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- W2556648357 abstract "RANK and RANKL, a receptor ligand pair belonging to the tumour necrosis factor family, are the critical regulators of osteoclast development and bone metabolism. Besides their essential function in bone, RANK and RANKL have also been identified as the key factors for the formation of a lactating mammary gland in pregnancy. Mechanistically, RANK and RANKL link the sex hormone progesterone with stem cell expansion and proliferation of mammary epithelial cells. Based on their normal physiology, RANKL/RANK control the onset of hormone-induced breast cancer through the expansion of mammary progenitor cells. Recently, we and others were able to show that RANK and RANKL are also critical regulators of BRCA1 -mutation-driven breast cancer. Currently, the preventive strategy for BRCA1 -mutation carriers includes preventive mastectomy, associated with wide-ranging risks and psychosocial effects. The search for an alternative non-invasive prevention strategy is therefore of paramount importance. As our work strongly implicates RANK and RANKL as key molecules involved in the initiation of BRCA1-associated breast cancer, we propose that anti-RANKL therapy could be a feasible preventive strategy for women carrying BRCA1 mutations, and by extension to other women with high risk of breast cancer." @default.
- W2556648357 created "2016-11-30" @default.
- W2556648357 creator A5030889614 @default.
- W2556648357 creator A5053226783 @default.
- W2556648357 creator A5059310975 @default.
- W2556648357 date "2016-11-01" @default.
- W2556648357 modified "2023-10-13" @default.
- W2556648357 title "RANKL/RANK: from bone loss to the prevention of breast cancer" @default.
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- W2556648357 doi "https://doi.org/10.1098/rsob.160230" @default.
- W2556648357 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5133443" @default.
- W2556648357 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27881737" @default.
- W2556648357 hasPublicationYear "2016" @default.
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