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|Ref Type||Journal Article|
|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.|
|Date||2014 06 19|
|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.|
|Molecular Profile||Treatment Approach|
|Gene Name||Source||Synonyms||Protein Domains||Gene Description||Gene Role|
|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|