Mutations in KRAS drive PDAC. (IMAGE)
Caption
Mutations in KRAS drive PDAC. (A) Illustration depicting different stages of PDAC, in which tumors originating in the pancreas (stage 1) first extend to lymph nodes and bile ducts (stage 2), then invade the superior mesenteric artery (stage 3) and metastasize to other organs, such as the liver (stage 4). (B) Prevalence of RAS mutations in pancreatic cancer. RAS are mutated in 19% of all tumors, whereas 77% of RAS-mutated tumors exhibit KRAS mutations. (C) KRAS dependency in PDAC. In the case of PDACs, 90% of tumors harbor mutations in KRAS with different factors (listed) contributing to this dependency in PDAC. (D) KRAS mutations in PDAC. Among KRAS mutations in PDAC, 40% of mutations are G12D, 29% are G12V, 15% are G12R, and 1% are G12C. All these mutations confer distinct functional impacts on KRAS, leading to aberrant downstream signaling and contributing to disease onset and progression in PDAC.
Credit
Cancer Biology & Medicine
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