PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system. - Wikidata - wikimedia - TriplyDB

PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system.

PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system.

http://www.wikidata.org/entity/Q27852473

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CIViC database CDK 4/6 inhibitors sensitize PIK3CA mutant breast cancer to PI3K inhibitors.AKT1E¹⁷K Is Oncogenic in Mouse Lung and Cooperates with Chemical Carcinogens in Inducing Lung Cancer Targeting AKT1-E17K and the PI3K/AKT Pathway with an Allosteric AKT Inhibitor, ARQ 092 Using Ontology Fingerprints to disambiguate gene name entities in the biomedical literature Regulation of PI3K effector signalling in cancer by the phosphoinositide phosphatases Activating Akt1 mutations alter DNA double strand break repair and radiosensitivity.DNA microarray reveals ZNF195 and SBF1 are potential biomarkers for gemcitabine sensitivity in head and neck squamous cell carcinoma cell lines Genomic Sequencing Identifies ELF3 as a Driver of Ampullary Carcinoma.Loss of ARID1A expression sensitizes cancer cells to PI3K- and AKT-inhibition SU2C phase Ib study of paclitaxel and MK-2206 in advanced solid tumors and metastatic breast cancer Linking tumor mutations to drug responses via a quantitative chemical-genetic interaction map.AKT1 (E17K) mutation profiling in breast cancer: prevalence, concurrent oncogenic alterations, and blood-based detection.HER2 missense mutations have distinct effects on oncogenic signaling and migration.Aberrant amino acid signaling promotes growth and metastasis of hepatocellular carcinomas through Rab1A-dependent activation of mTORC1 by Rab1A Mutant AKT1-E17K is oncogenic in lung epithelial cells Mutations in PIK3CA sensitize breast cancer cells to physiologic levels of aspirin Recurrent AKT mutations in human cancers: functional consequences and effects on drug sensitivity Oncogenic AKT1(E17K) mutation induces mammary hyperplasia but prevents HER2-driven tumorigenesis.Pancancer modelling predicts the context-specific impact of somatic mutations on transcriptional programs.Multicenter phase II study of the AKT inhibitor MK-2206 in recurrent or metastatic nasopharyngeal carcinoma from patients in the mayo phase II consortium and the cancer therapeutics research group (MC1079).PIK3CA mutations and TP53 alterations cooperate to increase cancerous phenotypes and tumor heterogeneity.Genetic landscape of meningioma.Triple Akt inhibition as a new therapeutic strategy in T-cell acute lymphoblastic leukemia.AKT1E17K mutations cluster with meningothelial and transitional meningiomas and can be detected by SFRP1 immunohistochemistry.Improved prediction of breast cancer outcome by identifying heterogeneous biomarkers.GATA3 frameshift mutation promotes tumor growth in human luminal breast cancer cells and induces transcriptional changes seen in primary GATA3 mutant breast cancers.E-cadherin loss induces targetable autocrine activation of growth factor signalling in lobular breast cancer Emerging Medical Treatments for Meningioma in the Molecular Era

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PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system.

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Anandita Rajpurohit

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Ben Ho Park

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D Marc Rosen

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John P Gustin

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Julia A Beaver

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P2860

Comprehensive molecular portraits of human breast tumours

The COSMIC (Catalogue of Somatic Mutations in Cancer) database and website

Knockin of mutant PIK3CA activates multiple oncogenic pathways

Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses

A transforming mutation in the pleckstrin homology domain of AKT1 in cancer

The identification of 2-(1H-indazol-4-yl)-6-(4-methanesulfonyl-piperazin-1-ylmethyl)-4-morpholin-4-yl-thieno[3,2-d]pyrimidine (GDC-0941) as a potent, selective, orally bioavailable inhibitor of class I PI3 kinase for the treatment of cancer

NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.

The phosphoinositide 3-kinase pathway

Insulin-modulated Akt subcellular localization determines Akt isoform-specific signaling.

mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt

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