Journal
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
Volume 20, Issue 1-2, Pages 75-91Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10911-015-9344-1
Keywords
Endocrine hormones; Hormone-sensing cells; Luminal progenitors; Androgen; Prolactin
Categories
Funding
- National Health and Medical Research Council of Australia [1008349, 1084416]
- Cancer Australia [627229]
- National Breast Cancer Foundation [PS-15-041]
- US Department of Defense Breast Cancer Research Program (BCRP) [W81XWH-11-1-0592]
- Royal Adelaide Hospital Research Foundation
- National Health and Medical Research Council of Australia [1084416] Funding Source: NHMRC
- National Breast Cancer Foundation [PS-15-041, PD-13-03] Funding Source: researchfish
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The hormone-sensing mammary epithelial cell (HS-MEC-expressing oestrogen receptor-alpha (ER alpha) and progesterone receptor (PGR)) is often represented as being terminally differentiated and lacking significant progenitor activity after puberty. Therefore while able to profoundly influence the proliferation and function of other MEC populations, HS-MECs are purported not to respond to sex hormone signals by engaging in significant cell proliferation during adulthood. This is a convenient and practical simplification that overshadows the sublime, and potentially critical, phenotypic plasticity found within the adult HS-MEC population. This concept is exemplified by the large proportion (similar to 80 %) of human breast cancers expressing PGR and/or ER alpha, demonstrating that HS-MECs clearly proliferate in the context of breast cancer. Understanding how HS-MEC proliferation and differentiation is driven could be key to unraveling the mechanisms behind uncontrolled HS-MEC proliferation associated with ER alpha- and/or PGR-positive breast cancers. Herein we review evidence for the existence of a HS-MEC progenitor and the emerging plasticity of the HS-MEC population in general. This is followed by an analysis of hormones other than oestrogen and progesterone that are able to influence HS-MEC proliferation and differentiation: androgens, prolactin and transforming growth factor-beta1.
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