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Gastrointestinal Cancer: From Pathophysiology to Novel Therapeutic Approaches
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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: 20 March 2025 | Viewed by 4259

Special Issue Editor

Dr. Marlena Brzozowa-Zasada

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

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Keywords

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

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Published Papers (3 papers)

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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 1426
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
(This article belongs to the Special Issue Gastrointestinal Cancer: From Pathophysiology to Novel Therapeutic Approaches)
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22 pages, 4213 KiB  
Article
Association of KRAS Mutation and Gene Pathways in Colorectal Carcinoma: A Transcriptome- and Methylome-Wide Study and Potential Implications for Therapy
by Farzana Jasmine, Armando Almazan, Yuliia Khamkevych, Marc Bissonnette, Habibul Ahsan and Muhammad G. Kibriya
Int. J. Mol. Sci. 2024, 25(15), 8094; https://doi.org/10.3390/ijms25158094 - 25 Jul 2024
Viewed by 1256
Abstract
Kirsten Rat Sarcoma (KRAS) is the most commonly mutated oncogene in colorectal carcinoma (CRC). We have previously reported the interactions between microsatellite instability (MSI), DNA promoter methylation, and gene expression. In this study, we looked for associations between KRAS mutation, gene [...] Read more.
Kirsten Rat Sarcoma (KRAS) is the most commonly mutated oncogene in colorectal carcinoma (CRC). We have previously reported the interactions between microsatellite instability (MSI), DNA promoter methylation, and gene expression. In this study, we looked for associations between KRAS mutation, gene expression, and methylation that may help with precision medicine. Genome-wide gene expression and DNA methylation were done in paired CRC tumor and surrounding healthy tissues. The results suggested that (a) the magnitude of dysregulation of many major gene pathways in CRC was significantly greater in patients with the KRAS mutation, (b) the up- and down-regulation of these dysregulated gene pathways could be correlated with the corresponding hypo- and hyper-methylation, and (c) the up-regulation of CDKN2A was more pronounced in tumors with the KRAS mutation. A recent cell line study showed that there were higher CDKN2A levels in 5-FU-resistant CRC cells and that these could be down-regulated by Villosol. Our findings suggest the possibility of a better response to anti-CDKN2A therapy with Villosol in KRAS-mutant CRC. Also, the more marked up-regulation of genes in the proteasome pathway in CRC tissue, especially with the KRAS mutation and MSI, may suggest a potential role of a proteasome inhibitor (bortezomib, carfilzomib, or ixazomib) in selected CRC patients if necessary. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Pathophysiology to Novel Therapeutic Approaches)
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14 pages, 977 KiB  
Review
Enhanced CRC Growth in Iron-Rich Environment, Facts and Speculations
by Marcello Chieppa, Marianna Kashyrina, Alessandro Miraglia and Diana Vardanyan
Int. J. Mol. Sci. 2024, 25(22), 12389; https://doi.org/10.3390/ijms252212389 - 19 Nov 2024
Viewed by 894
Abstract
The contribution of nutritional factors to disease development has been demonstrated for several chronic conditions including obesity, type 2 diabetes, metabolic syndrome, and about 30 percent of cancers. Nutrients include macronutrients and micronutrients, which are required in large and trace quantities, respectively. Macronutrients, [...] Read more.
The contribution of nutritional factors to disease development has been demonstrated for several chronic conditions including obesity, type 2 diabetes, metabolic syndrome, and about 30 percent of cancers. Nutrients include macronutrients and micronutrients, which are required in large and trace quantities, respectively. Macronutrients, which include protein, carbohydrates, and lipids, are mainly involved in energy production and biomolecule synthesis; micronutrients include vitamins and minerals, which are mainly involved in immune functions, enzymatic reactions, blood clotting, and gene transcription. Among the numerous micronutrients potentially involved in disease development, the present review will focus on iron and its relation to tumor development. Recent advances in the understanding of iron-related proteins accumulating in the tumor microenvironment shed light on the pivotal role of iron availability in sustaining pathological tumor hallmarks, including cell cycle regulation, angiogenesis, and metastasis. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Pathophysiology to Novel Therapeutic Approaches)
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