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1. ERF mutations reveal a balance of ETS factors controlling prostate oncogenesis.

Author

Bose, Rohit, Karthaus, Wouter R, Armenia, Joshua, Abida, Wassim, Iaquinta, Phillip J, Zhang, Zeda, Wongvipat, John, Wasmuth, Elizabeth V, Shah, Neel, Sullivan, Patrick S, Doran, Michael G, Wang, Ping, Patruno, Anna, Zhao, Yilin, International SU2C/PCF Prostate Cancer Dream Team, Zheng, Deyou, Schultz, Nikolaus, and Sawyers, Charles L

Subjects
International SU2C/PCF Prostate Cancer Dream Team, Prostate, Cell Line, Tumor, Animals, Humans, Mice, Prostatic Neoplasms, Serine Endopeptidases, Tumor Suppressor Proteins, Receptors, Androgen, Repressor Proteins, Androgens, Signal Transduction, Up-Regulation, Mutation, Genes, Male, Proto-Oncogene Proteins c-ets, Protein Stability, Transcriptome, Carcinogenesis, Transcriptional Regulator ERG, Cell Line, Tumor, Receptors, Androgen, MD Multidisciplinary, General Science & Technology
Abstract

Half of all prostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expression of the normally silent E26 transformation-specific (ETS) transcription factor ERG in prostate cells. Recent genomic landscape studies of such cancers have reported recurrent point mutations and focal deletions of another ETS member, the ETS2 repressor factor ERF. Here we show these ERF mutations cause decreased protein stability and mostly occur in tumours without ERG upregulation. ERF loss recapitulates the morphological and phenotypic features of ERG gain in normal mouse prostate cells, including expansion of the androgen receptor transcriptional repertoire, and ERF has tumour suppressor activity in the same genetic background of Pten loss that yields oncogenic activity by ERG. In the more common scenario of ERG upregulation, chromatin immunoprecipitation followed by sequencing indicates that ERG inhibits the ability of ERF to bind DNA at consensus ETS sites both in normal and in cancerous prostate cells. Consistent with a competition model, ERF overexpression blocks ERG-dependent tumour growth, and ERF loss rescues TMPRSS2-ERG-positive prostate cancer cells from ERG dependency. Collectively, these data provide evidence that the oncogenicity of ERG is mediated, in part, by competition with ERF and they raise the larger question of whether other gain-of-function oncogenic transcription factors might also inactivate endogenous tumour suppressors.

Published
2017

2. Tumor Microenvironment-Derived NRG1 Promotes Antiandrogen Resistance in Prostate Cancer

Author

Zhang, Zeda, Karthaus, Wouter R., Lee, Young Sun, Gao, Vianne R., Wu, Chao, Russo, Joshua W., Liu, Menghan, Mota, Jose Mauricio, Abida, Wassim, Linton, Eliot, Lee, Eugine, Barnes, Spencer D., Chen, Hsuan-An, Mao, Ninghui, Wongvipat, John, Choi, Danielle, Chen, Xiaoping, Zhao, Huiyong, Manova-Todorova, Katia, de Stanchina, Elisa, Taplin, Mary-Ellen, Balk, Steven P., Rathkopf, Dana E., Gopalan, Anuradha, Carver, Brett S., Mu, Ping, Jiang, Xuejun, Watson, Philip A., and Sawyers, Charles L.

Published
2020
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3. Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation

Author

Zhang, Zeda, Zhou, Chuanli, Li, Xiaoling, Barnes, Spencer D., Deng, Su, Hoover, Elizabeth, Chen, Chi-Chao, Lee, Young Sun, Zhang, Yanxiao, Wang, Choushi, Metang, Lauren A., Wu, Chao, Tirado, Carla Rodriguez, Johnson, Nickolas A., Wongvipat, John, Navrazhina, Kristina, Cao, Zhen, Choi, Danielle, Huang, Chun-Hao, Linton, Eliot, Chen, Xiaoping, Liang, Yupu, Mason, Christopher E., de Stanchina, Elisa, Abida, Wassim, Lujambio, Amaia, Li, Sheng, Lowe, Scott W., Mendell, Joshua T., Malladi, Venkat S., Sawyers, Charles L., and Mu, Ping

Published
2020
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4. Applying 89Zr-Transferrin To Study the Pharmacology of Inhibitors to BET Bromodomain Containing Proteins

Author

Doran, Michael G, Carnazza, Kathryn E, Steckler, Jeffrey M, Spratt, Daniel E, Truillet, Charles, Wongvipat, John, Sawyers, Charles L, Lewis, Jason S, and Evans, Michael J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Genetics, Cancer, Rare Diseases, Lymphoma, Animals, Apoptosis, Cell Proliferation, Gene Expression Regulation, Neoplastic, Histone Acetyltransferases, Histone Chaperones, Humans, Male, Mice, Mice, SCID, Nuclear Proteins, Positron-Emission Tomography, Prostatic Neoplasms, Proto-Oncogene Proteins c-myc, Radiopharmaceuticals, Receptors, Transferrin, Transferrin, Xenograft Model Antitumor Assays, Zirconium, PET, lymphoma, prostate cancer, MYC, transferrin receptor, BRD4, Macromolecular and Materials Chemistry, Pharmacology and Pharmaceutical Sciences, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

Chromatin modifying proteins are attractive drug targets in oncology, given the fundamental reliance of cancer on altered transcriptional activity. Multiple transcription factors can be impacted downstream of primary target inhibition, thus making it challenging to understand the driving mechanism of action of pharmacologic inhibition of chromatin modifying proteins. This in turn makes it difficult to identify biomarkers predictive of response and pharmacodynamic tools to optimize drug dosing. In this report, we show that (89)Zr-transferrin, an imaging tool we developed to measure MYC activity in cancer, can be used to identify cancer models that respond to broad spectrum inhibitors of transcription primarily due to MYC inhibition. As a proof of concept, we studied inhibitors of BET bromodomain containing proteins, as they can impart antitumor effects in a MYC dependent or independent fashion. In vitro, we show that transferrin receptor biology is inhibited in multiple MYC positive models of prostate cancer and double hit lymphoma when MYC biology is impacted. Moreover, we show that bromodomain inhibition in one lymphoma model results in transferrin receptor expression changes large enough to be quantified with (89)Zr-transferrin and positron emission tomography (PET) in vivo. Collectively, these data further underscore the diagnostic utility of the relationship between MYC and transferrin in oncology, and provide the rationale to incorporate transferrin-based PET into early clinical trials with bromodomain inhibitors for the treatment of solid tumors.

Published
2016

5. Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E, Evans, Michael J, Davis, Brian J, Doran, Michael G, Lee, Man Xia, Shah, Neel, Wongvipat, John, Carnazza, Kathryn E, Klee, George G, Polkinghorn, William, Tindall, Donald J, Lewis, Jason S, and Sawyers, Charles L

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Urologic Diseases, Prostate Cancer, Aging, Cancer, Animals, Blotting, Western, Cell Line, Tumor, Comet Assay, Fluorescent Antibody Technique, Humans, Luminescent Measurements, Male, Mice, Mice, SCID, Prostatic Neoplasms, Radiation Tolerance, Real-Time Polymerase Chain Reaction, Receptors, Androgen, Up-Regulation, Xenograft Model Antitumor Assays, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Clinical trials have established the benefit of androgen deprivation therapy (ADT) combined with radiotherapy in prostate cancer. ADT sensitizes prostate cancer to radiotherapy-induced death at least in part through inhibition of DNA repair machinery, but for unknown reasons, adjuvant ADT provides further survival benefits. Here, we show that androgen receptor (AR) expression and activity are durably upregulated following radiotherapy in multiple human prostate cancer models in vitro and in vivo. Moreover, the degree of AR upregulation correlates with survival in vitro and time to tumor progression in animal models. We also provide evidence of AR pathway upregulation, measured by a rise in serum levels of AR-regulated hK2 protein, in nearly 20% of patients after radiotherapy. Furthermore, these men were three-fold more likely to experience subsequent biochemical failure. Collectively, these data demonstrate that radiotherapy can upregulate AR signaling after therapy to an extent that negatively affects disease progression and/or survival.

Published
2015

7. Annotating STEAP1 Regulation in Prostate Cancer with 89Zr Immuno-PET

Author

Doran, Michael G, Watson, Philip A, Cheal, Sarah M, Spratt, Daniel E, Wongvipat, John, Steckler, Jeffrey M, Carrasquillo, Jorge A, Evans, Michael J, and Lewis, Jason S

Subjects
Prostate Cancer, Biotechnology, Aging, Cancer, Urologic Diseases, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Antigens, Neoplasm, Cell Line, Tumor, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Immunoconjugates, Male, Mice, Oxidoreductases, Positron-Emission Tomography, Prostatic Neoplasms, Radioisotopes, Radiopharmaceuticals, Tissue Distribution, Zirconium, PET, prostate cancer, androgen receptor, Clinical Sciences, Nuclear Medicine & Medical Imaging
Abstract

UnlabelledAntibodies and antibody-drug conjugates targeting the cell surface protein 6 transmembrane epithelial antigen of prostate 1 (STEAP1) are in early clinical development for the treatment of castration-resistant prostate cancer (PCa). In general, antigen expression directly affects the bioactivity of therapeutic antibodies, and the biologic regulation of STEAP1 is unusually complicated in PCa. Paradoxically, STEAP1 can be induced or repressed by the androgen receptor (AR) in different human PCa models, while also expressed in AR-null PCa. Consequently, there is an urgent need to translate diagnostic strategies to establish which regulatory mechanism predominates in patients to situate the appropriate therapy within standard of care therapies inhibiting AR.MethodsTo this end, we prepared and evaluated (89)Zr-labeled MSTP2109A ((89)Zr-2109A), a radiotracer for PET derived from a fully humanized monoclonal antibody to STEAP1 in preclinical PCa models.Results(89)Zr-2109A specifically localized to the STEAP1-positive human PCa models CWR22Pc, 22Rv1, and PC3. Moreover, (89)Zr-2109A sensitively measured treatment-induced changes (∼66% decline) in STEAP1 expression in CWR22PC in vitro and in vivo, a model we showed to express STEAP1 in an AR-dependent manner.ConclusionThese findings highlight the ability of immuno-PET with (89)Zr-2109A to detect acute changes in STEAP1 expression and argue for an expansion of ongoing efforts to image PCa patients with (89)Zr-2109A to maximize the clinical benefit associated with antibodies or antibody-drug conjugates to STEAP1.

Published
2014

8. 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

9. Overcoming mutation-based resistance to antiandrogens with rational drug design.

Author

Balbas, Minna D, Evans, Michael J, Hosfield, David J, Wongvipat, John, Arora, Vivek K, Watson, Philip A, Chen, Yu, Greene, Geoffrey L, Shen, Yang, and Sawyers, Charles L

Subjects
Cell Line, Humans, Prostatic Neoplasms, Androgen Antagonists, Drug Design, Drug Resistance, Neoplasm, Mutation, Male, Molecular Dynamics Simulation, Human, Mouse, androgen receptor, drug resistance, prostate cancer, Drug Resistance, Neoplasm, Biochemistry and Cell Biology
Abstract

The second-generation antiandrogen enzalutamide was recently approved for patients with castration-resistant prostate cancer. Despite its success, the duration of response is often limited. For previous antiandrogens, one mechanism of resistance is mutation of the androgen receptor (AR). To prospectively identify AR mutations that might confer resistance to enzalutamide, we performed a reporter-based mutagenesis screen and identified a novel mutation, F876L, which converted enzalutamide into an AR agonist. Ectopic expression of AR F876L rescued the growth inhibition of enzalutamide treatment. Molecular dynamics simulations performed on antiandrogen-AR complexes suggested a mechanism by which the F876L substitution alleviates antagonism through repositioning of the coactivator recruiting helix 12. This model then provided the rationale for a focused chemical screen which, based on existing antiandrogen scaffolds, identified three novel compounds that effectively antagonized AR F876L (and AR WT) to suppress the growth of prostate cancer cells resistant to enzalutamide. DOI:http://dx.doi.org/10.7554/eLife.00499.001.

Published
2013

10. 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

11. Aberrant Activation of a Gastrointestinal Transcriptional Circuit in Prostate Cancer Mediates Castration Resistance

Author

Shukla, Shipra, Cyrta, Joanna, Murphy, Devan A., Walczak, Edward G., Ran, Leili, Agrawal, Praveen, Xie, Yuanyuan, Chen, Yuedan, Wang, Shangqian, Zhan, Yu, Li, Dan, Wong, Elissa W.P., Sboner, Andrea, Beltran, Himisha, Mosquera, Juan Miguel, Sher, Jessica, Cao, Zhen, Wongvipat, John, Koche, Richard P., Gopalan, Anuradha, Zheng, Deyou, Rubin, Mark A., Scher, Howard I., Chi, Ping, and Chen, Yu

Published
2017
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12. COP1/DET1/ETS axis regulates ERK transcriptome and sensitivity to MAPK inhibitors

Author

Xie, Yuanyuan, Cao, Zhen, Wong, Elissa W.P., Guan, Youxin, Ma, Wenfu, Zhang, Jenny Q., Walczak, Edward G., Murphy, Devan, Ran, Leili, Sirota, Inna, Wang, Shangqian, Shukla, Shipra, Gao, Dong, Knott, Simon R.V., Chang, Kenneth, Leu, Justin, Wongvipat, John, Antonescu, Cristina R., Hannon, Gregory, Chi, Ping, and Chen, Yu

Subjects
Genetic aspects, Health aspects, Extracellular signal-regulated kinases -- Health aspects, Cellular signal transduction -- Genetic aspects -- Health aspects, Carcinogenesis -- Genetic aspects
Abstract

AU>Xie, Yuanyuan^Cao, Zhen^Wong, Elissa W.P.^Guan, Youxin^Ma, Wenfu^Zhang, Jenny Q.^Walczak, Edward G. ^Murphy, Devan^Ran, Leili^Sirota, Inna^Wang, Shangqian^Shukla, Shipra^Gao, Dong^Knott, Simon R.V. ^Chang, Kenneth^Leu, Justin^Wongvipat, John^Antonescu, Cristina R.^Hannon, Introduction The MAPK/ERK signaling [...], Aberrant activation of MAPK signaling leads to the activation of oncogenic transcriptomes. How MAPK signaling is coupled with the transcriptional response in cancer is not fully understood. In 2 MAPK- activated tumor types, gastrointestinal stromal tumor and melanoma, we found that ETV1 and other Pea3-ETS transcription factors are critical nuclear effectors of MAPK signaling that are regulated through protein stability. Expression of stabilized Pea3-ETS factors can partially rescue the MAPK transcriptome and cell viability after MAPK inhibition. To identify the players involved in this process, we performed a pooled genome-wide RNAi screen using a fluorescence-based ETV1 protein stability sensor and identified COP1, DET1, DDB1, UBE3C, PSMD4, and COP9 signalosome members. COP1 or DET1 loss led to decoupling between MAPK signaling and the downstream transcriptional response, where MAPK inhibition failed to destabilize Pea3 factors and fully inhibit the MAPK transcriptome, thus resulting in decreased sensitivity to MAPK pathway inhibitors. We identified multiple COP1 and DET1 mutations in human tumors that were defective in the degradation of Pea3-ETS factors. Two melanoma patients had de novo DET1 mutations arising after vemurafenib treatment. These observations indicate that MAPK signaling-dependent regulation of Pea3-ETS protein stability is a key signaling node in oncogenesis and therapeutic resistance to MAPK pathway inhibition.

Published
2018
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13. SOX2 promotes lineage plasticity and antiandrogen resistance in TP53 - and RB1 -deficient prostate cancer

Author

Mu, Ping, Zhang, Zeda, Benelli, Matteo, Karthaus, Wouter R., Hoover, Elizabeth, Chen, Chi-Chao, Wongvipat, John, Ku, Sheng-Yu, Gao, Dong, Cao, Zhen, Shah, Neel, Adams, Elizabeth J., Abida, Wassim, Watson, Philip A., Prandi, Davide, Huang, Chun-Hao, de Stanchina, Elisa, Lowe, Scott W., Ellis, Leigh, Beltran, Himisha, Rubin, Mark A., Goodrich, David W., Demichelis, Francesca, and Sawyers, Charles L.

Published
2017

14. 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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15. 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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16. Data from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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18. 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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19. Supplementary Table 1 from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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20. Supplementary Tables 1-16, Figures 1-15 from Imaging Androgen Receptor Signaling with a Radiotracer Targeting Free Prostate-Specific Antigen

Author

Ulmert, David, primary, Evans, Michael J., primary, Holland, Jason P., primary, Rice, Samuel L., primary, Wongvipat, John, primary, Pettersson, Kim, primary, Abrahamsson, Per-Anders, primary, Scardino, Peter T., primary, Larson, Steven M., primary, Lilja, Hans, primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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21. Supplementary Table 3 from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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22. Supplementary Figure Legends from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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23. Press Conference from Imaging Androgen Receptor Signaling with a Radiotracer Targeting Free Prostate-Specific Antigen

Author

Ulmert, David, primary, Evans, Michael J., primary, Holland, Jason P., primary, Rice, Samuel L., primary, Wongvipat, John, primary, Pettersson, Kim, primary, Abrahamsson, Per-Anders, primary, Scardino, Peter T., primary, Larson, Steven M., primary, Lilja, Hans, primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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24. Supplementary Table 2 from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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25. Supplementary Figures 1 - 6 from Combined Inhibition of MAP Kinase and KIT Signaling Synergistically Destabilizes ETV1 and Suppresses GIST Tumor Growth

Author

Ran, Leili, primary, Sirota, Inna, primary, Cao, Zhen, primary, Murphy, Devan, primary, Chen, Yuedan, primary, Shukla, Shipra, primary, Xie, Yuanyuan, primary, Kaufmann, Michael C., primary, Gao, Dong, primary, Zhu, Sinan, primary, Rossi, Ferdinando, primary, Wongvipat, John, primary, Taguchi, Takahiro, primary, Tap, William D., primary, Mellinghoff, Ingo K., primary, Besmer, Peter, primary, Antonescu, Cristina R., primary, Chen, Yu, primary, and Chi, Ping, primary

Published
2023
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27. Supplementary Methods from Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E., primary, Evans, Michael J., primary, Davis, Brian J., primary, Doran, Michael G., primary, Lee, Man Xia, primary, Shah, Neel, primary, Wongvipat, John, primary, Carnazza, Kathryn E., primary, Klee, George G., primary, Polkinghorn, William, primary, Tindall, Donald J., primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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28. Data from Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E., primary, Evans, Michael J., primary, Davis, Brian J., primary, Doran, Michael G., primary, Lee, Man Xia, primary, Shah, Neel, primary, Wongvipat, John, primary, Carnazza, Kathryn E., primary, Klee, George G., primary, Polkinghorn, William, primary, Tindall, Donald J., primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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29. Supplementary Figure Legends from Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E., primary, Evans, Michael J., primary, Davis, Brian J., primary, Doran, Michael G., primary, Lee, Man Xia, primary, Shah, Neel, primary, Wongvipat, John, primary, Carnazza, Kathryn E., primary, Klee, George G., primary, Polkinghorn, William, primary, Tindall, Donald J., primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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30. Supplementary Figure 2 from Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E., primary, Evans, Michael J., primary, Davis, Brian J., primary, Doran, Michael G., primary, Lee, Man Xia, primary, Shah, Neel, primary, Wongvipat, John, primary, Carnazza, Kathryn E., primary, Klee, George G., primary, Polkinghorn, William, primary, Tindall, Donald J., primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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31. SupplementaryFigure 1 from Androgen Receptor Upregulation Mediates Radioresistance after Ionizing Radiation

Author

Spratt, Daniel E., primary, Evans, Michael J., primary, Davis, Brian J., primary, Doran, Michael G., primary, Lee, Man Xia, primary, Shah, Neel, primary, Wongvipat, John, primary, Carnazza, Kathryn E., primary, Klee, George G., primary, Polkinghorn, William, primary, Tindall, Donald J., primary, Lewis, Jason S., primary, and Sawyers, Charles L., primary

Published
2023
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32. Supplementary Figure 3 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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33. Supplementary Figure 5 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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34. Supplementary Tables 1-7 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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35. Supplementary Figure 1 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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36. Supplementary Methods from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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37. Supplementary Figure 4 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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38. Supplementary Figure 2 from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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39. Data from ARN-509: A Novel Antiandrogen for Prostate Cancer Treatment

Author

Clegg, Nicola J., primary, Wongvipat, John, primary, Joseph, James D., primary, Tran, Chris, primary, Ouk, Samedy, primary, Dilhas, Anna, primary, Chen, Yu, primary, Grillot, Kate, primary, Bischoff, Eric D., primary, Cai, Ling, primary, Aparicio, Anna, primary, Dorow, Steven, primary, Arora, Vivek, primary, Shao, Gang, primary, Qian, Jing, primary, Zhao, Hong, primary, Yang, Guangbin, primary, Cao, Chunyan, primary, Sensintaffar, John, primary, Wasielewska, Teresa, primary, Herbert, Mark R., primary, Bonnefous, Celine, primary, Darimont, Beatrice, primary, Scher, Howard I., primary, Smith-Jones, Peter, primary, Klang, Mark, primary, Smith, Nicholas D., primary, De Stanchina, Elisa, primary, Wu, Nian, primary, Ouerfelli, Ouathek, primary, Rix, Peter J., primary, Heyman, Richard A., primary, Jung, Michael E., primary, Sawyers, Charles L., primary, and Hager, Jeffrey H., primary

Published
2023
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40. Organoid Cultures Derived from Patients with Advanced Prostate Cancer

Author

Gao, Dong, Vela, Ian, Sboner, Andrea, Iaquinta, Phillip J., Karthaus, Wouter R., Gopalan, Anuradha, Dowling, Catherine, Wanjala, Jackline N., Undvall, Eva A., Arora, Vivek K., Wongvipat, John, Kossai, Myriam, Ramazanoglu, Sinan, Barboza, Luendreo P., Di, Wei, Cao, Zhen, Zhang, Qi Fan, Sirota, Inna, Ran, Leili, MacDonald, Theresa Y., Beltran, Himisha, Mosquera, Juan-Miguel, Touijer, Karim A., Scardino, Peter T., Laudone, Vincent P., Curtis, Kristen R., Rathkopf, Dana E., Morris, Michael J., Danila, Daniel C., Slovin, Susan F., Solomon, Stephen B., Eastham, James A., Chi, Ping, Carver, Brett, Rubin, Mark A., Scher, Howard I., Clevers, Hans, Sawyers, Charles L., and Chen, Yu

Published
2014
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48. CANCER THERAPY: SOX2 promotes lineage plasticity and antiandrogen resistance in TP53-and RB1-deficient prostate cancer

Author

Mu, Ping, Zhang, Zeda, Benelli, Matteo, Karthaus, Wouter R., Hoover, Elizabeth, Chen, Chi-Chao, Wongvipat, John, Ku, Sheng-Yu, Gao, Dong, Cao, Zhen, Shah, Neel, Adams, Elizabeth J., Abida, Wassim, Watson, Philip A., Prandi, Davide, Huang, Chun-Hao, de Stanchina, Elisa, Lowe, Scott W., Ellis, Leigh, Beltran, Himisha, Rubin, Mark A., Goodrich, David W., Demichelis, Francesca, and Sawyers, Charles L.

Published
2017
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49. 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
Physiological aspects, Development and progression, Genetic aspects, Research, Risk factors, Prostate cancer -- Development and progression -- Genetic aspects -- Research, Binding proteins -- Physiological aspects -- Genetic aspects -- Research, Carcinogenesis -- Risk factors -- Development and progression -- Research
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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50. Annotating MYC status with [.sup.89]Zr-transferrin imaging

Author

Holland, Jason P., Evans, Michael J., Rice, Samuel L., Wongvipat, John, Sawyers, Charles L., and Lewis, Jason S.

Subjects
Diagnosis, Physiological aspects, Genetic aspects, Research, Methods, Positron emission tomography -- Methods -- Research, Transferrin -- Physiological aspects -- Genetic aspects -- Research, Prostate cancer -- Diagnosis -- Genetic aspects -- Research, Genetic markers -- Physiological aspects -- Research, PET imaging -- Methods -- Research
Abstract

Cancer cells generally express higher amounts of TFRC than do normal cells, presumably to accommodate the increase in iron usage required for various biological processes associated with cell proliferation (1), [...], A noninvasive technology that quantitatively measures the activity of oncogenic signaling pathways could have a broad impact on cancer diagnosis and treatment with targeted therapies. Here we describe the development of [.sup.89]Zr-desferrioxamine-labeled transferrin ([.sup.89]Zr-transferrin), a new positron emission tomography (PET) radiotracer that binds the transferrin receptor 1 (TFRC, CD71) with high avidity. The use of [.sup.89]Zr-transferrin produces high-contrast PET images that quantitatively reflect treatment-induced changes in MYC-regulated TFRC expression in a MYC-driven prostate cancer xenograft model. Moreover, [.sup.89]Zr-transferrin imaging can detect the in situ development of prostate cancer in a transgenic MYC prostate cancer model, as well as in prostatic intraepithelial neoplasia (PIN) before histological or anatomic evidence of invasive cancer. These preclinical data establish [.sup.89]Zr-transferrin as a sensitive tool for noninvasive measurement of oncogene-driven TFRC expression in prostate and potentially other cancers, with prospective near-term clinical application.

Published
2012
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