The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance
Open accessAbstract
Evading cancer drugs by identity fraud: Prostate cancer growth is fueled by male hormones called androgens. Drugs targeting the androgen receptor (AR) are initially efficacious, but most tumors eventually become resistant (see the Perspective by Kelly and Balk). Mu et al. found that prostate cancer cells escaped the effects of androgen deprivation therapy through a change in lineage identity. Functional loss of the tumor suppressors TP53 and RB1 promoted a shift from AR-dependent luminal epithelial cells to AR-independent basal-like cells. In related work, Ku et al. found that prostate cancer metastasis, lineage switching, and drug resistance were driven by the combined loss of the same tumor suppressors and were accompanied by increased expression of the epigenetic regulator Ezh2. Ezh2 inhibitors reversed the lineage switch and restored sensitivity to androgen deprivation therapy in experimental models. Science , this issue p. 84 , p. 78 ; see also p. 29
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Li, J., Yen, C., Liaw, D., Podsypanina, K., Bose, S., Wang, S. I., Puc, J., Miliaresis, C., Rodgers, L., McCombie, R., et al. (1997) · Science · doi:10.1126/science.275.5308.1943 · Cited by 4,785
Integrative Clinical Genomics of Advanced Prostate Cancer
Robinson, D., Van Allen, E. M., Wu, Y.-M., Schultz, N., Lonigro, R. J., Mosquera, J.-M., Montgomery, B., Taplin, M.-E., Pritchard, C. C., Attard, G., et al. (2015) · Cell · doi:10.1016/j.cell.2015.05.001 · Cited by 3,645
Self-citationGenotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis
Chen, Z., Trotman, L. C., Shaffer, D., Lin, H.-K., Dotan, Z. A., Niki, M., Koutcher, J. A., Scher, H. I., Ludwig, T., Gerald, W., et al. (2005) · Nature · doi:10.1038/nature03918 · Cited by 1,993
Transgenic strategies for combinatorial expression of fluorescent proteins in the nervous system
Livet, J., Weissman, T. A., Kang, H., Draft, R. W., Lu, J., Bennis, R. A., Sanes, J. R., & Lichtman, J. W. (2007) · Nature · doi:10.1038/nature06293 · Cited by 1,876
Suppression of induced pluripotent stem cell generation by the p53–p21 pathway
Hong, H., Takahashi, K., Ichisaka, T., Aoi, T., Kanagawa, O., Nakagawa, M., Okita, K., & Yamanaka, S. (2009) · Nature · doi:10.1038/nature08235 · Cited by 1,301
EZH2 is downstream of the pRB-E2F pathway, essential for proliferation and amplified in cancer.
Bracken, A. P., Pasini, D., Capra, M., Prosperini, E., Colli, E., & Helin, K. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg542 · Cited by 1,196
Wang, S., Gao, J., Lei, Q., Rozengurt, N., Pritchard, C., Jiao, J., Thomas, G. V., Li, G., Roy-Burman, P., Nelson, P. S., et al. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00215-0 · Cited by 1,109
RB loss in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer
Niederst, M. J., Sequist, L. V., Poirier, J. T., Mermel, C. H., Lockerman, E. L., Garcia, A. R., Katayama, R., Costa, C., Ross, K. N., Moran, T., et al. (2015) · Nature Communications · doi:10.1038/ncomms7377 · Cited by 647
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Genomic correlates of clinical outcome in advanced prostate cancer
Abida, W., Cyrta, J., Heller, G., Prandi, D., Armenia, J., Coleman, I., Cieslik, M., Benelli, M., Robinson, D., Van Allen, E. M., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1902651116 · Cited by 1,372
Self-citationAggarwal, R., Huang, J., Alumkal, J. J., Zhang, L., Feng, F. Y., Thomas, G. V., Weinstein, A. S., Friedl, V., Zhang, C., Witte, O. N., et al. (2018) · Journal of Clinical Oncology · doi:10.1200/jco.2017.77.6880 · Cited by 810
Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling
Bluemn, E. G., Coleman, I. M., Lucas, J. M., Coleman, R. T., Hernandez-Lopez, S., Tharakan, R., Bianchi-Frias, D., Dumpit, R. F., Kaipainen, A., Corella, A. N., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.09.003 · Cited by 744
Sartor, O., & de Bono, J. S. (2018) · New England Journal of Medicine · doi:10.1056/nejmra1701695 · Cited by 546
Cellular plasticity and the neuroendocrine phenotype in prostate cancer
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Metadata
- Authors
- Ku, S. Y., Rosario, S., Wang, Y., Mu, P., Seshadri, M., Goodrich, Z. W., Goodrich, M. M., Labbé, D. P., Gomez, E. C., Wang, J., Long, H. W., Xu, B., Brown, M., Loda, M., Sawyers, C. L., Ellis, L., & Goodrich, D. W.
- Venue
- Science
- Published
- 2017-01-06
- Volume
- 355
- Issue
- 6320
- Pages
- 78-83
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2571250257
- Cited by
- 1,089
- References
- 9
- FWCI
- 73.10
- Type
- journal article
- Language
- en
- Open access
- green
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- Ku, S. Y., Rosario, S., Wang, Y., Mu, P., Seshadri, M., Goodrich, Z. W., Goodrich, M. M., Labbé, D. P., Gomez, E. C., Wang, J., Long, H. W., Xu, B., Brown, M., Loda, M., Sawyers, C. L., Ellis, L., & Goodrich, D. W. (2017). Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance. Science. https://doi.org/10.1126/science.aah4199
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.