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Publication

KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function.

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Oncogene2018PMID 29755131PMC6107480stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (4)

How each link was made (MeSH, dictionary, registry reference, curation…) and whether it has been validated. Candidate links are not counted in entity statistics.

Validated 4

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
29755131
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
KMT2C Loss1
Aromatase InhibitorMalignant Breast NeoplasmPredictiveBSupports Resistance3accepted
EID6484

In the 746 metastatic breast tumors analyzed,KMT2C mutations were found in 9.8% of tumors, making it one of the most commonly mutated genes in breast cancer. Analysis of the 818 cases in the TCGA data… (full text at CIViC)

PMID 29755131 · Gala et al., 2018 · Open in CIViC

civic