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Article

Upregulation of IRS1 Enhances IGF1 Response in Y537S and D538G ESR1 Mutant Breast Cancer Cells.

Endocrinology - 1 Jan 2018

Li Zheqi, Levine Kevin M, Bahreini Amir, Wang Peilu, Chu David, Park Ben Ho, Oesterreich Steffi, Lee Adrian V

Abstract excerpt

Increased evidence suggests that somatic mutations in the ligand-binding domain of estrogen receptor [ER (ERα/ESR1)] are critical mediators of endocrine-resistant breast cancer progression. Insulinlike growth factor-1 (IGF1) is an essential regulator of breast development and tumorigenesis and also has a role in endocrine resistance. A recent study showed enhanced crosstalk between IGF1 and ERα in ESR1 mutant...

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Topics

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Share to Drug Synergism
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Insulin-Like Growth Factor I

Share to Insulin Receptor Substrate Proteins

Share to Phosphatidylinositol 3-Kinase

Share to Proto-Oncogene Proteins c-akt

Share to Receptor, IGF Type 1

Share to Receptors, Somatomedin

Source

Open in PubMed Open full text

Identifiers

PMID: 29029116
DOI: 10.1210/en.2017-00693
PMCID: PMC5761602

Genes

ESR1
IGF1
IRS1

Variants

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.

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