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Ref Type Journal Article
PMID (24919154)
Authors Ali K, Soond DR, Piñeiro R, Hagemann T, Pearce W, Lim EL, Bouabe H, Scudamore CL, Hancox T, Maecker H, Friedman L, Turner M, Okkenhaug K, Vanhaesebroeck B
Title Inactivation of PI(3)K p110δ breaks regulatory T-cell-mediated immune tolerance to cancer.
Journal Nature
Vol 510
Issue 7505
Date 2014 06 19
URL
Abstract Text Inhibitors against the p110δ isoform of phosphoinositide-3-OH kinase (PI(3)K) have shown remarkable therapeutic efficacy in some human leukaemias. As p110δ is primarily expressed in leukocytes, drugs against p110δ have not been considered for the treatment of solid tumours. Here we report that p110δ inactivation in mice protects against a broad range of cancers, including non-haematological solid tumours. We demonstrate that p110δ inactivation in regulatory T cells unleashes CD8(+) cytotoxic T cells and induces tumour regression. Thus, p110δ inhibitors can break tumour-induced immune tolerance and should be considered for wider use in oncology.

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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
PI-3065 PI-3065 1 0
Drug Name Trade Name Synonyms Drug Classes Drug Description
PI-3065 PIK3CD inhibitor 24 PI-3065 inhibits PIK3CD, which may block activation of the PI3K signaling pathway and inhibit tumor cell proliferation (PMID: 24919154, PMID: 28851839).
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
Unknown unknown pancreatic ductal adenocarcinoma not applicable PI-3065 Preclinical Actionable In a preclinical study, treatment with the PIK3-delta inhibitor PI-3065 resulted in increased host anti-tumor immune response and led to prolonged survival and decreased metastasis in an mouse model of KRAS G12D and TP53 R175H-expressing pancreatic ductal adenocarcinoma (PMID: 24919154). 24919154