Version 1
: Received: 28 October 2024 / Approved: 28 October 2024 / Online: 30 October 2024 (07:52:05 CET)
How to cite:
Duta-Ion, S. G.; Juganaru, I. R.; Hotinceanu, I. A.; Dan, A.; Burtavel, L. M.; Coman, M. C.; Focsa, I. O.; Zaruha, A. G.; Codreanu, P. C.; Bohiltea, L. C.; Rădoi, V. E. Actionable Molecular Pathways in Colorectal Cancer. Preprints2024, 2024102231. https://doi.org/10.20944/preprints202410.2231.v1
Duta-Ion, S. G.; Juganaru, I. R.; Hotinceanu, I. A.; Dan, A.; Burtavel, L. M.; Coman, M. C.; Focsa, I. O.; Zaruha, A. G.; Codreanu, P. C.; Bohiltea, L. C.; Rădoi, V. E. Actionable Molecular Pathways in Colorectal Cancer. Preprints 2024, 2024102231. https://doi.org/10.20944/preprints202410.2231.v1
Duta-Ion, S. G.; Juganaru, I. R.; Hotinceanu, I. A.; Dan, A.; Burtavel, L. M.; Coman, M. C.; Focsa, I. O.; Zaruha, A. G.; Codreanu, P. C.; Bohiltea, L. C.; Rădoi, V. E. Actionable Molecular Pathways in Colorectal Cancer. Preprints2024, 2024102231. https://doi.org/10.20944/preprints202410.2231.v1
APA Style
Duta-Ion, S. G., Juganaru, I. R., Hotinceanu, I. A., Dan, A., Burtavel, L. M., Coman, M. C., Focsa, I. O., Zaruha, A. G., Codreanu, P. C., Bohiltea, L. C., & Rădoi, V. E. (2024). Actionable Molecular Pathways in Colorectal Cancer. Preprints. https://doi.org/10.20944/preprints202410.2231.v1
Chicago/Turabian Style
Duta-Ion, S. G., Laurentiu Camil Bohiltea and Viorica Elena Rădoi. 2024 "Actionable Molecular Pathways in Colorectal Cancer" Preprints. https://doi.org/10.20944/preprints202410.2231.v1
Abstract
Colorectal cancer (CRC) arises through a combination of genetic and epigenetic alterations that affect key pathways involved in tumor growth and progression. This review examines the major molecular pathways driving CRC, including Chromosomal Instability (CIN), Microsatellite Instability (MSI), and the CpG Island Methylator Phenotype (CIMP). Key mutations in genes such as APC, KRAS, NRAS, BRAF, and TP53 activate signaling pathways like Wnt, EGFR, and PI3K/AKT, contributing to tumorigenesis and influencing responses to targeted therapies. Resistance mechanisms, including mutations that bypass drug action, remain challenging in CRC treatment. The review highlights the role of molecular profiling in guiding the use of targeted therapies such as tyrosine kinase inhibitors and immune checkpoint inhibitors. Novel combination treatments are also discussed as strategies to improve outcomes and overcome resistance. Understanding these molecular mechanisms is critical to advancing personalized treatment approaches in CRC and improving patient prognosis.
Medicine and Pharmacology, Oncology and Oncogenics
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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