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Comment
. 2009 Jul;150(7):2988-90.
doi: 10.1210/en.2009-0383.

Finally! A model for progesterone receptor action in normal human breast

John P Lydon  1 , Dean P Edwards
Affiliations
Comment

Finally! A model for progesterone receptor action in normal human breast

John P Lydon et al. Endocrinology. 2009 Jul.
No abstract available

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Figures

Figure 1
Figure 1
An emerging model for progesterone action in the human breast shares common features with a proposed paracrine mechanism of action model for progesterone in the rodent mammary gland (24,25,26). Based on findings of Graham et al., (21), the schematic outlines a hypothetical model to explain the role of progesterone (P4) signaling in the expansion and morphogenesis of the epithelial compartment in the human breast. A subset of mammary epithelial cells (red), which are PR positive, receive, transduce, and subsequently relay, in a paracrine fashion, the proliferative signal imparted by P4 hormone to a juxtacrine cell subgroup (green) that is PR negative. Gene profiling studies implicate the notch pathway as possibly one of a number of paracrine signals that project the proliferative effects of progesterone from PR-positive cells to a subset of PR-negative cells (green) that exhibit bipotent progenitor properties. Upon receiving paracrine signal inputs, the progenitor cell subtype reprograms and proliferates to generate both luminal and myoepithelial cell lineages. Luminal epithelial descendants can be positive or negative for PR expression, whereas myoepithelial cell are PR negative. Together, the expansion and differentiation of these cell lineages contribute to increased lobuloalveologenesis. Induction of DNA replication licensing factors, minichromosome maintenance proteins, and kinetochore formation proteins are possible early molecular changes that precede progesterone-induced progenitor cell reprogramming and subsequent proliferation.
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References

    1. Pike MC, Spicer DV, Dahmoush L, Press MF 1993 Estrogens, progestogens, normal breast cell proliferation, and breast cancer risk. Epidemiol Rev 15:17–35 - PubMed
    1. Fernandez-Valdivia R, Mukherjee A, Mulac-Jericevic B, Conneely OM, DeMayo FJ, Amato P, Lydon JP 2005 Revealing progesterone’s role in uterine and mammary gland biology: insights from the mouse. Semin Reprod Med 23:22–37 - PubMed
    1. Anderson E 2002 The role of oestrogen and progesterone receptors in human mammary development and tumorigenesis. Breast Cancer Res 4:197–201 - PMC - PubMed
    1. Hofseth LJ, Raafat AM, Osuch JR, Pathak DR, Slomski CA, Haslam SZ 1999 Hormone replacement therapy with estrogen or estrogen plus medroxyprogesterone acetate is associated with increased epithelial proliferation in the normal postmenopausal breast. J Clin Endocrinol Metab 84:4559–4565 - PubMed
    1. Beral V 2003 Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet 362:419–427 - PubMed

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