Identification of Pik3ca Mutation as a Genetic Driver of Prostate Cancer That Cooperates with Pten Loss to Accelerate Progression and Castration-Resistant Growth.

doi:10.1158/2159-8290.CD-17-0867

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Identification of Pik3ca Mutation as a Genetic Driver of Prostate Cancer That Cooperates with Pten Loss to Accelerate Progression and Castration-Resistant Growth.

Cancer discovery - 1 Jun 2018

Pearson Helen B, Li Jason, Meniel Valerie S, Fennell Christina M, Waring Paul, Montgomery Karen G, Rebello Richard J, Macpherson Arthi A, Koushyar Sarah, Furic Luc, Cullinane Carleen, Clarkson Richard W, Smalley Matthew J, Simpson Kaylene J, Phesse Toby J, Shepherd Peter R, Humbert Patrick O, Sansom Owen J, Phillips Wayne A

Abstract excerpt

Genetic alterations that potentiate PI3K signaling are frequent in prostate cancer, yet how different genetic drivers of the PI3K cascade contribute to prostate cancer is unclear. Here, we report PIK3CA mutation/amplification correlates with poor survival of patients with prostate cancer. To interrogate the requirement of different PI3K genetic drivers in prostate cancer, we employed a genetic approach to mutate...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Class I Phosphatidylinositol 3-Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Amplification

Share to Gene Deletion

Share to Neoplasm Invasiveness

Share to Neoplasms, Experimental

Share to Prostatic Neoplasms, Castration-Resistant

Share to PTEN Phosphohydrolase

Share to Survival Analysis

Source

Open in PubMed

Identifiers

PMID: 29581176
DOI: 10.1158/2159-8290.CD-17-0867

Genes

PTEN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identification of Pik3ca Mutation as a Genetic Driver of Prostate Cancer That Cooperates with Pten Loss to Accelerate Progression and Castration-Resistant Growth.PMID 29581176Read ↗

Prostate Power Play: Does Pik3ca Accelerate Pten -Deficient Cancer Progression?Semantic proximity Read ↗

PI3K signaling pathway is activated by PIK3CA mRNA overexpression and copy gain in prostate tumors, but PIK3CA, BRAF, KRAS and AKT1 mutations are infrequent events.Semantic proximity Read ↗

The Impact of PIK3R1 Mutations and Insulin-PI3K-Glycolytic Pathway Regulation in Prostate Cancer.Semantic proximity Read ↗

PTEN regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progressionSemantic proximity Read ↗

Prostate cancer, PI3K, PTEN and prognosis.Semantic proximity Read ↗

Differential impact of PI3K/AKT/mTOR signaling on tumor initiation and progression in animal models of prostate cancer.Semantic proximity Read ↗

PTEN loss and activation of K-RAS and β-catenin cooperate to accelerate prostate tumourigenesis.Semantic proximity Read ↗

SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling.Semantic proximity Read ↗

The PTEN Conundrum: How to Target PTEN-Deficient Prostate CancerSemantic proximity Read ↗

PIK3/Akt/mTOR pathway alterations in metastatic castration-sensitive prostate cancer.Semantic proximity Read ↗

Gata3 antagonizes cancer progression in Pten-deficient prostatesSemantic proximity Read ↗

Cooperation between FGF8b overexpression and PTEN deficiency in prostate tumorigenesis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.