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Article

PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition.

Cancer research - 4 Aug 2026

Ge Xiangyu, Singh Jaffarguriqbal, Li Wenxue, Markham Cassandra S, Ruiz Christian Felipe, Stites Edward C, Bhattacharyya Moitrayee, Liu Yansheng, Muzumdar Mandar Deepak

Abstract excerpt

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 showed here that phosphoinositide 3-kinase (PI3K) plays a major role in this resistance through upstream activation of wild-type (WT) RAS signaling-beyond its known KRAS effector function. The combination of...

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Share to Carcinoma, Pancreatic Ductal
Share to Class I Phosphatidylinositol 3-Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Pancreatic Neoplasms

Share to Phosphatidylinositol 3-Kinases

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Share to Proto-Oncogene Proteins p21(ras)

Source

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Identifiers

PMID: 42095550
DOI: 10.1158/0008-5472.CAN-25-3625
PMCID: PMC13237827

Genes

KRAS
EGFR
GAB1
PIK3CA
SOS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

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Research trail→

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PI3K Regulates Wild-type RAS Signaling to Confer Resistance to KRAS Inhibition.PMID 42095550Read ↗

Phosphoinositide 3-kinase regulates wild-type RAS signaling to confer resistance to KRAS inhibitionSemantic proximity Read ↗

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Oncogenic KRAS engages an RSK1/NF1 complex in pancreatic cancerSemantic proximity Read ↗

A Genome-scale CRISPR Screen Identifies the ERBB and mTOR Signaling Networks as Key Determinants of Response to PI3K Inhibition in Pancreatic CancerSemantic proximity Read ↗

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The Extracellular Niche and Tumor Microenvironment Enhance KRAS Inhibitor Efficacy in Pancreatic Cancer.Semantic proximity Read ↗

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