Title: Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics
Version: 2 Date: 23 Dec 2024
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: "Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics"
Thank you for the opportunity to review your manuscript.
The revised manuscript demonstrates significant improvements, particularly with the inclusion
of numerical details in the abstract, reorganization of patient descriptions, and clearer figure
legends. The addition of p-values where applicable strengthens the statistical rigor. However,
several aspects could still benefit from clarification and refinement.
The histological classifications and progression stages are well-described. Still, the presentation
of statistical data (e.g., comparisons of age and sex distributions across stages of cystic dilatation)
could be more thoroughly discussed in the text rather than relying solely on tables. While the
figures provide critical visual support, certain sections, such as Figure 2, remain somewhat
unclear despite the revisions. Adding more detailed commentary on the figure in the discussion
might improve accessibility.
The immunohistochemical findings, particularly the roles of markers such as MUC5AC and
Ki-67, are intriguing, but their implications for clinical practice or molecular mechanisms
of transformation are underexplored. Future studies focusing on these markers' diagnostic or
prognostic value would greatly enhance the impact of this work.
you can expand your discussion with adding : "The observed transformation of gastric mucosal
atrophy into cystic dilatation and subsequent neoplasia is likely influenced by inflammatory
and molecular disruptions, as suggested by Kuester et al. (2013). Their findings demonstrate
that Helicobacter pylori infection, combined with deficiencies in protease pathways such as
cathepsin x/z, induces premalignant host responses. These insights highlight potential molecular
mechanisms underlying the progression of atrophic lesions to cystic dilations and gastric
adenocarcinoma, reinforcing the need for further exploration into host-pathogen interactions in
gastric cancer pathogenesis."
This addition would enrich your discussion with a molecular perspective while maintaining the
focus on histopathological findings.
Ref: Kuester D, et al. (2013). Induction of premalignant host responses by cathepsin x/
z-deficiency in Helicobacter pylori-infected mice. PLoS One, 8(7):e70242. DOI:10.1371/
journal.pone.0070242
Overall, the manuscript provides valuable data on the pathogenesis of gastric mucosal atrophy
and cystic dilatation. The outlined stages and classifications could serve as a critical foundation
for future research into gastric cancer prevention and early detection. With minor adjustments,
the manuscript would be suitable for publication.
Kind regards,
Title: Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics
Version: 2 Date: 23 Dec 2024
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: "Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics"
Thank you for the opportunity to review your manuscript.
The revised manuscript demonstrates significant improvements, particularly with the inclusion
of numerical details in the abstract, reorganization of patient descriptions, and clearer figure
legends. The addition of p-values where applicable strengthens the statistical rigor. However,
several aspects could still benefit from clarification and refinement.
The histological classifications and progression stages are well-described. Still, the presentation
of statistical data (e.g., comparisons of age and sex distributions across stages of cystic dilatation)
could be more thoroughly discussed in the text rather than relying solely on tables. While the
figures provide critical visual support, certain sections, such as Figure 2, remain somewhat
unclear despite the revisions. Adding more detailed commentary on the figure in the discussion
might improve accessibility.
The immunohistochemical findings, particularly the roles of markers such as MUC5AC and
Ki-67, are intriguing, but their implications for clinical practice or molecular mechanisms
of transformation are underexplored. Future studies focusing on these markers' diagnostic or
prognostic value would greatly enhance the impact of this work.
you can expand your discussion with adding : "The observed transformation of gastric mucosal
atrophy into cystic dilatation and subsequent neoplasia is likely influenced by inflammatory
and molecular disruptions, as suggested by Kuester et al. (2013). Their findings demonstrate
that Helicobacter pylori infection, combined with deficiencies in protease pathways such as
cathepsin x/z, induces premalignant host responses. These insights highlight potential molecular
mechanisms underlying the progression of atrophic lesions to cystic dilations and gastric
adenocarcinoma, reinforcing the need for further exploration into host-pathogen interactions in
gastric cancer pathogenesis."
This addition would enrich your discussion with a molecular perspective while maintaining the
focus on histopathological findings.
Ref: Kuester D, et al. (2013). Induction of premalignant host responses by cathepsin x/
z-deficiency in Helicobacter pylori-infected mice. PLoS One, 8(7):e70242. DOI:10.1371/
journal.pone.0070242
Overall, the manuscript provides valuable data on the pathogenesis of gastric mucosal atrophy
and cystic dilatation. The outlined stages and classifications could serve as a critical foundation
for future research into gastric cancer prevention and early detection. With minor adjustments,
the manuscript would be suitable for publication.
Kind regards,
Please review this paper.
user
Title: Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics
Version: 2 Date: 23 Dec 2024
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: "Relationship Between Gastric Mucosal Atrophy, Cystic Dilatation, and Histopathological
Characteristics"
Thank you for the opportunity to review your manuscript.
The revised manuscript demonstrates significant improvements, particularly with the inclusion
of numerical details in the abstract, reorganization of patient descriptions, and clearer figure
legends. The addition of p-values where applicable strengthens the statistical rigor. However,
several aspects could still benefit from clarification and refinement.
The histological classifications and progression stages are well-described. Still, the presentation
of statistical data (e.g., comparisons of age and sex distributions across stages of cystic dilatation)
could be more thoroughly discussed in the text rather than relying solely on tables. While the
figures provide critical visual support, certain sections, such as Figure 2, remain somewhat
unclear despite the revisions. Adding more detailed commentary on the figure in the discussion
might improve accessibility.
The immunohistochemical findings, particularly the roles of markers such as MUC5AC and
Ki-67, are intriguing, but their implications for clinical practice or molecular mechanisms
of transformation are underexplored. Future studies focusing on these markers' diagnostic or
prognostic value would greatly enhance the impact of this work.
you can expand your discussion with adding : "The observed transformation of gastric mucosal
atrophy into cystic dilatation and subsequent neoplasia is likely influenced by inflammatory
and molecular disruptions, as suggested by Kuester et al. (2013). Their findings demonstrate
that Helicobacter pylori infection, combined with deficiencies in protease pathways such as
cathepsin x/z, induces premalignant host responses. These insights highlight potential molecular
mechanisms underlying the progression of atrophic lesions to cystic dilations and gastric
adenocarcinoma, reinforcing the need for further exploration into host-pathogen interactions in
gastric cancer pathogenesis."
This addition would enrich your discussion with a molecular perspective while maintaining the
focus on histopathological findings.
Ref: Kuester D, et al. (2013). Induction of premalignant host responses by cathepsin x/
z-deficiency in Helicobacter pylori-infected mice. PLoS One, 8(7):e70242. DOI:10.1371/
journal.pone.0070242
Overall, the manuscript provides valuable data on the pathogenesis of gastric mucosal atrophy
and cystic dilatation. The outlined stages and classifications could serve as a critical foundation
for future research into gastric cancer prevention and early detection. With minor adjustments,
the manuscript would be suitable for publication.
Kind regards,
assistant