Abstract

Mutational activations of KRas is one of the most common oncogenic events in human cancers and a heavily pursued target in therapeutic development for decades. Mutant KRas protein engages a host of signaling cascades that culminate in uncontrolled cell proliferation, enhanced survival, and set the stage for acquisition of further genetic events that propel cancer cells towards more malignant phenotypes. Direct targeting of KRas protein with inhibitors that disrupt its maturation and proper trafficking has not been successful in clinic. Instead, much attention is now focused on targeting the effector cascades that mutant KRas utilizes to exert its oncogenic feats, which include the PI3K/AKT/ mTOR and Raf/MEK/ERK cascades. Numerous inhibitors targeting these pathways have been developed and are being tested in clinic. However, durable clinical success will depend on identifying effective combinations with tolerable side effects and strategies to overcome resistance mechanisms.

Original languageEnglish
Title of host publicationCancer Therapeutic Targets
PublisherSpringer New York
Pages763-772
Number of pages10
Volume2-2
ISBN (Electronic)9781441907172
ISBN (Print)9781441907165
DOIs
StatePublished - Jan 1 2017

Keywords

  • Anti-EGFR monoclonal antibodies
  • Assessment
  • Cetuximab
  • Clinical trials
  • Effector
  • Epidermal growth factor receptors (EGFRs)
  • FOLFIRI
  • Farnesyl thiosalicylic acid
  • In human cancer
  • Kirsten rat sarcoma viral oncogene homolog (KRas)
  • Mutations
  • Ras GTPase activity
  • Ras GTPase-activating proteins
  • Ras guanine nucleotide exchange factor (RasGEF) proteins
  • SOS
  • Salirasib
  • Therapeutics
  • Tipifarnib
  • Tyrosine kinase inhibitor
  • Vemurafenib
  • mFOLFOX6

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  • Cite this

    Lim, K. H. (2017). K-Ras. In Cancer Therapeutic Targets (Vol. 2-2, pp. 763-772). Springer New York. https://doi.org/10.1007/978-1-4419-0717-2_73