Targeting KRAS in Cancer: Promising Therapeutic Strategies

DOI Web Site 1 Citations Open Access
  • Lisa Maria Mustachio
    Department of Epigenetics and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
  • Anca Chelariu-Raicu
    Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilian University of Munich, 80539 Munich, Germany
  • 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
  • Jason Roszik
    Department of Genomic Medicine, Division of Cancer Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

Description

<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>

Journal

  • Cancers

    Cancers 13 (6), 1204-, 2021-03-10

    MDPI AG

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