ID4 controls luminal lineage commitment in normal mammary epithelium and inhibits BRCA1 function in basal-like breast cancer
- 1The Kinghorn Cancer Centre and Cancer Research Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
- 2St Vincent’s Clinical School, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia
- Correspondence should be addressed to A Swarbrick; Email: a.swarbrick{at}garvan.org.au
Abstract
Inhibitor of differentiation (ID) proteins are key regulators of development and tumorigenesis. One member of this family, ID4, controls lineage commitment during mammary gland development by acting upstream of key developmental pathways. Recent evidence suggests an emerging role for ID4 as a lineage-dependent proto-oncogene that is overexpressed and amplified in a subset of basal-like breast cancers (BLBCs), conferring poor prognosis. Several lines of evidence suggest ID4 may suppress BRCA1 function in BLBC and in doing so, define a subset of BLBC patients who may respond to therapies traditionally used in BRCA1-mutant cancers. This review highlights recent advances in our understanding of the requirement for ID4 in mammary lineage commitment and the role for ID4 in BLBC. We address current shortfalls in this field and identify important areas of future research.
- Received 20 June 2016
- Accepted 13 July 2016
- Made available online as an Accepted Preprint 1 September 2016
- © 2016 Society for Endocrinology
