ijms-logo

Journal Browser

Journal Browser

Gastrointestinal Cancer: From Pathophysiology to Novel Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 446

Special Issue Editor


E-Mail Website
Guest Editor
Department of Histology and Cell Pathology in Zabrze, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 40-055 Katowice, Poland
Interests: colon cancer; gastric cancer; Notch signaling pathway; glutathione in cancer; antioxidant enzymes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gastrointestinal cancers include a broad range of malignant tumors affecting organs such as the esophagus, stomach, colon, liver, and pancreas. These cancers pose a significant global health burden, resulting in high morbidity and mortality.

The pathophysiology of gastrointestinal cancers involves complex molecular and genetic alterations. Genetic mutations, such as those in tumor suppressor genes (e.g., TP53) and oncogenes (e.g., KRAS), play a crucial role in driving oncogenesis and tumor growth. Environmental risk factors, such as tobacco smoking, alcohol consumption, obesity, and certain dietary habits, also significantly contribute to the development of gastrointestinal cancers. Recognizing the complexities of gastrointestinal cancer pathophysiology is essential for developing effective therapeutic strategies. Emerging therapeutic approaches: targeted therapies, such as inhibitors of specific molecular pathways (e.g., tyrosine kinases); immunotherapies, including immune checkpoint inhibitors and chimeric antigen receptor T-cell (CAR-T) therapy; nanomedicine and so on offer promising avenues to improve the outcomes of gastrointestinal cancers.

In conclusion, the pathophysiology of gastrointestinal cancers is multifaceted and involves complex molecular alterations. A comprehensive understanding of these processes paves the way for significant advances in therapeutic approaches.

This Special Issue “Gastrointestinal Cancer From Pathophysiology to Novel Therapeutic Approaches” of the International Journal of Molecular Sciences focuses on the study of molecular mechanisms and new therapeutic strategies for gastrointestinal cancers.

Dr. Marlena Brzozowa-Zasada
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • gastrointestinal cancer
  • molecular pathology
  • innovative therapies
  • targeted therapy
  • immunotherapy
  • cancer resistance

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:
13 pages, 3034 KiB  
Article
Characterization of MET Alterations in 37 Gastroesophageal Cancer Cell Lines for MET-Targeted Therapy
by Jin-Soo Kim, Mi Young Kim and Sungyoul Hong
Int. J. Mol. Sci. 2024, 25(11), 5975; https://doi.org/10.3390/ijms25115975 - 29 May 2024
Viewed by 213
Abstract
Capmatinib and savolitinib, selective MET inhibitors, are widely used to treat various MET-positive cancers. In this study, we aimed to determine the effects of these inhibitors on MET-amplified gastric cancer (GC) cells. Methods: After screening 37 GC cell lines, the following [...] Read more.
Capmatinib and savolitinib, selective MET inhibitors, are widely used to treat various MET-positive cancers. In this study, we aimed to determine the effects of these inhibitors on MET-amplified gastric cancer (GC) cells. Methods: After screening 37 GC cell lines, the following cell lines were found to be MET-positive with copy number variation >10: SNU-620, ESO51, MKN-45, SNU-5, and OE33 cell lines. Next, we assessed the cytotoxic response of these cell lines to capmatinib or savolitinib alone using cell counting kit-8 and clonogenic cell survival assays. Western blotting was performed to assess the effects of capmatinib and savolitinib on the MET signaling pathway. Xenograft studies were performed to evaluate the in vivo therapeutic efficacy of savolitinib in MKN-45 cells. Savolitinib and capmatinib exerted anti-proliferative effects on MET-amplified GC cell lines in a dose-dependent manner. Savolitinib inhibited the phosphorylation of MET and downstream signaling pathways, such as the protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) pathways, in MET-amplified GC cells. Additionally, savolitinib significantly decreased the number of colonies formed on the soft agar and exerted dose-dependent anti-tumor effects in an MKN-45 GC cell xenograft model. Furthermore, a combination of trastuzumab and capmatinib exhibited enhanced inhibition of AKT and ERK activation in human epidermal growth factor receptor-2 (HER2)- and MET-positive OE33 cells. Targeting MET with savolitinib and capmatinib efficiently suppressed the growth of MET-amplified GC cells. Moreover, these MET inhibitors exerted synergistic effects with trastuzumab on HER2- and MET-amplified GC cells. Full article
Show Figures

Figure 1

Back to TopTop