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Molecular Mechanisms and Therapies of Gastrointestinal Cancer

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 January 2026 | Viewed by 869

Special Issue Editor

Special Issue Information

Dear Colleagues,

Gastrointestinal (GI) cancers remain a major global health challenge due to their high morbidity and mortality rates. Despite advancements in early detection and treatment strategies, the prognosis for many GI cancer patients remains poor, underscoring the urgent need for improved therapeutic approaches. This Special Issue aims to explore the latest research on the molecular mechanisms driving GI cancer initiation, progression, and resistance to therapy, with a focus on identifying novel biomarkers and unraveling key signaling pathways. We seek contributions that delve into the genetic mutations and epigenetic changes that underpin tumorigenesis in these cancers. Key areas of interest include but are not limited to the role of tumor suppressor genes, oncogenes, and molecular networks involved in cell cycle regulation, metastasis, and immune evasion. Additionally, the issue will explore the impact of the tumor microenvironment, including stromal interactions and immune cell dynamics, in shaping cancer behavior. By bringing together cutting-edge research on molecular diagnostics, biomarkers, and treatment resistance, this issue aims to highlight promising therapeutic strategies and molecular targets for improving patient outcomes in GI cancer. We invite original research, reviews, and clinical studies that provide new insights into the molecular biology of GI cancers and innovative therapeutic approaches.

Dr. Donatella Delle Cave
Guest Editor

Manuscript Submission Information

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Keywords

  • tumor microenvironment
  • therapy resistance
  • genetic mutations
  • oncogenes
  • molecular diagnostics

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Published Papers (1 paper)

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Review

27 pages, 1375 KB  
Review
FBXW7 Gene Mutation and Expression in Colorectal Cancer (CRC): A Systematic Review from Molecular Mechanisms to Clinical Translation
by Giulia Arrivi, Gabriella Gentile, Michela Roberto and Donatella Delle Cave
Int. J. Mol. Sci. 2025, 26(23), 11318; https://doi.org/10.3390/ijms262311318 - 23 Nov 2025
Viewed by 567
Abstract
In the context of precision oncology, understanding the molecular drivers of colorectal cancer (CRC) is critical for improving prognosis and guiding targeted therapy. FBXW7 is a tumor suppressor that plays a pivotal role in CRC by regulating the degradation of key oncogenic proteins, [...] Read more.
In the context of precision oncology, understanding the molecular drivers of colorectal cancer (CRC) is critical for improving prognosis and guiding targeted therapy. FBXW7 is a tumor suppressor that plays a pivotal role in CRC by regulating the degradation of key oncogenic proteins, influencing tumor initiation, growth, therapeutic response, and metastatic behavior. Mutations in FBXW7 occur in 6–10% of CRC. Despite its biological relevance, the prognostic and predictive role of FBXW7 in CRC remains unclear, with inconsistent findings across studies. This systematic review collects and analyzes current evidence on FBXW7 mutations and expression in CRC, emphasizing its potential role in risk stratification, therapeutic response, and personalized treatment approaches. A total of 113 records were selected on PubMed, SCOPUS, Web of Science and Cochrane Central Register of Controlled Trials from 2015 and January 2025, of which 48 examined the preclinical landscape of FBXW7 in CRC and 65 focused on its clinical role. FBXW7 mutations are associated with different clinicopathological patterns, including early-onset disease, microsatellite instability, and co-occurring driver alterations, all of which shape prognosis and treatment outcomes. While some variants correlate with immune infiltration and better survival, others, especially when co-mutated, predict aggressive disease and poor outcomes. Furthermore, FBXW7 alterations contribute to chemoresistance and anti-EGFR therapy resistance but also reveal potential therapeutic vulnerabilities. These findings underscore FBXW7’s promise as a prognostic biomarker and a potential target for precision oncology strategies in colorectal cancer. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Gastrointestinal Cancer)
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