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476 results on '"Carver, Brett S."'

2. Rapid interrogation of cancer cell of origin through CRISPR editing

Author

Feng, Weiran, Cao, Zhen, Lim, Pei Xin, Zhao, Huiyong, Luo, Hanzhi, Mao, Ninghui, Lee, Young Sun, Rivera, Aura Agudelo, Choi, Danielle, Wu, Chao, Han, Teng, Romero, Rodrigo, de Stanchina, Elisa, Carver, Brett S., Wang, Qiao, Jasin, Maria, and Sawyers, Charles L.

Published
2021

6. The Molecular Taxonomy of Primary Prostate Cancer

Author

Network, The Cancer Genome Atlas Research, Abeshouse, Adam, Ahn, Jaeil, Akbani, Rehan, Ally, Adrian, Amin, Samirkumar, Andry, Christopher D, Annala, Matti, Aprikian, Armen, Armenia, Joshua, Arora, Arshi, Auman, J Todd, Balasundaram, Miruna, Balu, Saianand, Barbieri, Christopher E, Bauer, Thomas, Benz, Christopher C, Bergeron, Alain, Beroukhim, Rameen, Berrios, Mario, Bivol, Adrian, Bodenheimer, Tom, Boice, Lori, Bootwalla, Moiz S, dos Reis, Rodolfo Borges, Boutros, Paul C, Bowen, Jay, Bowlby, Reanne, Boyd, Jeffrey, Bradley, Robert K, Breggia, Anne, Brimo, Fadi, Bristow, Christopher A, Brooks, Denise, Broom, Bradley M, Bryce, Alan H, Bubley, Glenn, Burks, Eric, Butterfield, Yaron SN, Button, Michael, Canes, David, Carlotti, Carlos G, Carlsen, Rebecca, Carmel, Michel, Carroll, Peter R, Carter, Scott L, Cartun, Richard, Carver, Brett S, Chan, June M, Chang, Matthew T, Chen, Yu, Cherniack, Andrew D, Chevalier, Simone, Chin, Lynda, Cho, Juok, Chu, Andy, Chuah, Eric, Chudamani, Sudha, Cibulskis, Kristian, Ciriello, Giovanni, Clarke, Amanda, Cooperberg, Matthew R, Corcoran, Niall M, Costello, Anthony J, Cowan, Janet, Crain, Daniel, Curley, Erin, David, Kerstin, Demchok, John A, Demichelis, Francesca, Dhalla, Noreen, Dhir, Rajiv, Doueik, Alexandre, Drake, Bettina, Dvinge, Heidi, Dyakova, Natalya, Felau, Ina, Ferguson, Martin L, Frazer, Scott, Freedland, Stephen, Fu, Yao, Gabriel, Stacey B, Gao, Jianjiong, Gardner, Johanna, Gastier-Foster, Julie M, Gehlenborg, Nils, Gerken, Mark, Gerstein, Mark B, Getz, Gad, Godwin, Andrew K, Gopalan, Anuradha, Graefen, Markus, Graim, Kiley, Gribbin, Thomas, Guin, Ranabir, Gupta, Manaswi, Hadjipanayis, Angela, Haider, Syed, Hamel, Lucie, and Hayes, D Neil

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Human Genome, Cancer, Genetic Testing, Genetics, Urologic Diseases, Prostate Cancer, Good Health and Well Being, DNA Repair, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Gene Fusion, Humans, Male, Mutation, Neoplasm Metastasis, Phosphatidylinositol 3-Kinases, Prostatic Neoplasms, Receptors, Androgen, Signal Transduction, ras Proteins, Cancer Genome Atlas Research Network, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

There is substantial heterogeneity among primary prostate cancers, evident in the spectrum of molecular abnormalities and its variable clinical course. As part of The Cancer Genome Atlas (TCGA), we present a comprehensive molecular analysis of 333 primary prostate carcinomas. Our results revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1). Epigenetic profiles showed substantial heterogeneity, including an IDH1 mutant subset with a methylator phenotype. Androgen receptor (AR) activity varied widely and in a subtype-specific manner, with SPOP and FOXA1 mutant tumors having the highest levels of AR-induced transcripts. 25% of the prostate cancers had a presumed actionable lesion in the PI3K or MAPK signaling pathways, and DNA repair genes were inactivated in 19%. Our analysis reveals molecular heterogeneity among primary prostate cancers, as well as potentially actionable molecular defects.

Published
2015

7. Cabozantinib Resolves Bone Scans in Tumor-Naïve Mice Harboring Skeletal Injuries

Author

Doran, Michael G, Spratt, Daniel E, Wongvipat, John, Ulmert, David, Carver, Brett S, Sawyers, Charles L, and Evans, Michael J

Subjects
Engineering, Biomedical Engineering, Cancer, Urologic Diseases, Aging, Anilides, Animals, Axitinib, Bone Regeneration, Crizotinib, Fluorine Radioisotopes, Fractures, Bone, Imidazoles, Indazoles, Mice, Positron-Emission Tomography, Protein Kinase Inhibitors, Pyrazoles, Pyridines, Radiopharmaceuticals, Technetium Tc 99m Medronate, Tomography, Emission-Computed, Single-Photon, Nuclear Medicine & Medical Imaging, Biomedical engineering
Abstract

The receptor tyrosine kinase inhibitor cabozantinib (XL184, BMS-907351 Cometriq) has displayed impressive clinical activity against several indications, culminating in its recent approval for medullary thyroid cancer. Among malignancies with tropism for the bone (prostate, breast), one striking feature of early clinical reports about this drug has been the rapid and complete resolution of bone scans, a phenomenon almost never observed even among therapies already shown to confer survival benefit. In castration-resistant prostate cancer, not all conventional response indicators change as dramatically posttreatment, raising the possibility that cabozantinib may impair the ability of bone-seeking radionuclides to integrate within the remodeling bone. To test this hypothesis, we surgically induced bone remodeling via physical insult in non-tumor-bearing mice and performed 18F-sodium fluoride (18F-NaF) positron emission tomographic (PET) and technetium 99m-methylene diphosphonate (99mTc-MDP) single-photon emission computed tomographic (SPECT) scans pre- and posttreatment with cabozantinib and related inhibitors. A consistent reduction in the accumulation of either radiotracer at the site of bone remodeling was observed in animals treated with cabozantinib. Given that cabozantinib is known to inhibit several receptor tyrosine kinases, we drugged animals with various permutations of more selective inhibitors to attempt to refine the molecular basis of bone scan resolution. Neither the vascular endothelial growth factor receptor (VEGFR) inhibitor axitinib, the MET inhibitor crizotinib, nor the combination was capable of inhibiting 18F-NaF accumulation at known bioactive doses. In summary, although the mechanism by which cabozantinib suppresses radionuclide incorporation into foci undergoing bone remodeling remains unknown, that this phenomenon occurs in tumor-naïve models indicates that caution should be exercised in interpreting the clinical significance of this event.

Published
2014

8. MYC cooperates with AKT in prostate tumorigenesis and alters sensitivity to mTOR inhibitors.

Author

Clegg, Nicola J, Couto, Suzana S, Wongvipat, John, Hieronymus, Haley, Carver, Brett S, Taylor, Barry S, Ellwood-Yen, Katharine, Gerald, William L, Sander, Chris, and Sawyers, Charles L

Subjects
Prostate, Animals, Mice, Transgenic, Humans, Mice, Prostatic Intraepithelial Neoplasia, Prostatic Neoplasms, Neoplasm Invasiveness, Precancerous Conditions, Disease Models, Animal, Disease Progression, Proto-Oncogene Proteins c-myc, Protein Kinase Inhibitors, Signal Transduction, Apoptosis, Enzyme Activation, Protein Binding, Phenotype, Male, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Disease Models, Animal, Transgenic, General Science & Technology
Abstract

MYC and phosphoinositide 3-kinase (PI3K)-pathway deregulation are common in human prostate cancer. Through examination of 194 human prostate tumors, we observed statistically significant co-occurrence of MYC amplification and PI3K-pathway alteration, raising the possibility that these two lesions cooperate in prostate cancer progression. To investigate this, we generated bigenic mice in which both activated human AKT1 and human MYC are expressed in the prostate (MPAKT/Hi-MYC model). In contrast to mice expressing AKT1 alone (MPAKT model) or MYC alone (Hi-MYC model), the bigenic phenotype demonstrates accelerated progression of mouse prostate intraepithelial neoplasia (mPIN) to microinvasive disease with disruption of basement membrane, significant stromal remodeling and infiltration of macrophages, B- and T-lymphocytes, similar to inflammation observed in human prostate tumors. In contrast to the reversibility of mPIN lesions in young MPAKT mice after treatment with mTOR inhibitors, Hi-MYC and bigenic MPAKT/Hi-MYC mice were resistant. Additionally, older MPAKT mice showed reduced sensitivity to mTOR inhibition, suggesting that additional genetic events may dampen mTOR dependence. Since increased MYC expression is an early feature of many human prostate cancers, these data have implications for treatment of human prostate cancers with PI3K-pathway alterations using mTOR inhibitors.

Published
2011

10. ERG-driven prostate cancer emerges from basal-luminal hybrid cells

Author

Feng, Weiran, primary, Ladewig, Erik, additional, Salsabeel, Nazifa, additional, Zhao, Huiyong, additional, Lee, Young Sun, additional, Gopalan, Anuradha, additional, Luo, Hanzhi, additional, Kang, Wenfei, additional, Fan, Ning, additional, Rosiek, Eric, additional, Masilionis, Ignas, additional, Chaligne, Ronan, additional, De Stanchina, Elisa, additional, Chen, Yu, additional, Carver, Brett S., additional, Leslie, Christina S, additional, and Sawyers, Charles, additional

Published
2023
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11. Data from Androgen Receptor Signaling Regulates DNA Repair in Prostate Cancers

Author

Polkinghorn, William R., primary, Parker, Joel S., primary, Lee, Man X., primary, Kass, Elizabeth M., primary, Spratt, Daniel E., primary, Iaquinta, Phillip J., primary, Arora, Vivek K., primary, Yen, Wei-Feng, primary, Cai, Ling, primary, Zheng, Deyou, primary, Carver, Brett S., primary, Chen, Yu, primary, Watson, Philip A., primary, Shah, Neel P., primary, Fujisawa, Sho, primary, Goglia, Alexander G., primary, Gopalan, Anuradha, primary, Hieronymus, Haley, primary, Wongvipat, John, primary, Scardino, Peter T., primary, Zelefsky, Michael J., primary, Jasin, Maria, primary, Chaudhuri, Jayanta, primary, Powell, Simon N., primary, and Sawyers, Charles L., primary

Published
2023
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12. Supplementary Table S1 from Androgen Receptor Signaling Regulates DNA Repair in Prostate Cancers

Author

Polkinghorn, William R., primary, Parker, Joel S., primary, Lee, Man X., primary, Kass, Elizabeth M., primary, Spratt, Daniel E., primary, Iaquinta, Phillip J., primary, Arora, Vivek K., primary, Yen, Wei-Feng, primary, Cai, Ling, primary, Zheng, Deyou, primary, Carver, Brett S., primary, Chen, Yu, primary, Watson, Philip A., primary, Shah, Neel P., primary, Fujisawa, Sho, primary, Goglia, Alexander G., primary, Gopalan, Anuradha, primary, Hieronymus, Haley, primary, Wongvipat, John, primary, Scardino, Peter T., primary, Zelefsky, Michael J., primary, Jasin, Maria, primary, Chaudhuri, Jayanta, primary, Powell, Simon N., primary, and Sawyers, Charles L., primary

Published
2023
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13. Supplementary Figure S3 from Androgen Receptor Signaling Regulates DNA Repair in Prostate Cancers

Author

Polkinghorn, William R., primary, Parker, Joel S., primary, Lee, Man X., primary, Kass, Elizabeth M., primary, Spratt, Daniel E., primary, Iaquinta, Phillip J., primary, Arora, Vivek K., primary, Yen, Wei-Feng, primary, Cai, Ling, primary, Zheng, Deyou, primary, Carver, Brett S., primary, Chen, Yu, primary, Watson, Philip A., primary, Shah, Neel P., primary, Fujisawa, Sho, primary, Goglia, Alexander G., primary, Gopalan, Anuradha, primary, Hieronymus, Haley, primary, Wongvipat, John, primary, Scardino, Peter T., primary, Zelefsky, Michael J., primary, Jasin, Maria, primary, Chaudhuri, Jayanta, primary, Powell, Simon N., primary, and Sawyers, Charles L., primary

Published
2023
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14. Data from Suppression of CHK1 by ETS Family Members Promotes DNA Damage Response Bypass and Tumorigenesis

Author

Lunardi, Andrea, primary, Varmeh, Shohreh, primary, Chen, Ming, primary, Taulli, Riccardo, primary, Guarnerio, Jlenia, primary, Ala, Ugo, primary, Seitzer, Nina, primary, Ishikawa, Tomoki, primary, Carver, Brett S., primary, Hobbs, Robin M., primary, Quarantotti, Valentina, primary, Ng, Christopher, primary, Berger, Alice H., primary, Nardella, Caterina, primary, Poliseno, Laura, primary, Montironi, Rodolfo, primary, Castillo-Martin, Mireia, primary, Cordon-Cardo, Carlos, primary, Signoretti, Sabina, primary, and Pandolfi, Pier Paolo, primary

Published
2023
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15. Supplementary Figure S3 from Suppression of CHK1 by ETS Family Members Promotes DNA Damage Response Bypass and Tumorigenesis

Author

Lunardi, Andrea, primary, Varmeh, Shohreh, primary, Chen, Ming, primary, Taulli, Riccardo, primary, Guarnerio, Jlenia, primary, Ala, Ugo, primary, Seitzer, Nina, primary, Ishikawa, Tomoki, primary, Carver, Brett S., primary, Hobbs, Robin M., primary, Quarantotti, Valentina, primary, Ng, Christopher, primary, Berger, Alice H., primary, Nardella, Caterina, primary, Poliseno, Laura, primary, Montironi, Rodolfo, primary, Castillo-Martin, Mireia, primary, Cordon-Cardo, Carlos, primary, Signoretti, Sabina, primary, and Pandolfi, Pier Paolo, primary

Published
2023
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16. Supplementary Figure Legends from Suppression of CHK1 by ETS Family Members Promotes DNA Damage Response Bypass and Tumorigenesis

Author

Lunardi, Andrea, primary, Varmeh, Shohreh, primary, Chen, Ming, primary, Taulli, Riccardo, primary, Guarnerio, Jlenia, primary, Ala, Ugo, primary, Seitzer, Nina, primary, Ishikawa, Tomoki, primary, Carver, Brett S., primary, Hobbs, Robin M., primary, Quarantotti, Valentina, primary, Ng, Christopher, primary, Berger, Alice H., primary, Nardella, Caterina, primary, Poliseno, Laura, primary, Montironi, Rodolfo, primary, Castillo-Martin, Mireia, primary, Cordon-Cardo, Carlos, primary, Signoretti, Sabina, primary, and Pandolfi, Pier Paolo, primary

Published
2023
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17. Supplementary Table 1 from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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18. Data from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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19. Supplementary Figure Legend from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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20. Supplementary Figures from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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28. Copy number alteration burden predicts prostate cancer relapse

Author

Hieronymus, Haley, Schultz, Nikolaus, Gopalan, Anuradha, Carver, Brett S., Chang, Matthew T., Xiao, Yonghong, Heguy, Adriana, Huberman, Kety, Bernstein, Melanie, Assel, Melissa, Murali, Rajmohan, Vickers, Andrew, Scardino, Peter T., Sander, Chris, Reuter, Victor, Taylor, Barry S., and Sawyers, Charles L.

Published
2014

34. Identification of PHLPP1 as a Tumor Suppressor Reveals the Role of Feedback Activation in PTEN-Mutant Prostate Cancer Progression

Author

Chen, Muhan, Pratt, Christopher P., Zeeman, Martha E., Schultz, Nikolaus, Taylor, Barry S., O'Neill, Audrey, Castillo-Martin, Mireia, Nowak, Dawid G., Naguib, Adam, Grace, Danielle M., Murn, Jernej, Navin, Nick, Atwal, Gurinder S., Sander, Chris, Gerald, William L., Cordon-Cardo, Carlos, Newton, Alexandra C., Carver, Brett S., and Trotman, Lloyd C.

Published
2011
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36. Integrative Genomic Profiling of Human Prostate Cancer

Author

Taylor, Barry S., Schultz, Nikolaus, Hieronymus, Haley, Gopalan, Anuradha, Xiao, Yonghong, Carver, Brett S., Arora, Vivek K., Kaushik, Poorvi, Cerami, Ethan, Reva, Boris, Antipin, Yevgeniy, Mitsiades, Nicholas, Landers, Thomas, Dolgalev, Igor, Major, John E., Wilson, Manda, Socci, Nicholas D., Lash, Alex E., Heguy, Adriana, Eastham, James A., Scher, Howard I., Reuter, Victor E., Scardino, Peter T., Sander, Chris, Sawyers, Charles L., and Gerald, William L.

Published
2010
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41. ETS factors reprogram the androgen receptor cistrome and prime prostate tumorigenesis in response to PTEN loss

Author

Chen, Yu, Chi, Ping, Rockowitz, Shira, Iaquinta, Phillip J., Shamu, Tambudzai, Shukla, Shipra, Gao, Dong, Sirota, Inna, Carver, Brett S., Wongvipat, John, Scher, Howard I., Zheng, Deyou, and Sawyers, Charles L.

Subjects
Binding proteins -- Physiological aspects -- Genetic aspects -- Research, Prostate cancer -- Development and progression -- Genetic aspects -- Research, Carcinogenesis -- Risk factors -- Development and progression -- Research, Biological sciences, Health
Abstract

Studies of ETS-mediated prostate oncogenesis have been hampered by a lack of suitable experimental systems. Here we describe a new conditional mouse model that shows robust, homogenous ERG expression throughout [...]

Published
2013
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47. Four Cycles of Etoposide plus Cisplatin for Patients with Good-Risk Advanced Germ Cell Tumors

Author

Funt, Samuel A., primary, McHugh, Deaglan J., additional, Tsai, Stephanie, additional, Knezevic, Andrea, additional, O'Donnell, Devon, additional, Patil, Sujata, additional, Silber, Deborah, additional, Bromberg, Maria, additional, Carousso, Maryann, additional, Reuter, Victor E., additional, Carver, Brett S., additional, Sheinfeld, Joel, additional, Motzer, Robert J., additional, Bajorin, Dean F., additional, Bosl, George J., additional, and Feldman, Darren R., additional

Published
2021
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