Phosphoinositide 3-kinase regulates wild-type RAS signaling to confer resistance to KRAS inhibition

Abstract excerpt

<h4>SUMMARY</h4> Despite the availability of RAS inhibitors and the dependence of >90% of pancreatic ductal adenocarcinomas (PDAC) on oncogenic KRAS mutations, resistance to KRAS inhibition remains a serious obstacle. We show here that phosphoinositide 3-kinase (PI3K) plays a major role in this resistance through upstream activation of wild-type RAS signaling – beyond its known KRAS effector function. Combining...

Topics

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• Carcinoma, Pancreatic Ductal
• Class I Phosphatidylinositol 3-Kinases
• Drug Resistance, Neoplasm
• Pancreatic Neoplasms
• Phosphatidylinositol 3-Kinases
• Phosphoinositide-3 Kinase Inhibitors
• Protein Kinase Inhibitors
• Proto-Oncogene Proteins p21(ras)

Identifiers and source

Literature Corpus work

bf99929b-670f-5243-aa2b-fd68b361f8d8

DOI

10.1101/2025.06.20.660715