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Endocrine therapy: defining the path of least resistance

Abstract

One of the best-characterized oncogenic mechanisms in breast cancer is the aberrant activation of phosphatidylinositol-3-kinase, protein kinase B, and mammalian target of rapamycin signaling. In both endocrine-resistant disease and breast cancer stem cells, this is commonly caused by specific genetic lesions or amplification of key pathway components or both. These observations have generated two interesting hypotheses. Firstly, do these genetic anomalies provide clinically significant biomarkers predictive of endocrine resistance? Secondly, do tamoxifen-resistant breast cancer cells emerge from a stem-like cell population? New studies, published in Breast Cancer Research, raise the possibility that these hypotheses are intrinsically linked.

Type Journal
ISBN 1465-542X (Electronic) 1465-5411 (Linking)
Authors Stone, A.; Musgrove, E. A.
Responsible Garvan Author (missing name)
Publisher Name BREAST CANCER RES
Published Date 2014-05-22
Published Volume 16
Published Issue 3
Published Pages 101
Status Published in-print
DOI 10.1186/bcr3659
URL link to publisher's version http://www.ncbi.nlm.nih.gov/pubmed/25928145
OpenAccess link to author's accepted manuscript version https://publications.gimr.garvan.org.au/open-access/14124