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Coexistent <i>PTEN</i> and <i>PIK3CA</i> alterations hyperactivate mTORC1 signaling in endometrial cancers and cause their selective sensitivity to mTORC1 inhibition

2026-02-14

Abstract excerpt

In approximately half of endometrial carcinoma (EC), PTEN loss-of-function and activating PI3K mutants coexist. Unlike cells with either single mutation, PTEN / PIK3CA coexistent alterations result in elevated membrane phosphatidylinositol (3,4,5)-trisphosphate (PIP3) levels and mTORC1 hyperactivation, rendering PI3K or AKT inhibition ineffective in blocking mTORC1 activity and tumor growth. The bi-steric mTORC1...

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Literature Corpus work
98907026-9534-5b27-81a3-b3c2570736d3
DOI
10.64898/2026.02.12.705558
Open publication

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Coexistent <i>PTEN</i> and <i>PIK3CA</i> alterations hyperactivate mTORC1 signaling in endometrial cancers and cause their selective sensitivity to mTORC1 inhibitionDOI 10.64898/2026.02.12.705558
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