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Cancers
Special Issues
Unravelling Gastric Cancer Pathobiology: From Correa Cascade to Patchwork Vision
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Unravelling Gastric Cancer Pathobiology: From Correa Cascade to Patchwork Vision

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 5189

Special Issue Editors

Dr. Dominique Lamarque

E-Mail Website
Guest Editor
Department of Gastroenterology, Ambroise Paré Hospital, 92104 Boulogne-Billancourt, France
Interests: gastritis; inflammatory bowel diseases; optical biopsies; multispectral analysis; Helicobacter pylori; pre-neoplastic gastric lesions
Dr. Thomas Bazin

E-Mail Website
Guest Editor
Department of Gastroenterology, Ambroise Paré Hospital, 92104 Boulogne-Billancourt, France
Interests: mucosal inflammation; inflammatory bowel diseases; optical biopsies; multispectral analysis; microbiota; gut-on-chip; endoscopy; pre-neoplastic gastric lesions; biotherapies

Special Issue Information

Dear Colleagues,

Gastric cancer pathobiology has been explained by Dr Pelayo Correa as a linear cascade, with an evolution from normal gastric mucosa infected by cagA Helicobacter pylori to non-atrophic gastritis, then atrophic gastritis, intestinal metaplasia, gastric dysplasia and, ultimately, gastric adenocarcinoma. In the past decade, our knowledge of gastric carcinogenesis has improved, and this notion of linear progression has been called into question, in favor of a new selection model of the "adaptation and selection" type, quite different from the model of colon carcinogenesis, for example. Intestinal metaplasia is associated with an increased risk of gastric cancer because areas of dysplasia are genetically derived from one or more metaplastic clones and appear randomly, sometimes in multiple places. Moreover, dysplasia could also arise not only from intestinal metaplasia but also from pseudo-pyloric metaplastic clones. These new data are changing our understanding of carcinogenesis, and have implications for the screening and follow-up of patients.

Dr. Dominique Lamarque
Dr. Thomas Bazin
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • correa cascade
  • gastric adenocarcinoma
  • atrophic gastritis
  • intestinal metaplasia
  • gastric dysplasia
  • Helicobacter pylori
  • pseudo-pyloric metaplasia

Published Papers (2 papers)

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Research

11 pages, 1347 KiB  
Article
Creation of EGD-Derived Gastric Cancer Organoids to Predict Treatment Responses
by Hannah G. McDonald, Megan M. Harper, Kristen Hill, Anqi Gao, Angelica L. Solomon, Charles J. Bailey, Miranda Lin, Mautin Barry-Hundeyin, Michael J. Cavnar, Samuel H. Mardini, Prakash J. Pandalai, Reema A. Patel, Jill M. Kolesar, Justin A. Rueckert, Lawrence Hookey, Mark Ropeleski, Shaila J. Merchant, Joseph Kim and Mei Gao
Cancers 2023, 15(11), 3036; https://doi.org/10.3390/cancers15113036 - 2 Jun 2023
Cited by 1 | Viewed by 1649
Abstract
Gastric adenocarcinoma (GAd) is the third leading cause of cancer-related deaths worldwide. Most patients require perioperative chemotherapy, yet methods to accurately predict responses to therapy are lacking. Thus, patients may be unnecessarily exposed to considerable toxicities. Here, we present a novel methodology using [...] Read more.
Gastric adenocarcinoma (GAd) is the third leading cause of cancer-related deaths worldwide. Most patients require perioperative chemotherapy, yet methods to accurately predict responses to therapy are lacking. Thus, patients may be unnecessarily exposed to considerable toxicities. Here, we present a novel methodology using patient-derived organoids (PDOs) that rapidly and accurately predicts the chemotherapy efficacy for GAd patients. Methods: Endoscopic GAd biopsies were obtained from 19 patients, shipped overnight, and PDOs were developed within 24 h. Drug sensitivity testing was performed on PDO single-cells with current standard-of-care systemic GAd regimens and cell viability was measured. Whole exome sequencing was used to confirm the consistency of tumor-related gene mutations and copy number alterations between primary tumors, PDOs, and PDO single-cells. Results: Overall, 15 of 19 biopsies (79%) were appropriate for PDO creation and single-cell expansion within 24 h of specimen collection and overnight shipment. With our PDO single-cell technique, PDOs (53%) were successfully developed. Subsequently, two PDO lines were subjected to drug sensitivity testing within 12 days from initial biopsy procurement. Drug sensitivity assays revealed unique treatment response profiles for combination drug regimens in both of the two unique PDOs, which corresponded with the clinical response. Conclusions: The successful creation of PDOs within 24 h of endoscopic biopsy and rapid drug testing within 2 weeks demonstrate the feasibility of our novel approach for future applications in clinical decision making. This proof of concept sets the foundation for future clinical trials using PDOs to predict clinical responses to GAd therapies. Full article
(This article belongs to the Special Issue Unravelling Gastric Cancer Pathobiology: From Correa Cascade to Patchwork Vision)
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18 pages, 5238 KiB  
Article
Helicobacter pylori CagA Induces Cortactin Y-470 Phosphorylation-Dependent Gastric Epithelial Cell Scattering via Abl, Vav2 and Rac1 Activation
by Nicole Tegtmeyer, Aileen Harrer, Klemens Rottner and Steffen Backert
Cancers 2021, 13(16), 4241; https://doi.org/10.3390/cancers13164241 - 23 Aug 2021
Cited by 9 | Viewed by 2425
Abstract
The pathogen Helicobacter pylori is the first reported bacterial type-1 carcinogen playing a role in the development of human malignancies, including gastric adenocarcinoma. Cancer cell motility is an important process in this scenario, however, the molecular mechanisms are still not fully understood. Here, [...] Read more.
The pathogen Helicobacter pylori is the first reported bacterial type-1 carcinogen playing a role in the development of human malignancies, including gastric adenocarcinoma. Cancer cell motility is an important process in this scenario, however, the molecular mechanisms are still not fully understood. Here, we demonstrate that H. pylori subverts the actin-binding protein cortactin through its type-IV secretion system and injected oncoprotein CagA, e.g., by inducing tyrosine phosphorylation of cortactin at Y-470, which triggers gastric epithelial cell scattering and motility. During infection of AGS cells, cortactin was discovered to undergo tyrosine dephosphorylation at residues Y-421 and Y-486, which is mediated through inactivation of Src kinase. However, H. pylori also profoundly activates tyrosine kinase Abl, which simultaneously phosphorylates cortactin at Y-470. Phosphorylated cortactin interacts with the SH2-domain of Vav2, a guanine nucleotide exchange factor for the Rho-family of GTPases. The cortactin/Vav2 complex then stimulates a previously unrecognized activation cascade including the small GTPase Rac1, to effect actin rearrangements and cell scattering. We hypothesize that injected CagA targets cortactin to locally open the gastric epithelium in order to get access to certain nutrients. This may disturb the cellular barrier functions, likely contributing to the induction of cell motility, which is important in gastric cancer development. Full article
(This article belongs to the Special Issue Unravelling Gastric Cancer Pathobiology: From Correa Cascade to Patchwork Vision)
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