KRAS Mutation: Triggers of Colorectal Cancer
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 150
Special Issue Editor
Interests: KRAS signaling pathway; autophagy; colorectal cancer (CRC); yeast model; molecular target
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Colorectal cancer (CRC) is a leading cause of mortality in Europe, and its global therapeutics market is worth billions of euros. KRAS-activating mutations (KRASm), including KRASG13D, KRASG12D, and KRASG12V, are among the most frequent events found in CRC. Metastatic-CRC-harboring KRAS mutations are generally resistant to chemotherapy, namely, to epidermal growth factor receptor (EGFR) inhibitors. This is a relevant clinical problem that urges a resolution. Despite the billions of dollars spent by pharmaceutical companies, so far, the inhibition of mutated RAS has not been achieved.
The study of the role of KRAS mutations on colon carcinogenesis, tumor microenvironment, cell survival, autophagy, glycolytic metabolism, and invasion/metastization potential is an ever-growing field. A precise understanding of the mechanisms underlying KRAS in colorectal carcinogenesis might help in identifying new molecular targets to overcome the resistance in CRC-harboring KRAS mutations.
This Special Issue aims to highlight the most recent advances in studying the role of KRAS mutations on colorectal carcinogenesis using different cellular models and their possible therapeutic applications.
Dr. Ana Preto
Guest Editor
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