Discover Community Create You

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

Article

PI3K pathway dependencies in endometrioid endometrial cancer cell lines.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 Jul 2013

Weigelt Britta, Warne Patricia H, Lambros Maryou B, Reis-Filho Jorge S, Downward Julian

Abstract excerpt

PURPOSE: Endometrioid endometrial cancers (EEC) frequently harbor coexisting mutations in phosphoinositide 3-kinase (PI3K) pathway genes, including PTEN, PIK3CA, PIK3R1, and KRAS. We sought to define the genetic determinants of PI3K pathway inhibitor response in EEC cells, and whether PTEN-mutant EEC cell lines rely on p110β signaling for survival. EXPERIMENTAL DESIGN: Twenty-four human EEC cell lines were...

Read the complete abstract on PubMed

Topics

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

Share to Class Ia Phosphatidylinositol 3-Kinase
Share to Endometrial Neoplasms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Indazoles

Share to Phosphatidylinositol 3-Kinases

Share to Phosphoinositide-3 Kinase Inhibitors

Share to Proto-Oncogene Proteins c-akt

Share to PTEN Phosphohydrolase

Share to Sulfonamides

Source

Open in PubMed Open full text

Identifiers

PMID: 23674493
DOI: 10.1158/1078-0432.CCR-12-3815
PMCID: PMC3700760

Genes

KRAS
PTEN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PI3K pathway dependencies in endometrioid endometrial cancer cell lines.PMID 23674493Read ↗

Endometrial cancer cells exhibit high expression of p110β and its selective inhibition induces variable responses on PI3K signaling, cell survival and proliferation.Semantic proximity Read ↗

PIKing the type and pattern of PI3K pathway mutations in endometrioid endometrial carcinomas.Semantic proximity Read ↗

High frequency of PIK3R1 and PIK3R2 mutations in endometrial cancer elucidates a novel mechanism for regulation of PTEN protein stability.Semantic proximity Read ↗

Class I Phosphoinositide 3-Kinase PIK3CA/p110α and PIK3CB/p110β Isoforms in Endometrial CancerSemantic proximity Read ↗

PIK3R1 (p85α) is somatically mutated at high frequency in primary endometrial cancer.Semantic proximity Read ↗

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

Activation of PI3K/Akt/mTOR pathway and dual inhibitors of PI3K and mTOR in endometrial cancer.Semantic proximity Read ↗

PI3K pathway in gynecologic malignancies.Semantic proximity Read ↗

Oncogenic PIK3CA gene mutations and HER2/neu gene amplifications determine the sensitivity of uterine serous carcinoma cell lines to GDC-0980, a selective inhibitor of Class I PI3 kinase and mTOR kinase (TORC1/2).Semantic proximity Read ↗

Phase 2 study of LY3023414 in patients with advanced endometrial cancer harboring activating mutations in the PI3K pathway.Semantic proximity Read ↗

Activated mutant p110α causes endometrial carcinoma in the setting of biallelic Pten deletion.Semantic proximity Read ↗

PTEN loss is a context‐dependent outcome determinant in obese and non‐obese endometrioid endometrial cancer patientsSemantic proximity Read ↗

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