:
None□declared.
|
BMC
|
12885_2001_13_ReviewerReport_V2_R1.pdf
|
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"criticism": 0,
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's□report \n□Comparison□of□two□methods□based□on□cross-sectional□data□for□correcting□corpus□uterine□cancer□ Title: \nincidence□and□probabilities \nAuthors: \nRay□M□Merrill□( [email protected] )\nJoseph□L□Lyon□( [email protected] )\nCharles□Wiggins□( [email protected] )\n□2□ □8□Aug□2001 Version: Date: \n□Dr□Michael□Murphy Reviewer: \n□A□paper□of□limited□interest Level□of□interest: \n□Accept□without□revision Advice□on□publication: \nThis□paper□compares□two□methods□of□expressing□the□burden□of□corpus□uterine□cancer□in□relation□to□the□ \ntrue□population□at□risk□(ie□in□particular,□excluding□women□without□a□uterus□because□of□hysterectomy).□The \nauthors□have□reported□on□this□general□topic□before□and□this□study□presents□a□further□minor□development□ \nof□their□method.□I□have□few□criticisms□of□their□paper□except□that□I□am□not□convinced□of□the□practical□value□ \nor□the□theoretical□desirability□of□excluding□women□who□have□already□been□diagnosed□with□uterine□cancer□ \nfrom□the□denominator,□irrespective□of□whether□they□had□a□hysterectomy.□ \nAs□the□authors□point□out,□similar□methods□can□be□used□to□estimate□the□true□population□at□risk□of□other□ \ncancers□of□the□female□genital□tract,□such□as□cervix.□I□believe□that□this□application□is□particularly□important□ \nwhen□assessing□the□effects□of□screening□programmes□on□timetrends□in□the□occurrence□of□disease□(as□ \nwe□have□recently□done□for□Britain□:□Redburn□and□Murphy□in□Br□J□Obstet□&□Gynaecology□ \n2001;108:388-95).□ \nThe□use□of□operation□rate□data□to□calculate□cumulative□lifetime□risk□of□being□without□an□organ□has□quite□a□ \nlong□history,□and□is□not□confined□to□hysterectomy.□The□Oxford□Record□Linkage□Study□reported□on□e.g.□the \nchance□of□losing□your□gallbladder□or□appendix□nearly□40□years□ago.□Although□few□operations□are□as□ \ncommon□(in□the□USA□or□elsewhere)□as□hysterectomy,□the□use□of□the□methods□proposed□by□the□authors□ \nfor□calculating□other□types□of□organ□removal□cumulatively□should□be□valid□and□potentially□also□of□interest.□ \nMike□Murphy□ \nCompeting□interests: \nNone□declared. ",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-13
|
Reviewed - bmc_cancer
|
Reviewer's report
Comparison of two methods based on cross-sectional data for correcting corpus uterine cancer Title:
incidence and probabilities
Authors:
Ray M Merrill ([email protected] )
Joseph L Lyon ([email protected] )
Charles Wiggins ([email protected] )
2 8 Aug 2001 Version: Date:
Dr Riitta Luoto Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
Major comments:
Merrill et al study is an interesting and important piece of study based on long experience of the topic.
Methods and groups compared in the study are appropriate, although longer data from Hospital
Discharge Register might have revealed more changes in trends of hysterectomy. Minor changes are
needed to the text and figures.
Minor comments:
1. Running head of the study could be more descriptive- corrected rates does not clarify the findings of
this article.
2. Page 6, 3rd paragraph, reference 19 may be erroneous twice in this page.
3. In Figure 3, bars do not separate clearly- please clarify.
4. In page 11, the recommendation of the methods for countries which do not have much data available
could even be mentioned in the abstract.
5. Page 11, second paragraph: The discrepancy in Utah hysterectomy trends stays unresolved, please
discuss possible cohort effects etc. further. Survey methods of hysterectomy self-reports have been
published earlier- results have shown high validity of self-reports- please refer this study by Coulter et al.
6. Page 12, 3rd paragraph, 6th line a typing error in hysterectomy.
7. Figure 5 could be deleted since the information is in the text. Additionally, you could calculate
probability also for women over 50 years only- since the percentages may give an underestimated impression to health policy officials.
8. Please add as a table absolute numbers of hysterectomies from Hospital Discharge Data to describe
the changes in trends in other ways than proportions only.
Competing interests:
None declared.
|
Reviewer's report
Comparison of two methods based on cross-sectional data for correcting corpus uterine cancer Title:
incidence and probabilities
Authors:
Ray M Merrill ([email protected] )
Joseph L Lyon ([email protected] )
Charles Wiggins ([email protected] )
2 8 Aug 2001 Version: Date:
Dr Riitta Luoto Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
Major comments:
Merrill et al study is an interesting and important piece of study based on long experience of the topic.
Methods and groups compared in the study are appropriate, although longer data from Hospital
Discharge Register might have revealed more changes in trends of hysterectomy. Minor changes are
needed to the text and figures.
Minor comments:
1. Running head of the study could be more descriptive- corrected rates does not clarify the findings of
this article.
2. Page 6, 3rd paragraph, reference 19 may be erroneous twice in this page.
3. In Figure 3, bars do not separate clearly- please clarify.
4. In page 11, the recommendation of the methods for countries which do not have much data available
could even be mentioned in the abstract.
5. Page 11, second paragraph: The discrepancy in Utah hysterectomy trends stays unresolved, please
discuss possible cohort effects etc. further. Survey methods of hysterectomy self-reports have been
published earlier- results have shown high validity of self-reports- please refer this study by Coulter et al.
6. Page 12, 3rd paragraph, 6th line a typing error in hysterectomy.
7. Figure 5 could be deleted since the information is in the text. Additionally, you could calculate
probability also for women over 50 years only- since the percentages may give an underestimated impression to health policy officials.
8. Please add as a table absolute numbers of hysterectomies from Hospital Discharge Data to describe
the changes in trends in other ways than proportions only.
Competing interests:
None declared.
|
BMC
|
12885_2001_13_ReviewerReport_V2_R2.pdf
|
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"example": 5,
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"materials_and_methods": 6,
"praise": 2,
"presentation_and_reporting": 10,
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"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Comparison of two methods based on cross-sectional data for correcting corpus uterine cancer Title:\nincidence and probabilities\nAuthors:\nRay M Merrill ([email protected] )\nJoseph L Lyon ([email protected] )\nCharles Wiggins ([email protected] )\n 2 8 Aug 2001 Version: Date:\n Dr Riitta Luoto Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Accept after revision, which I do not need to see Advice on publication:\nMajor comments: \nMerrill et al study is an interesting and important piece of study based on long experience of the topic. \nMethods and groups compared in the study are appropriate, although longer data from Hospital \nDischarge Register might have revealed more changes in trends of hysterectomy. Minor changes are \nneeded to the text and figures. \nMinor comments: \n1. Running head of the study could be more descriptive- corrected rates does not clarify the findings of \nthis article. \n2. Page 6, 3rd paragraph, reference 19 may be erroneous twice in this page. \n3. In Figure 3, bars do not separate clearly- please clarify. \n4. In page 11, the recommendation of the methods for countries which do not have much data available \ncould even be mentioned in the abstract. \n5. Page 11, second paragraph: The discrepancy in Utah hysterectomy trends stays unresolved, please \ndiscuss possible cohort effects etc. further. Survey methods of hysterectomy self-reports have been \npublished earlier- results have shown high validity of self-reports- please refer this study by Coulter et al.\n6. Page 12, 3rd paragraph, 6th line a typing error in hysterectomy. \n7. Figure 5 could be deleted since the information is in the text. Additionally, you could calculate \nprobability also for women over 50 years only- since the percentages may give an underestimated impression to health policy officials. \n8. Please add as a table absolute numbers of hysterectomies from Hospital Discharge Data to describe \nthe changes in trends in other ways than proportions only. \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-12
|
Reviewed - bmc_cancer
|
Reviewer's report
Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:
Authors:
Luciano Mastronardi MD, PhD ([email protected] )
Antonio Guiducci MD ([email protected] )
Fabrizio Puzzilli MD ([email protected] )
1 5 Jun 2001 Version: Date:
Dr Regina Gandour-Edwards Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
This is a useful report on a challenging clinical problem, i.e. invasive pituitary adenomas. While,the
authors report no correlation between proliferation index, as measured by immunohistochemistry for
Ki-67, and tumor volume there was a difference in proliferation between invasive and non-invasive adenomas. The difference was not statistically significant but may reflect tumor biology and aggressiveness.
The study was well designed and analyzed and I recommend publication with some suggestions listed
below.
Comments
--------------------
Major suggestions: The report would be strengthened by radiologic images of
the different size/volume characteristics of the adenomas. I also recommend
a photograph of a histologic section stained with Ki-67.
Minor suggestions:
In the abstract, the authors refer to Ki-67 as a marker of tumoral
proliferation. It is indeed a marker of cell proliferation, normal and abnormal. There are scattered minor phrasing and spelling errors.
Competing interests:
None declared.
|
Reviewer's report
Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:
Authors:
Luciano Mastronardi MD, PhD ([email protected] )
Antonio Guiducci MD ([email protected] )
Fabrizio Puzzilli MD ([email protected] )
1 5 Jun 2001 Version: Date:
Dr Regina Gandour-Edwards Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
This is a useful report on a challenging clinical problem, i.e. invasive pituitary adenomas. While,the
authors report no correlation between proliferation index, as measured by immunohistochemistry for
Ki-67, and tumor volume there was a difference in proliferation between invasive and non-invasive adenomas. The difference was not statistically significant but may reflect tumor biology and aggressiveness.
The study was well designed and analyzed and I recommend publication with some suggestions listed
below.
Comments
--------------------
Major suggestions: The report would be strengthened by radiologic images of
the different size/volume characteristics of the adenomas. I also recommend
a photograph of a histologic section stained with Ki-67.
Minor suggestions:
In the abstract, the authors refer to Ki-67 as a marker of tumoral
proliferation. It is indeed a marker of cell proliferation, normal and abnormal. There are scattered minor phrasing and spelling errors.
Competing interests:
None declared.
|
BMC
|
12885_2001_12_ReviewerReport_V1_R1.pdf
|
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"importance_and_relevance": 1,
"materials_and_methods": 4,
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:\nAuthors:\nLuciano Mastronardi MD, PhD ([email protected] )\nAntonio Guiducci MD ([email protected] )\nFabrizio Puzzilli MD ([email protected] )\n 1 5 Jun 2001 Version: Date:\n Dr Regina Gandour-Edwards Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Accept after revision, which I do not need to see Advice on publication:\nThis is a useful report on a challenging clinical problem, i.e. invasive pituitary adenomas. While,the \nauthors report no correlation between proliferation index, as measured by immunohistochemistry for \nKi-67, and tumor volume there was a difference in proliferation between invasive and non-invasive adenomas. The difference was not statistically significant but may reflect tumor biology and aggressiveness. \nThe study was well designed and analyzed and I recommend publication with some suggestions listed \nbelow. \nComments \n-------------------- \nMajor suggestions: The report would be strengthened by radiologic images of \nthe different size/volume characteristics of the adenomas. I also recommend \na photograph of a histologic section stained with Ki-67. \nMinor suggestions: \nIn the abstract, the authors refer to Ki-67 as a marker of tumoral \nproliferation. It is indeed a marker of cell proliferation, normal and abnormal. There are scattered minor phrasing and spelling errors.\nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-12
|
Reviewed - bmc_cancer
|
Reviewer's report
Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:
Authors:
Luciano Mastronardi MD, PhD ([email protected] )
Antonio Guiducci MD ([email protected] )
Fabrizio Puzzilli MD ([email protected] )
1 27 Jun 2001 Version: Date:
Dr Marco Losa Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
In this study Mastronardi and coworkers report on the lack of correlation between Ki-67 labeling index
and volume (size indeed, see below) of anterior pituitary adenomas. At present there is controversy
about the clinical utility of assessing the Ki-67 LI in pituitary adenomas. The results of this study could be, then, of interest for all researchers in the field. The number of tumors studied is reasonably large. Moreover, tumor specimens were collected consecutively in a 5-year period, thus avoiding selection
bias.
However, the analysis of the data is, in my opinion, not convincing and I am, therefore, uncertain
whether the conclusions drawn by the authors are correct.
MAJOR CONCERNS
1) The principal variable investigated in the study is the Ki-67 LI, that is the percentage of cells showing
a positive staining with the MIB-1 monoclonal antibody. In my experience, this variable is not normally
distributed, at least in pituitary adenomas. The authors did not assess this point, but did use statistical tests, such as ANOVA, which require as a conditio sine qua non the normal distribution of the continuous variable. Looking at the results of Ki-67 LI, I strongly suspect that also in this series of
pituitary adenomas the Ki-67 LI was not normally distributed. In fact, there seems to be a large
dispersion of the data as suggested by the wide range of Ki-67 LI and the lack of reasonable correspondence between mean value and median. The authors should verify the assumption that Ki-67
LI values were normally distributed using an accepted statistical test. If the results confirm my suspicion,
all the analyses should be repeated either after log-transformation of the data or by implementing
nonparametric tests.
2) The data of all tumors are put together and then analyzed with respect to tumor size, invasiveness,
infiltration and so on. However, the different types of pituitary adenomas (GH-, PRL- ACTH- and
TSH-secreting and nonfunctioning adenomas) may intrinsically have different proliferation rates. I am particularly concerned because ACTH-secreting adenomas, which usually are microadenomas, seems
to have a higher proliferation index than other types of pituitary adenomas. In a previous paper (Losa et
al., Am J Pathol, 156:245-251, 2000) the mean Ki-67 LI in 51 ACTH-secreting adenomas was 4.7 +/-
1.0%. This value is higher than the average values (about 2.5%) we found in other series of
nonfunctioning and GH-secreting adenomas. Other authors also suggest that ACTH-secreting
adenomas have a higher proliferation index than the other types of adenoma (Shibuya et al, Acta
Neuropathol, 84:178-183, 1992; Landolt and, Shibata in: Pituitary Adenomas. New Trends in Basic and Clinical Research. Amsterdam: Excerpta Medica, 1991: 169-178). The problem of the possible interaction between tumor type, Ki-67 LI and the other variables, such as tumor size, can be overcome
by performing a multivariate analysis.
3) It is stated (pag. 4, lines 20-21) that 20 of 29 PRL-secreting tumors received preoperative medical
therapy with bromocriptine. In a previous study (Landolt et al. in Advances in Pituitary Adenoma
Research. Oxford: Pergamon Press, 1988: 53-62) it has been demonstrated that treated prolactinomas
had a lower Ki-67 LI than untreated ones. Similar observations have been reported in GH-secreting adenomas treated with somatostatin analogs and it is unclear whether acromegalic patients in the present study had been treated with drugs or not before surgery. Lastly, 21 or 23 patients had been
operated before. If second operation was performed because of tumor recurrence, it is hardly justifiable
to put both recurring and not recurring adenomas together. Again, history of previous treatment should
be controlled for in the statistical analysis and not completely ignored.
MINOR CONCERNS
1) The term "volume" referred to the pituitary adenomas in this paper is incorrect. What the authors
measured and report is tumor size.
2) Classification of tumor size (page 4, lines 4-9) should be simplified. It would be better to distinguish
separately micro- from macroadenomas and invasive (into the cavernous sinus) from not invasive
tumors. With less categories, statistical analysis would be simplified. Moreover, it should be stated how
many patients had a MRI and how many a CT scan. The latter technique is less precise in assessing cavernous sinus invasion.
3) The authors refer to surgically verified infiltration of dura or bone as "invasion". This is confusing
because usually invasiveness is related to the neuroradiological or intraoperative demonstration of involvement of the cavernous sinus or sphenoid sinus. I would prefer the words "infiltrating" and "not infiltrating".
4) Among the secreting tumors the authors describe one single FSH-secreting adenoma. The criterion
of this classification is not given. However, the percentage of endocrine-inactive adenomas shown at
immunocytochemistry to contain gonadotropins or their subunits is much higher, approaching 50-60% in
some series. The discrepancy between the authors' data and those of the literature must be clarified.
5) The first sentence of the Results details the mortality and morbidity of this surgical series. This is
irrelevant to the topic of the paper and should be deleted.
6) The first part of the discussion describes the radiological classification proposed several years ago by
Jules Hardy. As the authors did not follow this classification, I suggest to shorten or delete this part.
7) In the conclusion the authors state that "evaluation of the growth fraction......gives further information
about the infiltrative behaviour of pituitary adenomas and, thus, about the risk of recurrence". This
seems an unwarranted conclusion. In fact the authors do not report any data correlating the Ki-67 LI and
risk of recurrence of the pituitary tumors. If they are referring, as I suppose, to data in the literature, they
should thoroughly discuss this topic in the discussion and should not ignore other papers that did not
find the supposed correlation between Ki-67 LI and the risk of recurrence.
8) There are several grammatical errors throughout the paper.
Competing interests:
None declared.
|
Reviewer's report
Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:
Authors:
Luciano Mastronardi MD, PhD ([email protected] )
Antonio Guiducci MD ([email protected] )
Fabrizio Puzzilli MD ([email protected] )
1 27 Jun 2001 Version: Date:
Dr Marco Losa Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Unable to decide on acceptance or rejection until I see revised version Advice on publication:
In this study Mastronardi and coworkers report on the lack of correlation between Ki-67 labeling index
and volume (size indeed, see below) of anterior pituitary adenomas. At present there is controversy
about the clinical utility of assessing the Ki-67 LI in pituitary adenomas. The results of this study could be, then, of interest for all researchers in the field. The number of tumors studied is reasonably large. Moreover, tumor specimens were collected consecutively in a 5-year period, thus avoiding selection
bias.
However, the analysis of the data is, in my opinion, not convincing and I am, therefore, uncertain
whether the conclusions drawn by the authors are correct.
MAJOR CONCERNS
1) The principal variable investigated in the study is the Ki-67 LI, that is the percentage of cells showing
a positive staining with the MIB-1 monoclonal antibody. In my experience, this variable is not normally
distributed, at least in pituitary adenomas. The authors did not assess this point, but did use statistical tests, such as ANOVA, which require as a conditio sine qua non the normal distribution of the continuous variable. Looking at the results of Ki-67 LI, I strongly suspect that also in this series of
pituitary adenomas the Ki-67 LI was not normally distributed. In fact, there seems to be a large
dispersion of the data as suggested by the wide range of Ki-67 LI and the lack of reasonable correspondence between mean value and median. The authors should verify the assumption that Ki-67
LI values were normally distributed using an accepted statistical test. If the results confirm my suspicion,
all the analyses should be repeated either after log-transformation of the data or by implementing
nonparametric tests.
2) The data of all tumors are put together and then analyzed with respect to tumor size, invasiveness,
infiltration and so on. However, the different types of pituitary adenomas (GH-, PRL- ACTH- and
TSH-secreting and nonfunctioning adenomas) may intrinsically have different proliferation rates. I am particularly concerned because ACTH-secreting adenomas, which usually are microadenomas, seems
to have a higher proliferation index than other types of pituitary adenomas. In a previous paper (Losa et
al., Am J Pathol, 156:245-251, 2000) the mean Ki-67 LI in 51 ACTH-secreting adenomas was 4.7 +/-
1.0%. This value is higher than the average values (about 2.5%) we found in other series of
nonfunctioning and GH-secreting adenomas. Other authors also suggest that ACTH-secreting
adenomas have a higher proliferation index than the other types of adenoma (Shibuya et al, Acta
Neuropathol, 84:178-183, 1992; Landolt and, Shibata in: Pituitary Adenomas. New Trends in Basic and Clinical Research. Amsterdam: Excerpta Medica, 1991: 169-178). The problem of the possible interaction between tumor type, Ki-67 LI and the other variables, such as tumor size, can be overcome
by performing a multivariate analysis.
3) It is stated (pag. 4, lines 20-21) that 20 of 29 PRL-secreting tumors received preoperative medical
therapy with bromocriptine. In a previous study (Landolt et al. in Advances in Pituitary Adenoma
Research. Oxford: Pergamon Press, 1988: 53-62) it has been demonstrated that treated prolactinomas
had a lower Ki-67 LI than untreated ones. Similar observations have been reported in GH-secreting adenomas treated with somatostatin analogs and it is unclear whether acromegalic patients in the present study had been treated with drugs or not before surgery. Lastly, 21 or 23 patients had been
operated before. If second operation was performed because of tumor recurrence, it is hardly justifiable
to put both recurring and not recurring adenomas together. Again, history of previous treatment should
be controlled for in the statistical analysis and not completely ignored.
MINOR CONCERNS
1) The term "volume" referred to the pituitary adenomas in this paper is incorrect. What the authors
measured and report is tumor size.
2) Classification of tumor size (page 4, lines 4-9) should be simplified. It would be better to distinguish
separately micro- from macroadenomas and invasive (into the cavernous sinus) from not invasive
tumors. With less categories, statistical analysis would be simplified. Moreover, it should be stated how
many patients had a MRI and how many a CT scan. The latter technique is less precise in assessing cavernous sinus invasion.
3) The authors refer to surgically verified infiltration of dura or bone as "invasion". This is confusing
because usually invasiveness is related to the neuroradiological or intraoperative demonstration of involvement of the cavernous sinus or sphenoid sinus. I would prefer the words "infiltrating" and "not infiltrating".
4) Among the secreting tumors the authors describe one single FSH-secreting adenoma. The criterion
of this classification is not given. However, the percentage of endocrine-inactive adenomas shown at
immunocytochemistry to contain gonadotropins or their subunits is much higher, approaching 50-60% in
some series. The discrepancy between the authors' data and those of the literature must be clarified.
5) The first sentence of the Results details the mortality and morbidity of this surgical series. This is
irrelevant to the topic of the paper and should be deleted.
6) The first part of the discussion describes the radiological classification proposed several years ago by
Jules Hardy. As the authors did not follow this classification, I suggest to shorten or delete this part.
7) In the conclusion the authors state that "evaluation of the growth fraction......gives further information
about the infiltrative behaviour of pituitary adenomas and, thus, about the risk of recurrence". This
seems an unwarranted conclusion. In fact the authors do not report any data correlating the Ki-67 LI and
risk of recurrence of the pituitary tumors. If they are referring, as I suppose, to data in the literature, they
should thoroughly discuss this topic in the discussion and should not ignore other papers that did not
find the supposed correlation between Ki-67 LI and the risk of recurrence.
8) There are several grammatical errors throughout the paper.
Competing interests:
None declared.
|
BMC
|
12885_2001_12_ReviewerReport_V1_R2.pdf
|
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"content": "Please review this paper.",
"role": "user"
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"content": "Reviewer's report\n Lack of correlation between Ki-67 labelling index and volume of anterior pituitary adenomas. Title:\nAuthors:\nLuciano Mastronardi MD, PhD ([email protected] )\nAntonio Guiducci MD ([email protected] )\nFabrizio Puzzilli MD ([email protected] )\n 1 27 Jun 2001 Version: Date:\n Dr Marco Losa Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Unable to decide on acceptance or rejection until I see revised version Advice on publication:\nIn this study Mastronardi and coworkers report on the lack of correlation between Ki-67 labeling index \nand volume (size indeed, see below) of anterior pituitary adenomas. At present there is controversy \nabout the clinical utility of assessing the Ki-67 LI in pituitary adenomas. The results of this study could be, then, of interest for all researchers in the field. The number of tumors studied is reasonably large. Moreover, tumor specimens were collected consecutively in a 5-year period, thus avoiding selection \nbias. \nHowever, the analysis of the data is, in my opinion, not convincing and I am, therefore, uncertain \nwhether the conclusions drawn by the authors are correct. \nMAJOR CONCERNS \n1) The principal variable investigated in the study is the Ki-67 LI, that is the percentage of cells showing \na positive staining with the MIB-1 monoclonal antibody. In my experience, this variable is not normally \ndistributed, at least in pituitary adenomas. The authors did not assess this point, but did use statistical tests, such as ANOVA, which require as a conditio sine qua non the normal distribution of the continuous variable. Looking at the results of Ki-67 LI, I strongly suspect that also in this series of \npituitary adenomas the Ki-67 LI was not normally distributed. In fact, there seems to be a large \ndispersion of the data as suggested by the wide range of Ki-67 LI and the lack of reasonable correspondence between mean value and median. The authors should verify the assumption that Ki-67 \nLI values were normally distributed using an accepted statistical test. If the results confirm my suspicion,\nall the analyses should be repeated either after log-transformation of the data or by implementing \nnonparametric tests. \n2) The data of all tumors are put together and then analyzed with respect to tumor size, invasiveness, \ninfiltration and so on. However, the different types of pituitary adenomas (GH-, PRL- ACTH- and \nTSH-secreting and nonfunctioning adenomas) may intrinsically have different proliferation rates. I am particularly concerned because ACTH-secreting adenomas, which usually are microadenomas, seems \nto have a higher proliferation index than other types of pituitary adenomas. In a previous paper (Losa et \nal., Am J Pathol, 156:245-251, 2000) the mean Ki-67 LI in 51 ACTH-secreting adenomas was 4.7 +/- \n1.0%. This value is higher than the average values (about 2.5%) we found in other series of \nnonfunctioning and GH-secreting adenomas. Other authors also suggest that ACTH-secreting \nadenomas have a higher proliferation index than the other types of adenoma (Shibuya et al, Acta \nNeuropathol, 84:178-183, 1992; Landolt and, Shibata in: Pituitary Adenomas. New Trends in Basic and Clinical Research. Amsterdam: Excerpta Medica, 1991: 169-178). The problem of the possible interaction between tumor type, Ki-67 LI and the other variables, such as tumor size, can be overcome \nby performing a multivariate analysis. \n3) It is stated (pag. 4, lines 20-21) that 20 of 29 PRL-secreting tumors received preoperative medical \ntherapy with bromocriptine. In a previous study (Landolt et al. in Advances in Pituitary Adenoma \nResearch. Oxford: Pergamon Press, 1988: 53-62) it has been demonstrated that treated prolactinomas \nhad a lower Ki-67 LI than untreated ones. Similar observations have been reported in GH-secreting adenomas treated with somatostatin analogs and it is unclear whether acromegalic patients in the present study had been treated with drugs or not before surgery. Lastly, 21 or 23 patients had been \noperated before. If second operation was performed because of tumor recurrence, it is hardly justifiable \nto put both recurring and not recurring adenomas together. Again, history of previous treatment should \nbe controlled for in the statistical analysis and not completely ignored. \nMINOR CONCERNS \n1) The term \"volume\" referred to the pituitary adenomas in this paper is incorrect. What the authors \nmeasured and report is tumor size. \n2) Classification of tumor size (page 4, lines 4-9) should be simplified. It would be better to distinguish \nseparately micro- from macroadenomas and invasive (into the cavernous sinus) from not invasive \ntumors. With less categories, statistical analysis would be simplified. Moreover, it should be stated how \nmany patients had a MRI and how many a CT scan. The latter technique is less precise in assessing cavernous sinus invasion. \n3) The authors refer to surgically verified infiltration of dura or bone as \"invasion\". This is confusing \nbecause usually invasiveness is related to the neuroradiological or intraoperative demonstration of involvement of the cavernous sinus or sphenoid sinus. I would prefer the words \"infiltrating\" and \"not infiltrating\". \n4) Among the secreting tumors the authors describe one single FSH-secreting adenoma. The criterion \nof this classification is not given. However, the percentage of endocrine-inactive adenomas shown at \nimmunocytochemistry to contain gonadotropins or their subunits is much higher, approaching 50-60% in\nsome series. The discrepancy between the authors' data and those of the literature must be clarified. \n5) The first sentence of the Results details the mortality and morbidity of this surgical series. This is \nirrelevant to the topic of the paper and should be deleted. \n6) The first part of the discussion describes the radiological classification proposed several years ago by\nJules Hardy. As the authors did not follow this classification, I suggest to shorten or delete this part. \n7) In the conclusion the authors state that \"evaluation of the growth fraction......gives further information \nabout the infiltrative behaviour of pituitary adenomas and, thus, about the risk of recurrence\". This \nseems an unwarranted conclusion. In fact the authors do not report any data correlating the Ki-67 LI and\nrisk of recurrence of the pituitary tumors. If they are referring, as I suppose, to data in the literature, they \nshould thoroughly discuss this topic in the discussion and should not ignore other papers that did not \nfind the supposed correlation between Ki-67 LI and the risk of recurrence. \n8) There are several grammatical errors throughout the paper. \nCompeting interests:\nNone declared.",
"role": "assistant"
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] | 2,001
|
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0
| 0
|
Review for 10.1186/1471-2407-1-12
|
Reviewed - bmc_cancer
|
Reviewer's□report
□Lack□of□correlation□between□Ki-67□labelling□index□and□volume□of□anterior□pituitary□adenomas.□ Title:
Authors:
Luciano□Mastronardi□MD,□PhD□( [email protected] )
Antonio□Guiducci□MD□( [email protected] )
Fabrizio□Puzzilli□MD□( [email protected] )
□2□ □3□Aug□2001 Version: Date:
□Dr□Marco□Losa Reviewer:
□A□paper□whose□findings□are□important□to□those□with□closely□related□research□interests Level□of□interest:
□Other□(see□below) Advice□on□publication:
In□this□study□Mastronardi□and□coworkers□report□on□the□lack□of□correlation□between□Ki-67□labeling□index□
and□size□of□anterior□pituitary□adenomas□in□a□series□of□121□consecutively□operated□patients.□This□finding□
may□have□interesting□pathophysiological□implications□as□it□suggests□that□the□proliferative□activity□may□not be□the□most□important□factor□in□determining□the□size□of□pituitary□adenomas.□The□authors□postulate□that□ the□time□elapsed□from□tumoral□transformation□to□diagnosis□might□be□the□critical□factor□in□determining□
tumor□size,□but□still□other□factors,□such□as□the□fraction□of□cell□loss□due□to□apoptosis□and□necrosis,□might□
be□of□relevance.□
However,□before□we□accept□the□conclusion□that□the□proliferation□rate□of□pituitary□adenomas□is□not□
correlated□with□tumor□size,□we□need□to□consider□important□drawbacks□in□the□study□by□Mastronardi□and□
coworkers.□ The□results□of□tumors□with□different□endocrine□activity□have□been□analyzed□together□on□the□assumption□ that□the□different□histotype□has□no□independent□effect□on□the□Ki-67□LI.□However,□this□assumption□is□still□
unproven,□at□least□in□the□case□of□ACTH-secreting□adenomas,□which□have□been□shown□in□some□studies□
to□have□a□higher□Ki-67□LI□than□the□other□types□of□pituitary□adenomas□(Shibuya□et□al,□Acta□Neuropathol,□ 84:178-183,□1992;□Landolt□and,□Shibata□in:□Pituitary□Adenomas.□New□Trends□in□Basic□and□Clinical□
Research.□Amsterdam:□Excerpta□Medica,□1991:□169-178).□Therefore,□an□imbalance□in□the□distribution□of□
micro-□and□macroadenomas□among□the□different□types□of□pituitary□adenomas,□would□obscure□a□possible□
relationship□between□Ki-67□LI□and□tumor□size.□Indeed,□in□a□previous□paper□(Losa□et□al.,□Am□J□Pathol,□
156:245-251,□2000)□we□found□that□in□a□homogeneous□population□of□patients□with□Cushing's□disease□the□ Ki-67□LI□was□significantly□higher□in□macroadenomas□than□in□microadenomas□and□that□there□was□a□
significant□correlation□between□maximum□tumor□diameter□and□Ki-67□LI,□just□the□opposite□findings□of□
Mastronardi□and□coworkers.□A□multivariate□analysis□taking□into□account□the□endocrine□activity□of□the□ tumor□would□have□been□useful.□
Another□drawback□is□the□inclusion□of□patients□with□PRL-secreting□adenomas□previously□treated□with□
dopaminergic□drugs.□We□are□not□given□information□whether□the□drug□was□stopped□months□before□or□
continued□until□surgery.□In□a□previous□study□(Landolt□et□al.□in□Advances□in□Pituitary□Adenoma□Research.□ Oxford:□Pergamon□Press,□1988:□53-62)□it□has□been□demonstrated□that□treated□prolactinomas□had□a□ lower□Ki-67□LI□than□untreated□ones.□Again,□an□imbalance□in□the□distribution□of□micro-□and□
macroadenomas□among□patients□who□received□dopaminergic□drugs,□would□bias□the□analysis□performed□
by□the□authors.□A□similar□reasoning□can□also□be□done□for□the□inclusion□of□patients□with□recurrent□tumors.□
Again,□more□sophisticated□statistical□methods□to□control□for□imbalances□in□the□study□population□would□
have□been□more□appropriate.□
The□mechanisms□controlling□tumor□growth□in□pituitary□adenomas□are□still□partially□unknown.□The□paper□
by□Mastronardi□and□coworkers□represents□another□piece□of□knowledge□in□this□fascinating□field□of□
research.□
Competing□interests:
None□declared.
|
Reviewer's□report
□Lack□of□correlation□between□Ki-67□labelling□index□and□volume□of□anterior□pituitary□adenomas.□ Title:
Authors:
Luciano□Mastronardi□MD,□PhD□( [email protected] )
Antonio□Guiducci□MD□( [email protected] )
Fabrizio□Puzzilli□MD□( [email protected] )
□2□ □3□Aug□2001 Version: Date:
□Dr□Marco□Losa Reviewer:
□A□paper□whose□findings□are□important□to□those□with□closely□related□research□interests Level□of□interest:
□Other□(see□below) Advice□on□publication:
In□this□study□Mastronardi□and□coworkers□report□on□the□lack□of□correlation□between□Ki-67□labeling□index□
and□size□of□anterior□pituitary□adenomas□in□a□series□of□121□consecutively□operated□patients.□This□finding□
may□have□interesting□pathophysiological□implications□as□it□suggests□that□the□proliferative□activity□may□not be□the□most□important□factor□in□determining□the□size□of□pituitary□adenomas.□The□authors□postulate□that□ the□time□elapsed□from□tumoral□transformation□to□diagnosis□might□be□the□critical□factor□in□determining□
tumor□size,□but□still□other□factors,□such□as□the□fraction□of□cell□loss□due□to□apoptosis□and□necrosis,□might□
be□of□relevance.□
However,□before□we□accept□the□conclusion□that□the□proliferation□rate□of□pituitary□adenomas□is□not□
correlated□with□tumor□size,□we□need□to□consider□important□drawbacks□in□the□study□by□Mastronardi□and□
coworkers.□ The□results□of□tumors□with□different□endocrine□activity□have□been□analyzed□together□on□the□assumption□ that□the□different□histotype□has□no□independent□effect□on□the□Ki-67□LI.□However,□this□assumption□is□still□
unproven,□at□least□in□the□case□of□ACTH-secreting□adenomas,□which□have□been□shown□in□some□studies□
to□have□a□higher□Ki-67□LI□than□the□other□types□of□pituitary□adenomas□(Shibuya□et□al,□Acta□Neuropathol,□ 84:178-183,□1992;□Landolt□and,□Shibata□in:□Pituitary□Adenomas.□New□Trends□in□Basic□and□Clinical□
Research.□Amsterdam:□Excerpta□Medica,□1991:□169-178).□Therefore,□an□imbalance□in□the□distribution□of□
micro-□and□macroadenomas□among□the□different□types□of□pituitary□adenomas,□would□obscure□a□possible□
relationship□between□Ki-67□LI□and□tumor□size.□Indeed,□in□a□previous□paper□(Losa□et□al.,□Am□J□Pathol,□
156:245-251,□2000)□we□found□that□in□a□homogeneous□population□of□patients□with□Cushing's□disease□the□ Ki-67□LI□was□significantly□higher□in□macroadenomas□than□in□microadenomas□and□that□there□was□a□
significant□correlation□between□maximum□tumor□diameter□and□Ki-67□LI,□just□the□opposite□findings□of□
Mastronardi□and□coworkers.□A□multivariate□analysis□taking□into□account□the□endocrine□activity□of□the□ tumor□would□have□been□useful.□
Another□drawback□is□the□inclusion□of□patients□with□PRL-secreting□adenomas□previously□treated□with□
dopaminergic□drugs.□We□are□not□given□information□whether□the□drug□was□stopped□months□before□or□
continued□until□surgery.□In□a□previous□study□(Landolt□et□al.□in□Advances□in□Pituitary□Adenoma□Research.□ Oxford:□Pergamon□Press,□1988:□53-62)□it□has□been□demonstrated□that□treated□prolactinomas□had□a□ lower□Ki-67□LI□than□untreated□ones.□Again,□an□imbalance□in□the□distribution□of□micro-□and□
macroadenomas□among□patients□who□received□dopaminergic□drugs,□would□bias□the□analysis□performed□
by□the□authors.□A□similar□reasoning□can□also□be□done□for□the□inclusion□of□patients□with□recurrent□tumors.□
Again,□more□sophisticated□statistical□methods□to□control□for□imbalances□in□the□study□population□would□
have□been□more□appropriate.□
The□mechanisms□controlling□tumor□growth□in□pituitary□adenomas□are□still□partially□unknown.□The□paper□
by□Mastronardi□and□coworkers□represents□another□piece□of□knowledge□in□this□fascinating□field□of□
research.□
Competing□interests:
None□declared.
|
BMC
|
12885_2001_12_ReviewerReport_V2_R2.pdf
|
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},
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"content": "Reviewer's□report \n□Lack□of□correlation□between□Ki-67□labelling□index□and□volume□of□anterior□pituitary□adenomas.□ Title: \nAuthors: \nLuciano□Mastronardi□MD,□PhD□( [email protected] )\nAntonio□Guiducci□MD□( [email protected] )\nFabrizio□Puzzilli□MD□( [email protected] )\n□2□ □3□Aug□2001 Version: Date: \n□Dr□Marco□Losa Reviewer: \n□A□paper□whose□findings□are□important□to□those□with□closely□related□research□interests Level□of□interest: \n□Other□(see□below) Advice□on□publication: \nIn□this□study□Mastronardi□and□coworkers□report□on□the□lack□of□correlation□between□Ki-67□labeling□index□ \nand□size□of□anterior□pituitary□adenomas□in□a□series□of□121□consecutively□operated□patients.□This□finding□ \nmay□have□interesting□pathophysiological□implications□as□it□suggests□that□the□proliferative□activity□may□not be□the□most□important□factor□in□determining□the□size□of□pituitary□adenomas.□The□authors□postulate□that□ the□time□elapsed□from□tumoral□transformation□to□diagnosis□might□be□the□critical□factor□in□determining□ \ntumor□size,□but□still□other□factors,□such□as□the□fraction□of□cell□loss□due□to□apoptosis□and□necrosis,□might□ \nbe□of□relevance.□ \nHowever,□before□we□accept□the□conclusion□that□the□proliferation□rate□of□pituitary□adenomas□is□not□ \ncorrelated□with□tumor□size,□we□need□to□consider□important□drawbacks□in□the□study□by□Mastronardi□and□ \ncoworkers.□ The□results□of□tumors□with□different□endocrine□activity□have□been□analyzed□together□on□the□assumption□ that□the□different□histotype□has□no□independent□effect□on□the□Ki-67□LI.□However,□this□assumption□is□still□ \nunproven,□at□least□in□the□case□of□ACTH-secreting□adenomas,□which□have□been□shown□in□some□studies□ \nto□have□a□higher□Ki-67□LI□than□the□other□types□of□pituitary□adenomas□(Shibuya□et□al,□Acta□Neuropathol,□ 84:178-183,□1992;□Landolt□and,□Shibata□in:□Pituitary□Adenomas.□New□Trends□in□Basic□and□Clinical□ \nResearch.□Amsterdam:□Excerpta□Medica,□1991:□169-178).□Therefore,□an□imbalance□in□the□distribution□of□ \nmicro-□and□macroadenomas□among□the□different□types□of□pituitary□adenomas,□would□obscure□a□possible□ \nrelationship□between□Ki-67□LI□and□tumor□size.□Indeed,□in□a□previous□paper□(Losa□et□al.,□Am□J□Pathol,□ \n156:245-251,□2000)□we□found□that□in□a□homogeneous□population□of□patients□with□Cushing's□disease□the□ Ki-67□LI□was□significantly□higher□in□macroadenomas□than□in□microadenomas□and□that□there□was□a□ \nsignificant□correlation□between□maximum□tumor□diameter□and□Ki-67□LI,□just□the□opposite□findings□of□ \nMastronardi□and□coworkers.□A□multivariate□analysis□taking□into□account□the□endocrine□activity□of□the□ tumor□would□have□been□useful.□ \nAnother□drawback□is□the□inclusion□of□patients□with□PRL-secreting□adenomas□previously□treated□with□ \ndopaminergic□drugs.□We□are□not□given□information□whether□the□drug□was□stopped□months□before□or□ \ncontinued□until□surgery.□In□a□previous□study□(Landolt□et□al.□in□Advances□in□Pituitary□Adenoma□Research.□ Oxford:□Pergamon□Press,□1988:□53-62)□it□has□been□demonstrated□that□treated□prolactinomas□had□a□ lower□Ki-67□LI□than□untreated□ones.□Again,□an□imbalance□in□the□distribution□of□micro-□and□ \nmacroadenomas□among□patients□who□received□dopaminergic□drugs,□would□bias□the□analysis□performed□ \nby□the□authors.□A□similar□reasoning□can□also□be□done□for□the□inclusion□of□patients□with□recurrent□tumors.□ \nAgain,□more□sophisticated□statistical□methods□to□control□for□imbalances□in□the□study□population□would□ \nhave□been□more□appropriate.□ \nThe□mechanisms□controlling□tumor□growth□in□pituitary□adenomas□are□still□partially□unknown.□The□paper□ \nby□Mastronardi□and□coworkers□represents□another□piece□of□knowledge□in□this□fascinating□field□of□ \nresearch.□ \nCompeting□interests: \nNone□declared. ",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-11
|
Reviewed - bmc_cancer
|
Reviewer's report
An association study of digitoxin use and cancer. Title:
Authors:
Johan Haux ([email protected] )
Olbjorn Klepp ([email protected] )
Olav Spigset ([email protected] )
Steinar Tretli ([email protected] )
1 7 Jun 2001 Version: Date:
Dr Richard Havlik Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
In this report the authors test a hypothesis concerning digitalis use in patients and less cancer
incidence. They utilize a rather unique cohort of those with digitoxin levels measured in the blood paired
with available cancer registry data analyzed both after and importantly BEFORE the date of drug
initiation. The results of some of the analyses suggest that the relationships found are more likely due to
selective factors, because of apparent associations being present before medication use, while
prospective results are more consistent with the original hypothesis. However, the addition of more
detail about the hypothesis, interpretation of the data, and rationale for the conclusion would strengthen
the report.
1. There is quite a nice introduction, which was informative for me, about previous clinical and
laboratory research concerning digitalis and cancer. However, what was not well explained is the actual
mechanism of why digitoxin should show more of an effect but the more commonly used digoxin form
would be less. Also, it was not clear whether certain cancer types would be hypothesized to be more
controlled by apoptosis than others and be more sensitive to digitalis. The references refer to prostate
and breast cancer. To have designated these cancers a priori would have helped in interpreting the conclusions. My impression of cancer etiological dogma is to see each site as having a separate
etiology. In fact, these were not the cancers found to be associated in the results. There is always the
potential statistical bias of looking at multiple comparisons and identifying false positive associations. The authors could elaborate more on this aspect in the introduction and discussion.
2. The interpretation of the data analysis would be assisted by some additional considerations. The
findings in tables 1-2 about cardiovascular disease (CVD) are very interesting. The idea that there are risk factors common to both CVD and cancer seems possible, especially for smoking, but the relationship with cholesterol or hypertension is not so clear. Reference is made to the initial findings of
calcium channel blocker drugs (commonly used in those with CVD) being associated with cancer.
However, others and our own group have been unable to replicate the original findings. Also, the understanding of how melanoma (reversal of relationship between tables 1 and 2) would be affected is too conjectural. Sun exposure for melanoma usually occurs many years before the onset of CVD. The
discussion on these issues should be expanded.
3. The dose-response data in table 3 could be considered the strongest indication of a possible real
association. The statistical test used for the ?trend analysis? should be stated.. In fact, there seems to
be more of a threshold at 16 ng/ml rather than a trend, especially for kidney and all sites.
4. Finally, in terms of the conclusion it will not be possible to use digitalis in prospective clinical trials in
non-CVD cases and randomization in CVD cases would be problematic. So, at best
more descriptive clinical data collection will be necessary to understand possible relationships.
There are a few words that might be modified for better meaning. In the Results section of the Abstract
?start? should be ?starting?. There is a sentence that should be: ?This indicates that yet unknown
factors exist... Also, ?an internal? analysis, I think is better described as a ?dose-response? analysis. In
the Conclusion better to say: should be ?ascribed? rather than ?referred?. Table 1 should be:
International ?Classification? not ?Code?.
Competing interests:
None declared.
|
Reviewer's report
An association study of digitoxin use and cancer. Title:
Authors:
Johan Haux ([email protected] )
Olbjorn Klepp ([email protected] )
Olav Spigset ([email protected] )
Steinar Tretli ([email protected] )
1 7 Jun 2001 Version: Date:
Dr Richard Havlik Reviewer:
A paper whose findings are important to those with closely related research interests Level of interest:
Accept after revision, which I do not need to see Advice on publication:
In this report the authors test a hypothesis concerning digitalis use in patients and less cancer
incidence. They utilize a rather unique cohort of those with digitoxin levels measured in the blood paired
with available cancer registry data analyzed both after and importantly BEFORE the date of drug
initiation. The results of some of the analyses suggest that the relationships found are more likely due to
selective factors, because of apparent associations being present before medication use, while
prospective results are more consistent with the original hypothesis. However, the addition of more
detail about the hypothesis, interpretation of the data, and rationale for the conclusion would strengthen
the report.
1. There is quite a nice introduction, which was informative for me, about previous clinical and
laboratory research concerning digitalis and cancer. However, what was not well explained is the actual
mechanism of why digitoxin should show more of an effect but the more commonly used digoxin form
would be less. Also, it was not clear whether certain cancer types would be hypothesized to be more
controlled by apoptosis than others and be more sensitive to digitalis. The references refer to prostate
and breast cancer. To have designated these cancers a priori would have helped in interpreting the conclusions. My impression of cancer etiological dogma is to see each site as having a separate
etiology. In fact, these were not the cancers found to be associated in the results. There is always the
potential statistical bias of looking at multiple comparisons and identifying false positive associations. The authors could elaborate more on this aspect in the introduction and discussion.
2. The interpretation of the data analysis would be assisted by some additional considerations. The
findings in tables 1-2 about cardiovascular disease (CVD) are very interesting. The idea that there are risk factors common to both CVD and cancer seems possible, especially for smoking, but the relationship with cholesterol or hypertension is not so clear. Reference is made to the initial findings of
calcium channel blocker drugs (commonly used in those with CVD) being associated with cancer.
However, others and our own group have been unable to replicate the original findings. Also, the understanding of how melanoma (reversal of relationship between tables 1 and 2) would be affected is too conjectural. Sun exposure for melanoma usually occurs many years before the onset of CVD. The
discussion on these issues should be expanded.
3. The dose-response data in table 3 could be considered the strongest indication of a possible real
association. The statistical test used for the ?trend analysis? should be stated.. In fact, there seems to
be more of a threshold at 16 ng/ml rather than a trend, especially for kidney and all sites.
4. Finally, in terms of the conclusion it will not be possible to use digitalis in prospective clinical trials in
non-CVD cases and randomization in CVD cases would be problematic. So, at best
more descriptive clinical data collection will be necessary to understand possible relationships.
There are a few words that might be modified for better meaning. In the Results section of the Abstract
?start? should be ?starting?. There is a sentence that should be: ?This indicates that yet unknown
factors exist... Also, ?an internal? analysis, I think is better described as a ?dose-response? analysis. In
the Conclusion better to say: should be ?ascribed? rather than ?referred?. Table 1 should be:
International ?Classification? not ?Code?.
Competing interests:
None declared.
|
BMC
|
12885_2001_11_ReviewerReport_V1_R1.pdf
|
{
"criticism": 5,
"example": 2,
"importance_and_relevance": 3,
"materials_and_methods": 15,
"praise": 3,
"presentation_and_reporting": 11,
"results_and_discussion": 15,
"suggestion_and_solution": 16,
"total": 43
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|
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"criticism": 0.11627906976744186,
"example": 0.046511627906976744,
"importance_and_relevance": 0.06976744186046512,
"materials_and_methods": 0.3488372093023256,
"praise": 0.06976744186046512,
"presentation_and_reporting": 0.2558139534883721,
"results_and_discussion": 0.3488372093023256,
"suggestion_and_solution": 0.37209302325581395
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| 1.627907
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n An association study of digitoxin use and cancer. Title:\nAuthors:\nJohan Haux ([email protected] )\nOlbjorn Klepp ([email protected] )\nOlav Spigset ([email protected] )\nSteinar Tretli ([email protected] )\n 1 7 Jun 2001 Version: Date:\n Dr Richard Havlik Reviewer:\n A paper whose findings are important to those with closely related research interests Level of interest:\n Accept after revision, which I do not need to see Advice on publication:\nIn this report the authors test a hypothesis concerning digitalis use in patients and less cancer \nincidence. They utilize a rather unique cohort of those with digitoxin levels measured in the blood paired\nwith available cancer registry data analyzed both after and importantly BEFORE the date of drug \ninitiation. The results of some of the analyses suggest that the relationships found are more likely due to\nselective factors, because of apparent associations being present before medication use, while \nprospective results are more consistent with the original hypothesis. However, the addition of more \ndetail about the hypothesis, interpretation of the data, and rationale for the conclusion would strengthen \nthe report. \n1. There is quite a nice introduction, which was informative for me, about previous clinical and \nlaboratory research concerning digitalis and cancer. However, what was not well explained is the actual \nmechanism of why digitoxin should show more of an effect but the more commonly used digoxin form \nwould be less. Also, it was not clear whether certain cancer types would be hypothesized to be more \ncontrolled by apoptosis than others and be more sensitive to digitalis. The references refer to prostate \nand breast cancer. To have designated these cancers a priori would have helped in interpreting the conclusions. My impression of cancer etiological dogma is to see each site as having a separate \netiology. In fact, these were not the cancers found to be associated in the results. There is always the \npotential statistical bias of looking at multiple comparisons and identifying false positive associations. The authors could elaborate more on this aspect in the introduction and discussion. \n2. The interpretation of the data analysis would be assisted by some additional considerations. The \nfindings in tables 1-2 about cardiovascular disease (CVD) are very interesting. The idea that there are risk factors common to both CVD and cancer seems possible, especially for smoking, but the relationship with cholesterol or hypertension is not so clear. Reference is made to the initial findings of \ncalcium channel blocker drugs (commonly used in those with CVD) being associated with cancer. \nHowever, others and our own group have been unable to replicate the original findings. Also, the understanding of how melanoma (reversal of relationship between tables 1 and 2) would be affected is too conjectural. Sun exposure for melanoma usually occurs many years before the onset of CVD. The \ndiscussion on these issues should be expanded. \n3. The dose-response data in table 3 could be considered the strongest indication of a possible real \nassociation. The statistical test used for the ?trend analysis? should be stated.. In fact, there seems to \nbe more of a threshold at 16 ng/ml rather than a trend, especially for kidney and all sites. \n4. Finally, in terms of the conclusion it will not be possible to use digitalis in prospective clinical trials in \nnon-CVD cases and randomization in CVD cases would be problematic. So, at best \nmore descriptive clinical data collection will be necessary to understand possible relationships. \nThere are a few words that might be modified for better meaning. In the Results section of the Abstract \n?start? should be ?starting?. There is a sentence that should be: ?This indicates that yet unknown \nfactors exist... Also, ?an internal? analysis, I think is better described as a ?dose-response? analysis. In \nthe Conclusion better to say: should be ?ascribed? rather than ?referred?. Table 1 should be: \nInternational ?Classification? not ?Code?. \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
||
0
| 0
|
Review for 10.1186/1471-2407-1-10
|
Reviewed - bmc_cancer
|
Reviewer's report
Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug resistance Title:
and telomere elongation
Authors:
Noritsugu Kuranaga ([email protected] )
Nariyoshi Shinomiya ([email protected] )
Hidetaka Mochizuki ([email protected] )
1 11 Jun 2001 Version: Date:
Dr Monika Engelhardt Reviewer:
A paper of limited interest Level of interest:
Other (see below) Advice on publication:
The article Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug
resistance and telomere elongation by N. Kuranaga et al describes cell growth kinetics of 2 colorectal cell lines cultivated with two anti-cancer drugs with respect to population doublings, telomere length, telomerase activity, mRNA expression of telomerase components and acquisition of mdr expression.
Major criticisms:
1. The English phrasing and grammar needs much more attention and correct spelling, grammar and
expressions/wording would greatly improve the manuscript. Some of these major flaws are mentioned in the section 'minor criticism', but could not be named in full detail by the reviewer. In general, the
whole paper needs rewriting and rephrasing to ameliorate understanding its contents.
2. In the 'background section', the authors claim that the relationship between the role of telomerase
activation in the progression of cancer cells has not been explained, this seems inadequately phrased, since there are numerous papers focusing on that aspect, please either rephrase or take out.
3. The cancer drugs used in the paper, such as 5-FU or CDDP should be fully mentioned and explained
in its action in the background and methods section. It also does not help, if these are not given by their
full name, but abbreviation in the whole text, even in the incomplete abbreviation list on page 14, these
are not explained, please name and explain all words when used in abbreviated terms throughout the entire manuscript.
4. On page 5, the authors should name why the fluorescence at 560nm and 590 nm wavelength was
measured, in order to determine cell numbers? 5. Since it is well known that best distribution of telomeres are performed in low concentration agarose gels, the high concentration of 1% is a little surprising, please explain why lower concentrations as
previously published were not used. Moreover, running the gel at 50V for only 75 min seems very short
indeed, time error here? 6. (page 7, statistical analysis): The two groups that were tested by the Student's t-test remain unclear, are CDDP plus 5-FU in both cell lines or each as compared to its control meant? Please clarify.
7. Why in both tumor cell lines - with addition of both anti-cancer drugs - the authors conclude that
growth kinetics and speed were almost as high as in the controls, remains unclear, since this is most
certainly not the case. Please correct. It would also be of interest to mention what happened with both
cell lines, both the control and with addition of both anti-cancer drugs beyond d 100 as well as with the
addition of each single anti-cancer drug alone.
8. It remains unclear to the reviewer why different cut-offs for PDL were chosen for the measurement of
the proliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the
same ones to better compare both with each other.
9. The effect of clonality measured by DNA histogram analysis does not completely convince the reviewer that in each cell line chromosomal changes did not occur, this seems to be better excluded using FISH analyses rather than by DNA histogram pattern, please comment.
10. Figure 4 shows the expression of mdr-1 and MRP, but neither convincingly demonstrates their
upregulation nor does it show potential changes in the control cell lines grown without anti-cancer treatment. Please improve or exchange the figure. 11. The elongation of telomeres in figure 5 is not completely convincing for DLD-1 cells, especially the
claimed telomere elongation from 7.96 to 9.3kbp, the latter even appears shorter or at the utmost both
seem similar in length. Please also give mean TRF values as compared to peak TRFs and comment ontheir differences. 12. In figure 6, telomerase activity does not seem to be extremely or as given 'strongly' upregulated,
rather than increased at moderate values. Also, in DLD-1 telomerase at all time points, with 7, 27 and 58
PDL seem very comparable or similar, please change the text and interpretation accordingly or
improve/exchange the figure. 13. In figure 7 the upregulation of mRNA expressions are not convincingly displayed either. Please
exchange figure to better display these changes.
14. The plateau that is mentioned by the authors in the discussion (page 10) seems misleading, since both cell lines with CDDP and 5 FU addition did not reach a plateau at all, however, grew slower but gradually as compared to the control.
15. The authors claim that their cell lines after some time after the addition of both anti-cancer drugs
acquired drug resistance. How can they safely prove that? What was the half life of both drugs? How often was each anti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it once added and never later again? Please comment in detail.
16. Please rephrase: These may be different conclusions from one in which there is active telomere
elongation. This is not well understood and needs to be rephrased. 17. Although this may be the first report on drug resistance and telomere elongation as claimed by the authors, these results have substatial shortcomings, seem less well understood and are certainly not
very well presented: first the continuous and/or frequent addition of both drugs to both cell lines does not
seem to have taken place, secondly telomere elongation at least for DLD-1 seems less well
documented and is not convincing and thirdly telomerase changes / activation during cell growth was very moderate. Bearing these substantial shortcomings of the manuscript in mind, the authors should
be much more carefully when interpreting their results than performed so far.
18. The very low telomerase activity (page 11) during the first PDL are not shown and should probably be included in figure 5. 19. The final conclusion that telomere elongation was not due to abnormal clones rather than
upregulation of telomerase seems very unlikely to be the only and final conclusion to the observed
phenomenon and should be more carefully addressed. Clonal appearance was not carefully tested, nor telomerase upregulation very substantial. Other factors than those named might most likely have had a substantial input in the observed changes and discussion of these would greatly improve the
manuscript.
Minor criticisms:
Abstract:
1. In the abstract, in the results section: please change: ....during the observation period, an
abnormal.....
2. Rephrase: Telomere length gradually increased with progressive PDL.
3. In the conclusions: .... and elongation of telomeres have some ..... . Colorectal carcinoma cells with longer telomeres may be selected.......
Background
4. We often encounter patients.... 5. An acceleration of the.... 6. ....(1-3) which have proved to play.....
7. MDR-1 and MRP genes have been reported.....and to frequently exist on.....
8. Telomere shortening has been reported to be involved in the..... 9. It has also been clarified that once tumor cells acquire telomerase activity telomere length is maintained.
10. Up to now, the relationship.......and to various characteristics of tumor cells......
11. Instead of `for a long period of time' use the exact time of observation, e.g. 100 days. 12. ....and obtained cancer cells that were highly resistant to anti-cancer drugs and grew rapidly. 13. ...., including telomere length.....
Material and methods
14. Take out:...... and used as study materials. 15. Rephrase (page 4): ...used for cell passage. The cell passage was performed when cells had
reached confluence.
16. (page 4, last paragraph)...in triplicates. 17. (page 5): Ten ml of diluted Alamar blue were added to each well and incubated...... 18. (page 5): Telomerase activity was determined using a modified TRAP assay. .......with minor
modifications.
Results
19. (page 8): ....growth was almost completely suppressed until (or: up to) day 14.
20. ....growth speed gradually increased.
21. Please note that in relative sentences, starting with who, which or that, there is no comma. Please change accordingly in the whole text. 22. (page 9) ... in the passages cells were observed.
Discussion
23. However, it is also possible that cells that possess high telomerase ....... 24. In their study, critically short telomeres in tumor-derived cell lines ......
25. (page 11): This is the first report....... and elongation of telomeres.
Specific questions:
1. Are the conclusions drawn adequately supported by the data shown: if not, what are the
shortcomings and could they be overcome?
As named in detail in the major comments sections from 1.-19., there are several shortcomings of the
paper that need to be addressed.
2. Are sufficient details provided to allow replication of the work or comparison with related analyses: if
not, what is missing?
Although there is sufficient data presented as well as enough details given in the methods section to
allow replication of the data, numerous points as listed in 1.-19. need to be carefully addressed, such as
the high concentration of the agarose gel and running the gel at 50V for only 75 min. Moreover, the
statistical analyses are either unclear or not very extensively performed at all, these need to be performed with more regard and in more detail. It also remains unclear why in both tumor cell lines -
with addition of both anti-cancer drugs - the authors conclude that growth kinetics and speed were
almost as high as in the controls. As already explained above, it would also be of interest to mention
what happened with both cell lines, beyond d 100 and with the addition of each single anti-cancer drug
alone. Of concern is as well, why different cut-offs for PDL were chosen for the measurement of the
proliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the
same ones to better compare both with each other. As mentioned, especially figures 4, 6 and 7 do not
adequately display what is meant to be described by the authors, these have to be improved or exchanged. Finally, the authors claim that their cell lines acquired drug resistance needs better clarification. How can they safely prove that? What was the half life of both drugs? How often was each
anti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it
once added band never later again? This needs to be addressed in detail.
3. Does the manuscript adhere to the relevant standards for reporting and data deposition: if not, in
what ways?
Bearing in mind the extensive major and minor comments, these need to be addresses, if the authors
can improve and/or clarify all of these comments raised this will help to greatly improve the manuscript and ensure that the relevant standards of reporting are met.
4. Is the writing acceptable?
The English phrasing and grammar needs much more attention. Correct spelling, expressions and grammar will greatly improve the manuscript. Some of these major flaws are mentioned in the section
'minor criticism', but could not be named in full detail by the reviewer. In general, the whole paper needs
extensive rewriting and rephrasing to ameliorate understanding its contents.
Level of interest: limited
Advice on publication: accept after extensive revision
Quality of written English: poor, not acceptable for publication unless it is rewritten
Competing interests:
None declared.
|
Reviewer's report
Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug resistance Title:
and telomere elongation
Authors:
Noritsugu Kuranaga ([email protected] )
Nariyoshi Shinomiya ([email protected] )
Hidetaka Mochizuki ([email protected] )
1 11 Jun 2001 Version: Date:
Dr Monika Engelhardt Reviewer:
A paper of limited interest Level of interest:
Other (see below) Advice on publication:
The article Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug
resistance and telomere elongation by N. Kuranaga et al describes cell growth kinetics of 2 colorectal cell lines cultivated with two anti-cancer drugs with respect to population doublings, telomere length, telomerase activity, mRNA expression of telomerase components and acquisition of mdr expression.
Major criticisms:
1. The English phrasing and grammar needs much more attention and correct spelling, grammar and
expressions/wording would greatly improve the manuscript. Some of these major flaws are mentioned in the section 'minor criticism', but could not be named in full detail by the reviewer. In general, the
whole paper needs rewriting and rephrasing to ameliorate understanding its contents.
2. In the 'background section', the authors claim that the relationship between the role of telomerase
activation in the progression of cancer cells has not been explained, this seems inadequately phrased, since there are numerous papers focusing on that aspect, please either rephrase or take out.
3. The cancer drugs used in the paper, such as 5-FU or CDDP should be fully mentioned and explained
in its action in the background and methods section. It also does not help, if these are not given by their
full name, but abbreviation in the whole text, even in the incomplete abbreviation list on page 14, these
are not explained, please name and explain all words when used in abbreviated terms throughout the entire manuscript.
4. On page 5, the authors should name why the fluorescence at 560nm and 590 nm wavelength was
measured, in order to determine cell numbers? 5. Since it is well known that best distribution of telomeres are performed in low concentration agarose gels, the high concentration of 1% is a little surprising, please explain why lower concentrations as
previously published were not used. Moreover, running the gel at 50V for only 75 min seems very short
indeed, time error here? 6. (page 7, statistical analysis): The two groups that were tested by the Student's t-test remain unclear, are CDDP plus 5-FU in both cell lines or each as compared to its control meant? Please clarify.
7. Why in both tumor cell lines - with addition of both anti-cancer drugs - the authors conclude that
growth kinetics and speed were almost as high as in the controls, remains unclear, since this is most
certainly not the case. Please correct. It would also be of interest to mention what happened with both
cell lines, both the control and with addition of both anti-cancer drugs beyond d 100 as well as with the
addition of each single anti-cancer drug alone.
8. It remains unclear to the reviewer why different cut-offs for PDL were chosen for the measurement of
the proliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the
same ones to better compare both with each other.
9. The effect of clonality measured by DNA histogram analysis does not completely convince the reviewer that in each cell line chromosomal changes did not occur, this seems to be better excluded using FISH analyses rather than by DNA histogram pattern, please comment.
10. Figure 4 shows the expression of mdr-1 and MRP, but neither convincingly demonstrates their
upregulation nor does it show potential changes in the control cell lines grown without anti-cancer treatment. Please improve or exchange the figure. 11. The elongation of telomeres in figure 5 is not completely convincing for DLD-1 cells, especially the
claimed telomere elongation from 7.96 to 9.3kbp, the latter even appears shorter or at the utmost both
seem similar in length. Please also give mean TRF values as compared to peak TRFs and comment ontheir differences. 12. In figure 6, telomerase activity does not seem to be extremely or as given 'strongly' upregulated,
rather than increased at moderate values. Also, in DLD-1 telomerase at all time points, with 7, 27 and 58
PDL seem very comparable or similar, please change the text and interpretation accordingly or
improve/exchange the figure. 13. In figure 7 the upregulation of mRNA expressions are not convincingly displayed either. Please
exchange figure to better display these changes.
14. The plateau that is mentioned by the authors in the discussion (page 10) seems misleading, since both cell lines with CDDP and 5 FU addition did not reach a plateau at all, however, grew slower but gradually as compared to the control.
15. The authors claim that their cell lines after some time after the addition of both anti-cancer drugs
acquired drug resistance. How can they safely prove that? What was the half life of both drugs? How often was each anti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it once added and never later again? Please comment in detail.
16. Please rephrase: These may be different conclusions from one in which there is active telomere
elongation. This is not well understood and needs to be rephrased. 17. Although this may be the first report on drug resistance and telomere elongation as claimed by the authors, these results have substatial shortcomings, seem less well understood and are certainly not
very well presented: first the continuous and/or frequent addition of both drugs to both cell lines does not
seem to have taken place, secondly telomere elongation at least for DLD-1 seems less well
documented and is not convincing and thirdly telomerase changes / activation during cell growth was very moderate. Bearing these substantial shortcomings of the manuscript in mind, the authors should
be much more carefully when interpreting their results than performed so far.
18. The very low telomerase activity (page 11) during the first PDL are not shown and should probably be included in figure 5. 19. The final conclusion that telomere elongation was not due to abnormal clones rather than
upregulation of telomerase seems very unlikely to be the only and final conclusion to the observed
phenomenon and should be more carefully addressed. Clonal appearance was not carefully tested, nor telomerase upregulation very substantial. Other factors than those named might most likely have had a substantial input in the observed changes and discussion of these would greatly improve the
manuscript.
Minor criticisms:
Abstract:
1. In the abstract, in the results section: please change: ....during the observation period, an
abnormal.....
2. Rephrase: Telomere length gradually increased with progressive PDL.
3. In the conclusions: .... and elongation of telomeres have some ..... . Colorectal carcinoma cells with longer telomeres may be selected.......
Background
4. We often encounter patients.... 5. An acceleration of the.... 6. ....(1-3) which have proved to play.....
7. MDR-1 and MRP genes have been reported.....and to frequently exist on.....
8. Telomere shortening has been reported to be involved in the..... 9. It has also been clarified that once tumor cells acquire telomerase activity telomere length is maintained.
10. Up to now, the relationship.......and to various characteristics of tumor cells......
11. Instead of `for a long period of time' use the exact time of observation, e.g. 100 days. 12. ....and obtained cancer cells that were highly resistant to anti-cancer drugs and grew rapidly. 13. ...., including telomere length.....
Material and methods
14. Take out:...... and used as study materials. 15. Rephrase (page 4): ...used for cell passage. The cell passage was performed when cells had
reached confluence.
16. (page 4, last paragraph)...in triplicates. 17. (page 5): Ten ml of diluted Alamar blue were added to each well and incubated...... 18. (page 5): Telomerase activity was determined using a modified TRAP assay. .......with minor
modifications.
Results
19. (page 8): ....growth was almost completely suppressed until (or: up to) day 14.
20. ....growth speed gradually increased.
21. Please note that in relative sentences, starting with who, which or that, there is no comma. Please change accordingly in the whole text. 22. (page 9) ... in the passages cells were observed.
Discussion
23. However, it is also possible that cells that possess high telomerase ....... 24. In their study, critically short telomeres in tumor-derived cell lines ......
25. (page 11): This is the first report....... and elongation of telomeres.
Specific questions:
1. Are the conclusions drawn adequately supported by the data shown: if not, what are the
shortcomings and could they be overcome?
As named in detail in the major comments sections from 1.-19., there are several shortcomings of the
paper that need to be addressed.
2. Are sufficient details provided to allow replication of the work or comparison with related analyses: if
not, what is missing?
Although there is sufficient data presented as well as enough details given in the methods section to
allow replication of the data, numerous points as listed in 1.-19. need to be carefully addressed, such as
the high concentration of the agarose gel and running the gel at 50V for only 75 min. Moreover, the
statistical analyses are either unclear or not very extensively performed at all, these need to be performed with more regard and in more detail. It also remains unclear why in both tumor cell lines -
with addition of both anti-cancer drugs - the authors conclude that growth kinetics and speed were
almost as high as in the controls. As already explained above, it would also be of interest to mention
what happened with both cell lines, beyond d 100 and with the addition of each single anti-cancer drug
alone. Of concern is as well, why different cut-offs for PDL were chosen for the measurement of the
proliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the
same ones to better compare both with each other. As mentioned, especially figures 4, 6 and 7 do not
adequately display what is meant to be described by the authors, these have to be improved or exchanged. Finally, the authors claim that their cell lines acquired drug resistance needs better clarification. How can they safely prove that? What was the half life of both drugs? How often was each
anti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it
once added band never later again? This needs to be addressed in detail.
3. Does the manuscript adhere to the relevant standards for reporting and data deposition: if not, in
what ways?
Bearing in mind the extensive major and minor comments, these need to be addresses, if the authors
can improve and/or clarify all of these comments raised this will help to greatly improve the manuscript and ensure that the relevant standards of reporting are met.
4. Is the writing acceptable?
The English phrasing and grammar needs much more attention. Correct spelling, expressions and grammar will greatly improve the manuscript. Some of these major flaws are mentioned in the section
'minor criticism', but could not be named in full detail by the reviewer. In general, the whole paper needs
extensive rewriting and rephrasing to ameliorate understanding its contents.
Level of interest: limited
Advice on publication: accept after extensive revision
Quality of written English: poor, not acceptable for publication unless it is rewritten
Competing interests:
None declared.
|
BMC
|
12885_2001_10_ReviewerReport_V1_R1.pdf
|
{
"criticism": 22,
"example": 17,
"importance_and_relevance": 1,
"materials_and_methods": 33,
"praise": 1,
"presentation_and_reporting": 37,
"results_and_discussion": 13,
"suggestion_and_solution": 37,
"total": 127
}
|
{
"criticism": 0.1732283464566929,
"example": 0.13385826771653545,
"importance_and_relevance": 0.007874015748031496,
"materials_and_methods": 0.25984251968503935,
"praise": 0.007874015748031496,
"presentation_and_reporting": 0.29133858267716534,
"results_and_discussion": 0.10236220472440945,
"suggestion_and_solution": 0.29133858267716534
}
| 1.267717
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Reviewer's report\n Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug resistance Title:\nand telomere elongation\nAuthors:\nNoritsugu Kuranaga ([email protected] )\nNariyoshi Shinomiya ([email protected] )\nHidetaka Mochizuki ([email protected] )\n 1 11 Jun 2001 Version: Date:\n Dr Monika Engelhardt Reviewer:\n A paper of limited interest Level of interest:\n Other (see below) Advice on publication:\nThe article Long-term cultivation of colorectal carcinoma cells with anti-cancer drugs induces drug \nresistance and telomere elongation by N. Kuranaga et al describes cell growth kinetics of 2 colorectal cell lines cultivated with two anti-cancer drugs with respect to population doublings, telomere length, telomerase activity, mRNA expression of telomerase components and acquisition of mdr expression. \nMajor criticisms: \n1. The English phrasing and grammar needs much more attention and correct spelling, grammar and \nexpressions/wording would greatly improve the manuscript. Some of these major flaws are mentioned in the section 'minor criticism', but could not be named in full detail by the reviewer. In general, the \nwhole paper needs rewriting and rephrasing to ameliorate understanding its contents. \n2. In the 'background section', the authors claim that the relationship between the role of telomerase \nactivation in the progression of cancer cells has not been explained, this seems inadequately phrased, since there are numerous papers focusing on that aspect, please either rephrase or take out. \n3. The cancer drugs used in the paper, such as 5-FU or CDDP should be fully mentioned and explained \nin its action in the background and methods section. It also does not help, if these are not given by their \nfull name, but abbreviation in the whole text, even in the incomplete abbreviation list on page 14, these \nare not explained, please name and explain all words when used in abbreviated terms throughout the entire manuscript. \n4. On page 5, the authors should name why the fluorescence at 560nm and 590 nm wavelength was \nmeasured, in order to determine cell numbers? 5. Since it is well known that best distribution of telomeres are performed in low concentration agarose gels, the high concentration of 1% is a little surprising, please explain why lower concentrations as \npreviously published were not used. Moreover, running the gel at 50V for only 75 min seems very short \nindeed, time error here? 6. (page 7, statistical analysis): The two groups that were tested by the Student's t-test remain unclear, are CDDP plus 5-FU in both cell lines or each as compared to its control meant? Please clarify. \n7. Why in both tumor cell lines - with addition of both anti-cancer drugs - the authors conclude that \ngrowth kinetics and speed were almost as high as in the controls, remains unclear, since this is most \ncertainly not the case. Please correct. It would also be of interest to mention what happened with both \ncell lines, both the control and with addition of both anti-cancer drugs beyond d 100 as well as with the \naddition of each single anti-cancer drug alone. \n8. It remains unclear to the reviewer why different cut-offs for PDL were chosen for the measurement of \nthe proliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the\nsame ones to better compare both with each other. \n9. The effect of clonality measured by DNA histogram analysis does not completely convince the reviewer that in each cell line chromosomal changes did not occur, this seems to be better excluded using FISH analyses rather than by DNA histogram pattern, please comment. \n10. Figure 4 shows the expression of mdr-1 and MRP, but neither convincingly demonstrates their \nupregulation nor does it show potential changes in the control cell lines grown without anti-cancer treatment. Please improve or exchange the figure. 11. The elongation of telomeres in figure 5 is not completely convincing for DLD-1 cells, especially the \nclaimed telomere elongation from 7.96 to 9.3kbp, the latter even appears shorter or at the utmost both \nseem similar in length. Please also give mean TRF values as compared to peak TRFs and comment ontheir differences. 12. In figure 6, telomerase activity does not seem to be extremely or as given 'strongly' upregulated, \nrather than increased at moderate values. Also, in DLD-1 telomerase at all time points, with 7, 27 and 58\nPDL seem very comparable or similar, please change the text and interpretation accordingly or \nimprove/exchange the figure. 13. In figure 7 the upregulation of mRNA expressions are not convincingly displayed either. Please \nexchange figure to better display these changes. \n14. The plateau that is mentioned by the authors in the discussion (page 10) seems misleading, since both cell lines with CDDP and 5 FU addition did not reach a plateau at all, however, grew slower but gradually as compared to the control. \n15. The authors claim that their cell lines after some time after the addition of both anti-cancer drugs \nacquired drug resistance. How can they safely prove that? What was the half life of both drugs? How often was each anti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it once added and never later again? Please comment in detail. \n16. Please rephrase: These may be different conclusions from one in which there is active telomere \nelongation. This is not well understood and needs to be rephrased. 17. Although this may be the first report on drug resistance and telomere elongation as claimed by the authors, these results have substatial shortcomings, seem less well understood and are certainly not \nvery well presented: first the continuous and/or frequent addition of both drugs to both cell lines does not\nseem to have taken place, secondly telomere elongation at least for DLD-1 seems less well \ndocumented and is not convincing and thirdly telomerase changes / activation during cell growth was very moderate. Bearing these substantial shortcomings of the manuscript in mind, the authors should \nbe much more carefully when interpreting their results than performed so far. \n18. The very low telomerase activity (page 11) during the first PDL are not shown and should probably be included in figure 5. 19. The final conclusion that telomere elongation was not due to abnormal clones rather than \nupregulation of telomerase seems very unlikely to be the only and final conclusion to the observed \nphenomenon and should be more carefully addressed. Clonal appearance was not carefully tested, nor telomerase upregulation very substantial. Other factors than those named might most likely have had a substantial input in the observed changes and discussion of these would greatly improve the \nmanuscript. \nMinor criticisms: \nAbstract: \n1. In the abstract, in the results section: please change: ....during the observation period, an \nabnormal..... \n2. Rephrase: Telomere length gradually increased with progressive PDL. \n3. In the conclusions: .... and elongation of telomeres have some ..... . Colorectal carcinoma cells with longer telomeres may be selected....... \nBackground \n4. We often encounter patients.... 5. An acceleration of the.... 6. ....(1-3) which have proved to play..... \n7. MDR-1 and MRP genes have been reported.....and to frequently exist on..... \n8. Telomere shortening has been reported to be involved in the..... 9. It has also been clarified that once tumor cells acquire telomerase activity telomere length is maintained. \n10. Up to now, the relationship.......and to various characteristics of tumor cells...... \n11. Instead of `for a long period of time' use the exact time of observation, e.g. 100 days. 12. ....and obtained cancer cells that were highly resistant to anti-cancer drugs and grew rapidly. 13. ...., including telomere length..... \nMaterial and methods \n14. Take out:...... and used as study materials. 15. Rephrase (page 4): ...used for cell passage. The cell passage was performed when cells had \nreached confluence. \n16. (page 4, last paragraph)...in triplicates. 17. (page 5): Ten ml of diluted Alamar blue were added to each well and incubated...... 18. (page 5): Telomerase activity was determined using a modified TRAP assay. .......with minor \nmodifications. \nResults \n19. (page 8): ....growth was almost completely suppressed until (or: up to) day 14. \n20. ....growth speed gradually increased. \n21. Please note that in relative sentences, starting with who, which or that, there is no comma. Please change accordingly in the whole text. 22. (page 9) ... in the passages cells were observed. \nDiscussion \n23. However, it is also possible that cells that possess high telomerase ....... 24. In their study, critically short telomeres in tumor-derived cell lines ...... \n25. (page 11): This is the first report....... and elongation of telomeres. \nSpecific questions: \n1. Are the conclusions drawn adequately supported by the data shown: if not, what are the \nshortcomings and could they be overcome? \nAs named in detail in the major comments sections from 1.-19., there are several shortcomings of the \npaper that need to be addressed. \n2. Are sufficient details provided to allow replication of the work or comparison with related analyses: if \nnot, what is missing? \nAlthough there is sufficient data presented as well as enough details given in the methods section to \nallow replication of the data, numerous points as listed in 1.-19. need to be carefully addressed, such as\nthe high concentration of the agarose gel and running the gel at 50V for only 75 min. Moreover, the \nstatistical analyses are either unclear or not very extensively performed at all, these need to be performed with more regard and in more detail. It also remains unclear why in both tumor cell lines - \nwith addition of both anti-cancer drugs - the authors conclude that growth kinetics and speed were \nalmost as high as in the controls. As already explained above, it would also be of interest to mention \nwhat happened with both cell lines, beyond d 100 and with the addition of each single anti-cancer drug \nalone. Of concern is as well, why different cut-offs for PDL were chosen for the measurement of the \nproliferative activity of both cells lines, namely 19 and 39 vs. 27 and 58 rather than using exactly the \nsame ones to better compare both with each other. As mentioned, especially figures 4, 6 and 7 do not \nadequately display what is meant to be described by the authors, these have to be improved or exchanged. Finally, the authors claim that their cell lines acquired drug resistance needs better clarification. How can they safely prove that? What was the half life of both drugs? How often was each \nanti-cancer drug renewed in the culture to ensure their activity on both cell lines up to late PDs, or was it\nonce added band never later again? This needs to be addressed in detail. \n3. Does the manuscript adhere to the relevant standards for reporting and data deposition: if not, in \nwhat ways? \nBearing in mind the extensive major and minor comments, these need to be addresses, if the authors \ncan improve and/or clarify all of these comments raised this will help to greatly improve the manuscript and ensure that the relevant standards of reporting are met. \n4. Is the writing acceptable? \nThe English phrasing and grammar needs much more attention. Correct spelling, expressions and grammar will greatly improve the manuscript. Some of these major flaws are mentioned in the section \n'minor criticism', but could not be named in full detail by the reviewer. In general, the whole paper needs\nextensive rewriting and rephrasing to ameliorate understanding its contents. \nLevel of interest: limited \nAdvice on publication: accept after extensive revision \nQuality of written English: poor, not acceptable for publication unless it is rewritten \nCompeting interests:\nNone declared.",
"role": "assistant"
}
] | 2,001
|
BMC Cancer Peer Reviews
This dataset contains peer reviews from BMC, standardized to match the format of the pawin205/PeerRT dataset.
Dataset Structure
Each record contains the following attributes:
relative_rank: Default value (0).win_prob: Default value (0.0).title: Title of the paper.abstract: Abstract of the paper.full_text: Full text of the paper (or review text if unavailable).review: The peer review text.source: Source of the data ('BMC').review_src: Original filename of the review.criteria_count: Dictionary containing counts of specific criteria in the review (e.g., criticism, praise).dimension_scores: Dictionary containing scores for various dimensions.overall_score: Computed overall score (reward value).thinking_trace: Placeholder (empty).prompt: Placeholder (empty).prompt_length: Placeholder (0).conversations: List of dictionaries representing the conversation (User/Assistant format).year: Year of publication (if available).
Usage
from datasets import load_dataset
dataset = load_dataset("JerMa88/BMC_Cancer_Peer_Reviews")
print(dataset['train'][0])
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