Reviewer's report
Title:Selenoprotein S (SEPS1) gene -105G>A promoter polymorphism
influences the susceptibility of Japanese to gastric cancer
Version: 2Date:4 October 2008
Reviewer: Charles Foster
Reviewer's report:
Overview: This study tests the hypothesis that a polymorphism in the gene
selenoprotein S, enhances the pro-inflammatory cytokine response and
modulates the risk for progressing from H. pylori induced gastritis to gastric
cancer. The G-105A polymorphism was typed in 268 men with gastric cancer
and 306 controls. The major finding was that in patients with Lauren's Intestinal
type cancer GG homozygotes were over represented (OR 1.99, p = 0.047). The
authors conclude that these data support the hypothesis that selenoprotein S
polymorphisms may modify the risk of Intestinal type gastric cancer.
Major Compulsory Revisions:
1) The statistical analysis should include a discussion of whether the data is in
Hardy-Weinberg Equilibrium.
2) The discussion should comment on whether selenium status is known to
influence susceptibility to H. pylori, gastritis, or gastric cancer. Is it known
whether selenium deficiency is common in your population?
3) Cigarette smoke exposure is known to modify the risk of colon and prostate
cancer in selenium deficient patients. Were patients asked about smoking
status? Does smoking modify the strength of the association?
4) In rats selenium deficiency induces eosinophilic enteritis (Hong CB. Exp Mol
Pathol. 1988 Apr;48(2):182-92.); does the polymorphism correlate with the
degree of eosinophilia on gastric biopsies?
Minor Essential Revisions:
1) There are quite a few awkward phrases throughtout the manuscript. A native
English speaking scientific editor should be consulted to assist with revisions. For
example: "Selenoprotein S is the molecule related with the control of
inflammatory response in Endoplasmic reticulum." This might be re-written as
"Selenoprotein S is an Endoplasmic reticulum localized protein that may control
inflammatory response." AND "It is suggested this SEPS1 polymorphism possibly
associated with the process of chronic gastric inflammation to carcinogenesis."
This could be re-written as "Since polymorphisms in SEPS1 influence
inflammatory cytokine response, it is possible that the G-105A polymorphism
influences progression from chronic gastric inflammation to gastric cancer."
2) In the discussion, the authors say that the results of previous association
studies exploring the role of the G-105A polymorphsim in chronic inflammatory
disease are controversial. Without further elaboration, it is not clear to the reader
why these results are controversial.
Discretionary Revisions:
1) If tissue is available, it would be most interesting to directly determine whether
the polymorphism correlates with tissue mRNA or protein levels of
pro-inflammatory cytokines such as IL-1b.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:Selenoprotein S (SEPS1) gene -105G>A promoter polymorphism
influences the susceptibility of Japanese to gastric cancer
Version: 2Date:4 October 2008
Reviewer: Charles Foster
Reviewer's report:
Overview: This study tests the hypothesis that a polymorphism in the gene
selenoprotein S, enhances the pro-inflammatory cytokine response and
modulates the risk for progressing from H. pylori induced gastritis to gastric
cancer. The G-105A polymorphism was typed in 268 men with gastric cancer
and 306 controls. The major finding was that in patients with Lauren's Intestinal
type cancer GG homozygotes were over represented (OR 1.99, p = 0.047). The
authors conclude that these data support the hypothesis that selenoprotein S
polymorphisms may modify the risk of Intestinal type gastric cancer.
Major Compulsory Revisions:
1) The statistical analysis should include a discussion of whether the data is in
Hardy-Weinberg Equilibrium.
2) The discussion should comment on whether selenium status is known to
influence susceptibility to H. pylori, gastritis, or gastric cancer. Is it known
whether selenium deficiency is common in your population?
3) Cigarette smoke exposure is known to modify the risk of colon and prostate
cancer in selenium deficient patients. Were patients asked about smoking
status? Does smoking modify the strength of the association?
4) In rats selenium deficiency induces eosinophilic enteritis (Hong CB. Exp Mol
Pathol. 1988 Apr;48(2):182-92.); does the polymorphism correlate with the
degree of eosinophilia on gastric biopsies?
Minor Essential Revisions:
1) There are quite a few awkward phrases throughtout the manuscript. A native
English speaking scientific editor should be consulted to assist with revisions. For
example: "Selenoprotein S is the molecule related with the control of
inflammatory response in Endoplasmic reticulum." This might be re-written as
"Selenoprotein S is an Endoplasmic reticulum localized protein that may control
inflammatory response." AND "It is suggested this SEPS1 polymorphism possibly
associated with the process of chronic gastric inflammation to carcinogenesis."
This could be re-written as "Since polymorphisms in SEPS1 influence
inflammatory cytokine response, it is possible that the G-105A polymorphism
influences progression from chronic gastric inflammation to gastric cancer."
2) In the discussion, the authors say that the results of previous association
studies exploring the role of the G-105A polymorphsim in chronic inflammatory
disease are controversial. Without further elaboration, it is not clear to the reader
why these results are controversial.
Discretionary Revisions:
1) If tissue is available, it would be most interesting to directly determine whether
the polymorphism correlates with tissue mRNA or protein levels of
pro-inflammatory cytokines such as IL-1b.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:Selenoprotein S (SEPS1) gene -105G>A promoter polymorphism
influences the susceptibility of Japanese to gastric cancer
Version: 2Date:4 October 2008
Reviewer: Charles Foster
Reviewer's report:
Overview: This study tests the hypothesis that a polymorphism in the gene
selenoprotein S, enhances the pro-inflammatory cytokine response and
modulates the risk for progressing from H. pylori induced gastritis to gastric
cancer. The G-105A polymorphism was typed in 268 men with gastric cancer
and 306 controls. The major finding was that in patients with Lauren's Intestinal
type cancer GG homozygotes were over represented (OR 1.99, p = 0.047). The
authors conclude that these data support the hypothesis that selenoprotein S
polymorphisms may modify the risk of Intestinal type gastric cancer.
Major Compulsory Revisions:
1) The statistical analysis should include a discussion of whether the data is in
Hardy-Weinberg Equilibrium.
2) The discussion should comment on whether selenium status is known to
influence susceptibility to H. pylori, gastritis, or gastric cancer. Is it known
whether selenium deficiency is common in your population?
3) Cigarette smoke exposure is known to modify the risk of colon and prostate
cancer in selenium deficient patients. Were patients asked about smoking
status? Does smoking modify the strength of the association?
4) In rats selenium deficiency induces eosinophilic enteritis (Hong CB. Exp Mol
Pathol. 1988 Apr;48(2):182-92.); does the polymorphism correlate with the
degree of eosinophilia on gastric biopsies?
Minor Essential Revisions:
1) There are quite a few awkward phrases throughtout the manuscript. A native
English speaking scientific editor should be consulted to assist with revisions. For
example: "Selenoprotein S is the molecule related with the control of
inflammatory response in Endoplasmic reticulum." This might be re-written as
"Selenoprotein S is an Endoplasmic reticulum localized protein that may control
inflammatory response." AND "It is suggested this SEPS1 polymorphism possibly
associated with the process of chronic gastric inflammation to carcinogenesis."
This could be re-written as "Since polymorphisms in SEPS1 influence
inflammatory cytokine response, it is possible that the G-105A polymorphism
influences progression from chronic gastric inflammation to gastric cancer."
2) In the discussion, the authors say that the results of previous association
studies exploring the role of the G-105A polymorphsim in chronic inflammatory
disease are controversial. Without further elaboration, it is not clear to the reader
why these results are controversial.
Discretionary Revisions:
1) If tissue is available, it would be most interesting to directly determine whether
the polymorphism correlates with tissue mRNA or protein levels of
pro-inflammatory cytokines such as IL-1b.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
assistant