Advances and Challenges in KRAS Mutation Detection and Clinical Implications
Aberrant activation of the RAS signaling pathway is a halmark of various cancers. This activation, is often caused by mutations in RAS genes or other pathway components and, drivesi uncontrolled cell growth and proliferation. Studies have demonstrated that certain codon mutations can significantly influence the clinical outcomes of cancer patients. Historically, KRAS was considered "undruggable"; however, recent advancements in drug discovery have led to the development of promising KRAS inhibitors. Accurately identifying the specific type of KRAS mutation in a patient is essential for making optimal treatment decisions. Several methods have been developed for detecting KRAS mutations to address this need, focusing on creating robust, rapid, sensitive, accurate, and cost-effective approaches, particularly for point-of-care applications. Starting with the Ras family and RASopathies, this review provides a comprehensive overview of KRAS mutation detection methods, ranging from research-use-only techniques to in vitro diagnostic-certified tests. Published results are critically evaluated in terms of accuracy, sensitivity, cost, throughput, and suitability for various sample types and clinical settings. This, offers researchers and clinicians an up-to-date resource for.
Authors
- Samira Nomiri (ORCID: https://orcid.org/0000-0002-3569-4650)
- Javad Razaviyan (ORCID: https://orcid.org/0000-0003-2122-7012)
- Mohammad Réza Ahmadian
- Meer-Taher Shabani-Rad
- Tooba Yousefi
- Esmail Pishbin
- Maryam Sadat Mirlohi
- Siamak Salami
Institutions
- University of Calgary (CA)
- University of Victoria (CA)
- Iranian Research Organization for Science and Technology (IR)
- Calgary Laboratory Services (CA)
- Heinrich Heine University Düsseldorf (DE)
- Shahid Beheshti University of Medical Sciences (IR)
Publication Details
- Journal
- Cancers
- Published
- 2025-12-22
- DOI
- https://doi.org/10.3390/cancers18010031
- Primary Topic
- Protein Kinase Regulation and GTPase Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00