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Cited by 175

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

RANKL/RANK control Brca1 mutation-driven mammary tumors

Open access
Sigl, Verena, Owusu-Boaitey, Kwadwo, Joshi, Purna A, Kavirayani, Anoop, Wirnsberger, Gerald, Novatchkova, Maria, Kozieradzki, Ivona, Schramek, Daniel, Edokobi, Nnamdi, Hersl, Jerome, Sampson, Aishia, Odai-Afotey, Ashley, Lazaro, Conxi, Gonzalez-Suarez, Eva, Pujana, Miguel A, CIMBA, for, Heyn, Holger, Vidal, Enrique, Cruickshank, Jennifer, Berman, Hal, Sarao, Renu, Ticevic, Melita, Uribesalgo, Iris, Tortola, Luigi, Rao, Shuan, Tan, Yen, Pfeiler, Georg, Lee, Eva YHP, Bago-Horvath, Zsuzsanna, Kenner, Lukas, Popper, Helmuth, Singer, Christian, Khokha, Rama, Jones, Laundette P, Penninger, Josef M·2016·Cell Research
DOI 10.1038/cr.2016.69
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Abstract

Breast cancer is the most common female cancer, affecting approximately one in eight women during their life-time. Besides environmental triggers and hormones, inherited mutations in the breast cancer 1 (BRCA1) or BRCA2 genes markedly increase the risk for the development of breast cancer. Here, using two different mouse models, we show that genetic inactivation of the key osteoclast differentiation factor RANK in the mammary epithelium markedly delayed onset, reduced incidence, and attenuated progression of Brca1;p53 mutation-driven mammary cancer. Long-term pharmacological inhibition of the RANK ligand RANKL in mice abolished the occurrence of Brca1 mutation-driven pre-neoplastic lesions. Mechanistically, genetic inactivation of Rank or RANKL/RANK blockade impaired proliferation and expansion of both murine Brca1;p53 mutant mammary stem cells and mammary progenitors from human BRCA1 mutation carriers. In addition, genome variations within the RANK locus were significantly associated with risk of developing breast cancer in women with BRCA1 mutations. Thus, RANKL/RANK control progenitor cell expansion and tumorigenesis in inherited breast cancer. These results present a viable strategy for the possible prevention of breast cancer in BRCA1 mutant patients.

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Authors
Sigl, V., Owusu-Boaitey, K., Joshi, P. A., Kavirayani, A., Wirnsberger, G., Novatchkova, M., Kozieradzki, I., Schramek, D., Edokobi, N., Hersl, J., Sampson, A., Odai-Afotey, A., Lazaro, C., Gonzalez-Suarez, E., Pujana, M. A., CIMBA, F., Heyn, H., Vidal, E., Cruickshank, J., Berman, H., Sarao, R., Ticevic, M., Uribesalgo, I., Tortola, L., Rao, S., Tan, Y., Pfeiler, G., Lee, E. Y., Bago-Horvath, Z., Kenner, L., Popper, H., Singer, C., Khokha, R., Jones, L. P., & Penninger, J. M.
Venue
Cell Research
Publisher
Springer Science and Business Media LLC
Published
2016-05-31
Volume
26
Issue
7
Pages
761-774
ISSN
  • 1001-0602 (ISSN-L)
  • 1748-7838
DOI
10.1038/cr.2016.69
OpenAlex
W2414274468
Cited by
175
References
6
FWCI
17.86
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: RANKL/RANK control Brca1 mutation-driven mammary tumors. https://app.cochat.ai/papers/10.1038/cr.2016.69
The paper
Sigl, V., Owusu-Boaitey, K., Joshi, P. A., Kavirayani, A., Wirnsberger, G., Novatchkova, M., Kozieradzki, I., Schramek, D., Edokobi, N., Hersl, J., Sampson, A., Odai-Afotey, A., Lazaro, C., Gonzalez-Suarez, E., Pujana, M. A., CIMBA, F., Heyn, H., Vidal, E., Cruickshank, J., . . . Penninger, J. M. (2016). RANKL/RANK control Brca1 mutation-driven mammary tumors. Cell Research. https://doi.org/10.1038/cr.2016.69

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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