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These studies suggest that oncogenic KRAS can directly activate PI3K signaling through the catalytic subunit P110α of PI3K.
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Oncogenic KRAS mutations are prevalent in various cancers, including pancreatic ductal adenocarcinoma (PDAC). These mutations are known to activate several downstream signaling pathways, including the phosphoinositide 3-kinase (PI3K) pathway. This synthesis aims to determine whether oncogenic KRAS can directly activate PI3K signaling through the catalytic subunit p110α of PI3K.
Dependence on p110α for Pancreatic Cancer Initiation:
Activation of p110α by Oncogenic Mutations:
Requirement of p110α for KRAS-Induced Tumorigenesis:
The evidence strongly supports that oncogenic KRAS can directly activate PI3K signaling through the catalytic subunit p110α. This activation is crucial for the initiation and progression of pancreatic cancer, as p110α is necessary for the reprogramming of acinar cells, proliferation of epithelial cells, and activation of downstream effectors like RAC1.
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