RANK ligand mediates progestin-induced mammary epithelial proliferation and carcinogenesis

Eva Gonzalez-Suarez, Allison P. Jacob, Jon Jones, Robert Miller, Martine P. Roudier-Meyer, Ryan Erwert, Jan Pinkas, Dan Branstetter and William C. Dougall ()
Additional contact information
Eva Gonzalez-Suarez: Amgen Inc
Allison P. Jacob: Amgen Inc
Jon Jones: Amgen Inc
Robert Miller: Amgen Inc
Martine P. Roudier-Meyer: Amgen Inc
Ryan Erwert: Amgen Inc
Jan Pinkas: Amgen Inc
Dan Branstetter: Amgen Inc
William C. Dougall: Amgen Inc

Nature, 2010, vol. 468, issue 7320, 103-107

Abstract: Progestins and breast cancer Progestins, used in contraceptives and hormone replacement therapy, have been linked to breast cancer. Two teams working independently have now found a mechanistic basis for this association. Schramek et al. show in a mouse model that synthetic progestins can promote mammary tumour formation by inducing the osteoclast differentiation factor RANKL, which acts on mammary epithelial cells through the RANKL receptor RANK. Gonzalez-Suarez et al. find that inhibition of RANKL reduces tumorigenesis in hormone-induced as well as in other mouse mammary gland tumour models, suggesting a new therapeutic approach. One RANKL inhibitor (denosumab) is in clinical trials as a treatment for bone loss in post-menopausal osteoporosis and for the treatment of skeletal-related symptoms in metastatic bone disease.

Date: 2010
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DOI: 10.1038/nature09495

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