| Literature DB >> 33801965 |
Lisa Maria Mustachio1,2, Anca Chelariu-Raicu3, Lorant Szekvolgyi4, Jason Roszik5,6.
Abstract
The Kirsten rat sarcoma viral oncogene homolog (KRAS) is mutated in approximately 25% of all human cancers and is known to be a major player promoting and maintaining tumorigenesis through the RAS/MAPK pathway. Over the years, a large number of studies have identified strategies at different regulatory levels to tackle this 'difficult-to-target' oncoprotein. Yet, the most ideal strategy to overcome KRAS and its downstream effects has yet to be uncovered. This review summarizes the role of KRAS activating mutations in multiple cancer types as well as the key findings for potential strategies inhibiting its oncogenic behavior. A comprehensive analysis of the different pathways and mechanisms associated with KRAS activity in tumors will ultimately pave the way for promising future work that will identify optimum therapeutic strategies.Entities:
Keywords: EGFR; KRAS; MAPK; cancer; mutations; targeted-therapy
Year: 2021 PMID: 33801965 PMCID: PMC7999304 DOI: 10.3390/cancers13061204
Source DB: PubMed Journal: Cancers (Basel) ISSN: 2072-6694 Impact factor: 6.639