Reviewer's report
Title:Association of polymorphism of PTPN 11 encoding SHP-2 with gastric
atrophy but not gastric cancer in Helicobacter pylori seropositive Chinese
population
Version: 1Date:11 May 2012
Reviewer: Kazuhiro Tsukamoto
Reviewer's report:
BMC Gastroenterology
To editor:
This manuscript by Jiang J, et al. entitled “Association of polymorphism of
PTPN11 encoding SHP-2 with gastric atrophy but not gastric cancer in
Helicobacter pylori seropositive Chinese population“ reports that a new gastric
atrophy-susceptibility SNP in PTPN11 was confirmed by a single candidate
gene-based association study for 109 patients with gastric atrophy and 923
healthy control subjects in the Chinese population.
This is concise, easily readable, and has accurately statistical analyses.
Furthermore, this study is one of the replication studies, indicating that a new
SNP in PTPN11 is associated with susceptibility to H. pylori-seropositive gastric
atrophy in the Chinese population. However, PTPN11 is already known as a
disease-susceptibility gene related to gastric atrophy in the Japanese population
in several reports, although the associated SNP in this manuscript is different
from that associated in the Japanese population. This manuscript is involved in
the same manner of the leading studies. There are no new idea, study design,
suggestions, and attractive prospects on the molecular mechanisms, which are
related to the predisposition to the onset of gastric atrophy, but not gastric
cancer. Therefore, the study design with SNP analysis of 6 tag SNPs of one
gene, results, and explanation of a pathophysiological perspective are not
enough for publication. My recommendation is to reject this manuscript and to
publish it to another journal.
My minor comments are following below.
1. The total number of the healthy control subjects is described as 932 in Table
1. However, 923 was subject to the following analysis.
2. The authors suggest that an intronic enhancer may be located within or around
the rs12423190 SNP site in PTPN11 as shown in the Discussion section (Lines
20-21 in page 12). This putative enhance may induce the overexpression of
PTPN11, thereby resulting in the gain-of-function of SHP-2. As another
mechanism, the gain-of-function of SNP-2 may accelerate the downregulation of
T-cell and B-cell activation through CTLA-4/PD-1 as well as IL-6/STAT3
signalings, eventually leading to a decrease in inflammation. This point shows a
discrepancy in the suggestion of this manuscript.
I declare that I have no competing interests.
Level of interest: An article of limited interest
Quality of written English: Acceptable
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:Association of polymorphism of PTPN 11 encoding SHP-2 with gastric
atrophy but not gastric cancer in Helicobacter pylori seropositive Chinese
population
Version: 1Date:11 May 2012
Reviewer: Kazuhiro Tsukamoto
Reviewer's report:
BMC Gastroenterology
To editor:
This manuscript by Jiang J, et al. entitled “Association of polymorphism of
PTPN11 encoding SHP-2 with gastric atrophy but not gastric cancer in
Helicobacter pylori seropositive Chinese population“ reports that a new gastric
atrophy-susceptibility SNP in PTPN11 was confirmed by a single candidate
gene-based association study for 109 patients with gastric atrophy and 923
healthy control subjects in the Chinese population.
This is concise, easily readable, and has accurately statistical analyses.
Furthermore, this study is one of the replication studies, indicating that a new
SNP in PTPN11 is associated with susceptibility to H. pylori-seropositive gastric
atrophy in the Chinese population. However, PTPN11 is already known as a
disease-susceptibility gene related to gastric atrophy in the Japanese population
in several reports, although the associated SNP in this manuscript is different
from that associated in the Japanese population. This manuscript is involved in
the same manner of the leading studies. There are no new idea, study design,
suggestions, and attractive prospects on the molecular mechanisms, which are
related to the predisposition to the onset of gastric atrophy, but not gastric
cancer. Therefore, the study design with SNP analysis of 6 tag SNPs of one
gene, results, and explanation of a pathophysiological perspective are not
enough for publication. My recommendation is to reject this manuscript and to
publish it to another journal.
My minor comments are following below.
1. The total number of the healthy control subjects is described as 932 in Table
1. However, 923 was subject to the following analysis.
2. The authors suggest that an intronic enhancer may be located within or around
the rs12423190 SNP site in PTPN11 as shown in the Discussion section (Lines
20-21 in page 12). This putative enhance may induce the overexpression of
PTPN11, thereby resulting in the gain-of-function of SHP-2. As another
mechanism, the gain-of-function of SNP-2 may accelerate the downregulation of
T-cell and B-cell activation through CTLA-4/PD-1 as well as IL-6/STAT3
signalings, eventually leading to a decrease in inflammation. This point shows a
discrepancy in the suggestion of this manuscript.
I declare that I have no competing interests.
Level of interest: An article of limited interest
Quality of written English: Acceptable
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:Association of polymorphism of PTPN 11 encoding SHP-2 with gastric
atrophy but not gastric cancer in Helicobacter pylori seropositive Chinese
population
Version: 1Date:11 May 2012
Reviewer: Kazuhiro Tsukamoto
Reviewer's report:
BMC Gastroenterology
To editor:
This manuscript by Jiang J, et al. entitled “Association of polymorphism of
PTPN11 encoding SHP-2 with gastric atrophy but not gastric cancer in
Helicobacter pylori seropositive Chinese population“ reports that a new gastric
atrophy-susceptibility SNP in PTPN11 was confirmed by a single candidate
gene-based association study for 109 patients with gastric atrophy and 923
healthy control subjects in the Chinese population.
This is concise, easily readable, and has accurately statistical analyses.
Furthermore, this study is one of the replication studies, indicating that a new
SNP in PTPN11 is associated with susceptibility to H. pylori-seropositive gastric
atrophy in the Chinese population. However, PTPN11 is already known as a
disease-susceptibility gene related to gastric atrophy in the Japanese population
in several reports, although the associated SNP in this manuscript is different
from that associated in the Japanese population. This manuscript is involved in
the same manner of the leading studies. There are no new idea, study design,
suggestions, and attractive prospects on the molecular mechanisms, which are
related to the predisposition to the onset of gastric atrophy, but not gastric
cancer. Therefore, the study design with SNP analysis of 6 tag SNPs of one
gene, results, and explanation of a pathophysiological perspective are not
enough for publication. My recommendation is to reject this manuscript and to
publish it to another journal.
My minor comments are following below.
1. The total number of the healthy control subjects is described as 932 in Table
1. However, 923 was subject to the following analysis.
2. The authors suggest that an intronic enhancer may be located within or around
the rs12423190 SNP site in PTPN11 as shown in the Discussion section (Lines
20-21 in page 12). This putative enhance may induce the overexpression of
PTPN11, thereby resulting in the gain-of-function of SHP-2. As another
mechanism, the gain-of-function of SNP-2 may accelerate the downregulation of
T-cell and B-cell activation through CTLA-4/PD-1 as well as IL-6/STAT3
signalings, eventually leading to a decrease in inflammation. This point shows a
discrepancy in the suggestion of this manuscript.
I declare that I have no competing interests.
Level of interest: An article of limited interest
Quality of written English: Acceptable
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