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- Lisa Maria Mustachio
- Department of Epigenetics and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
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- Anca Chelariu-Raicu
- Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilian University of Munich, 80539 Munich, Germany
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- Lorant Szekvolgyi
- Genome Architecture and Recombination Research Group, Department of Biochemistry and Molecular Biology, MTA-DE Momentum, Faculty of Medicine, University of Debrecen, 4002 Debrecen, Hungary
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- Jason Roszik
- Department of Genomic Medicine, Division of Cancer Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
説明
<jats:p>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.</jats:p>
収録刊行物
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- Cancers
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Cancers 13 (6), 1204-, 2021-03-10
MDPI AG
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キーワード
詳細情報 詳細情報について
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- CRID
- 1360017287064383360
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- ISSN
- 20726694
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- データソース種別
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- Crossref
- OpenAIRE