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• W2516180175 abstract "Ras protein was discovered more than 30 years ago and since then extensive research in the area of ras biology has clearly established the diverse roles of this master regulator in cancer. Nevertheless, this knowledge could not be translated into the development of clinically viable therapeutic agents against ras. The primary reason is the lack of possible drug-binding pockets within the ras structure itself as well as its high affinity to GTP that does not allow easy access to small molecule drugs. Alternatively, researchers have focused on targeting the upstream [epidermal growth factor receptor, insulin-like growth factor 1 receptor (IGF1R)] and downstream signaling pathways [such as the rapidly accelerated fibrosarcoma (RAF), mitogen-activated protein kinase kinase (MEK), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)] among others. However, none of these targets proved to be actionable and showed limited clinical benefits or often time acute toxicity in patients. Lack of response to downstream targets have been attributed to the diverse cross talk and feedback mechanisms in ras signaling and such attempts are yet to yield any clinically viable candidate molecules. Over the last decade the small GTPases such as Rho, Rac, and CDC42 have also been explored as potential therapeutic targets within the mutant ras signaling. The p21 activated kinases (PAKs) Rho GTPase effectors that are emerging to play a key role in cancer therapy resistance and stemness. There are two groups of PAKs [group I PAKs (1, 2, and 3) and group II PAKs (4, 5, and 6)]. This chapter highlights the multi-faceted roles of PAKs in cancer signaling and also brings forward some of the recent attempts to target key players particularly belonging to the group II kinases." @default.
• W2516180175 created "2016-09-16" @default.
• W2516180175 creator A5015800200 @default.
• W2516180175 creator A5056962753 @default.
• W2516180175 date "2017-01-01" @default.
• W2516180175 modified "2023-10-16" @default.
• W2516180175 title "Targeting Rho, Rac, CDC42 GTPase Effector p21 Activated Kinases in Mutant K-Ras-Driven Cancer" @default.
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