ReviewMolecular and cellular endocrinology2012
From the ranks of mammary progesterone mediators, RANKL takes the spotlight.
Review in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Paracrine activation of WNT/β-catenin pathway in uterine leiomyoma stem cells promotes tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Α Humanized RANKL Transgenic Mouse Model of Progestin-Induced Mammary Carcinogenesis for Evaluation of Novel Therapeutics.Cancers · 2023Article
- Histopathologic and transcriptomic phenotypes of a conditional RANKL transgenic mouse thymus.Cytokine · 2022Article
- Hormone and receptor activator of NF-κB (RANK) pathway gene expression in plasma and mammographic breast density in postmenopausal women.Breast cancer research : BCR · 2022Article
- Role of sex hormones in modulating breast and ovarian cancer associated pain.Molecular and cellular endocrinology · 2021Article
- Origins of Alterations toInternational journal of molecular sciences · 2020Article
- New Selective Progesterone Receptor Modulators and Their Impact on the RANK/RANKL Complex Activity.Molecules (Basel, Switzerland) · 2020Article
- Short-term RANKL exposure initiates a neoplastic transcriptional program in the basal epithelium of the murine salivary gland.Cytokine · 2019Article
- Clinical and translational pharmacology of drugs for the prevention and treatment of bone metastases and cancer-induced bone loss.British journal of clinical pharmacology · 2019Review
- Circulating Receptor Activator of Nuclear Factor-κB (RANK), RANK ligand (RANKL), and Mammographic Density in Premenopausal Women.Cancer prevention research (Philadelphia, Pa.) · 2018Observational
- Prolactin Alters the Mammary Epithelial Hierarchy, Increasing Progenitors and Facilitating Ovarian Steroid Action.Stem cell reports · 2017Article
- RANK ligand as a potential target for breast cancer prevention in BRCA1-mutation carriers.Nature medicine · 2016Article
- Dissecting the Biology of Menstrual Cycle-Associated Breast Cancer Risk.Frontiers in oncology · 2016Review
- Aberrant Activation of the RANK Signaling Receptor Induces Murine Salivary Gland Tumors.PloS one · 2015Article
- Early pregnancy sex steroids and maternal breast cancer: a nested case-control study.Cancer research · 2014Article
- Mammary stem cells and the differentiation hierarchy: current status and perspectives.Genes & development · 2014Review
- The effects of diet induced obesity on breast cancer associated pathways in mice deficient in SFRP1.Molecular cancer · 2014Article
- Progesterone receptor and Stat5 signaling cross talk through RANKL in mammary epithelial cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Where Do Bone-Targeted Agents RANK in Breast Cancer Treatment?Journal of clinical medicine · 2013Review
- A model for breast cancer risk based on stem-cell theory.Current oncology (Toronto, Ont.) · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Whether during the diestrus phase of the estrous cycle or with pregnancy onset, the mitogenic effects of progesterone are well-established in the murine mammary epithelium. Importantly, progesterone-induced mitogenicity is critical for mammary tumor promotion, providing one explanation for the increase in breast cancer-risk observed with prolonged progestin-based hormone therapy. At the cellular level, progesterone projects its mitogenic influence through an evolutionary conserved paracrine mechanism of action. In this regard, recent studies provide compelling support for receptor activator of NF-kB ligand (RANKL) as a key paracrine mediator of the progesterone mitogenic signal. Induction of RANKL is sufficient to elicit mammary ductal side-branching and alveologenesis, the very morphogenetic responses elicited by progesterone during pregnancy and at diestrus. Significantly, the proliferative and pro-survival signals triggered by RANKL are also required for progestin-promotion of mammary tumorigenesis, underscoring a dual role for RANKL in progesterone-dependent mammary morphogenesis and tumorigenesis. Recently, RANKL has been shown to be critical for progesterone-induced expansion of the mammary stem cell population (and its lineal descendents), thereby advancing our conceptual understanding not only of RANKL's involvement in normal mammary morphogenesis but also in breast cancer risk associated with sustained hormone exposure. Finally, these studies together suggest that chemotherapeutic intervention of RANKL signaling represents a feasible approach for the effective prevention and/or treatment of hormone-responsive breast cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.