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2. Distinct mesenchymal cell states mediate prostate cancer progression

Author

Pakula, Hubert, Omar, Mohamed, Carelli, Ryan, Pederzoli, Filippo, Fanelli, Giuseppe Nicolò, Pannellini, Tania, Socciarelli, Fabio, Van Emmenis, Lucie, Rodrigues, Silvia, Fidalgo-Ribeiro, Caroline, Nuzzo, Pier Vitale, Brady, Nicholas J., Dinalankara, Wikum, Jere, Madhavi, Valencia, Itzel, Saladino, Christopher, Stone, Jason, Unkenholz, Caitlin, Garner, Richard, Alexanderani, Mohammad K., Khani, Francesca, de Almeida, Francisca Nunes, Abate-Shen, Cory, Greenblatt, Matthew B., Rickman, David S., Barbieri, Christopher E., Robinson, Brian D., Marchionni, Luigi, and Loda, Massimo

Published
2024
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3. Transcriptomic Profiling of Primary Prostate Cancers and Nonlocalized Disease on Prostate-Specific Membrane Antigen Positron Emission Tomography/Computed Tomography: A Multicenter Retrospective Study

Author

Nikitas, John, Subramanian, Kritika, Gozal, Nimrod Barashi, Ricaurte-Fajardo, Andres, Li, Eric, Proudfoot, James A., Davicioni, Elai, Marciscano, Ariel E., Osborne, Joseph R., Barbieri, Christopher E., Armstrong, Wesley R., Smith, Clayton P., Valle, Luca F., Steinberg, Michael L., Boutros, Paul C., Nickols, Nicholas G., Rettig, Matthew B., Reiter, Robert, Weiner, Adam B., Calais, Jeremie, Czernin, Johannes, Ross, Ashley Evan, Kim, Eric H., Nagar, Himanshu, and Kishan, Amar U.

Published
2024
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4. Cross-modality Knowledge Transfer for Prostate Segmentation from CT Scans

Author

Liu, Yucheng, Khosravan, Naji, Liu, Yulin, Stember, Joseph, Shoag, Jonathan, Barbieri, Christopher E., Bagci, Ulas, and Jambawalikar, Sachin

Subjects
Electrical Engineering and Systems Science - Image and Video Processing, Computer Science - Machine Learning, Physics - Medical Physics, Statistics - Machine Learning
Abstract

Creating large scale high-quality annotations is a known challenge in medical imaging. In this work, based on the CycleGAN algorithm, we propose leveraging annotations from one modality to be useful in other modalities. More specifically, the proposed algorithm creates highly realistic synthetic CT images (SynCT) from prostate MR images using unpaired data sets. By using SynCT images (without segmentation labels) and MR images (with segmentation labels available), we have trained a deep segmentation network for precise delineation of prostate from real CT scans. For the generator in our CycleGAN, the cycle consistency term is used to guarantee that SynCT shares the identical manually-drawn, high-quality masks originally delineated on MR images. Further, we introduce a cost function based on structural similarity index (SSIM) to improve the anatomical similarity between real and synthetic images. For segmentation followed by the SynCT generation from CycleGAN, automatic delineation is achieved through a 2.5D Residual U-Net. Quantitative evaluation demonstrates comparable segmentation results between our SynCT and radiologist drawn masks for real CT images, solving an important problem in medical image segmentation field when ground truth annotations are not available for the modality of interest., Comment: 9 pages, 3 figures, 2019 MICCAI-DART workshop

Published
2019

7. Identifying synergistic high-order 3D chromatin conformations from genome-scale nanopore concatemer sequencing

Author

Deshpande, Aditya S., Ulahannan, Netha, Pendleton, Matthew, Dai, Xiaoguang, Ly, Lynn, Behr, Julie M., Schwenk, Stefan, Liao, Will, Augello, Michael A., Tyer, Carly, Rughani, Priyesh, Kudman, Sarah, Tian, Huasong, Otis, Hannah G., Adney, Emily, Wilkes, David, Mosquera, Juan Miguel, Barbieri, Christopher E., Melnick, Ari, Stoddart, David, Turner, Daniel J., Juul, Sissel, Harrington, Eoghan, and Imieliński, Marcin

Published
2022
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8. FOXA1 mutations alter pioneering activity, differentiation and prostate cancer phenotypes

Author

Adams, Elizabeth J, Karthaus, Wouter R, Hoover, Elizabeth, Liu, Deli, Gruet, Antoine, Zhang, Zeda, Cho, Hyunwoo, DiLoreto, Rose, Chhangawala, Sagar, Liu, Yang, Watson, Philip A, Davicioni, Elai, Sboner, Andrea, Barbieri, Christopher E, Bose, Rohit, Leslie, Christina S, and Sawyers, Charles L

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Biomedical and Clinical Sciences, Genetics, Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Prostate Cancer, Aging, Cancer, Urologic Diseases, Human Genome, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Amino Acid Sequence, Animals, Base Sequence, Binding Sites, Cell Differentiation, Cell Lineage, Chromatin, Disease Progression, Gene Expression Regulation, Neoplastic, Hepatocyte Nuclear Factor 3-alpha, Humans, Male, Mice, Mice, Inbred NOD, Mutation, Nucleotide Motifs, Organoids, Phenotype, Prostatic Neoplasms, General Science & Technology
Abstract

Mutations in the transcription factor FOXA1 define a unique subset of prostate cancers but the functional consequences of these mutations and whether they confer gain or loss of function is unknown1-9. Here, by annotating the landscape of FOXA1 mutations from 3,086 human prostate cancers, we define two hotspots in the forkhead domain: Wing2 (around 50% of all mutations) and the highly conserved DNA-contact residue R219 (around 5% of all mutations). Wing2 mutations are detected in adenocarcinomas at all stages, whereas R219 mutations are enriched in metastatic tumours with neuroendocrine histology. Interrogation of the biological properties of wild-type FOXA1 and fourteen FOXA1 mutants reveals gain of function in mouse prostate organoid proliferation assays. Twelve of these mutants, as well as wild-type FOXA1, promoted an exaggerated pro-luminal differentiation program, whereas two different R219 mutants blocked luminal differentiation and activated a mesenchymal and neuroendocrine transcriptional program. Assay for transposase-accessible chromatin using sequencing (ATAC-seq) of wild-type FOXA1 and representative Wing2 and R219 mutants revealed marked, mutant-specific changes in open chromatin at thousands of genomic loci and exposed sites of FOXA1 binding and associated increases in gene expression. Of note, ATAC-seq peaks in cells expressing R219 mutants lacked the canonical core FOXA1-binding motifs (GTAAAC/T) but were enriched for a related, non-canonical motif (GTAAAG/A), which was preferentially activated by R219-mutant FOXA1 in reporter assays. Thus, FOXA1 mutations alter its pioneering function and perturb normal luminal epithelial differentiation programs, providing further support for the role of lineage plasticity in cancer progression.

Published
2019

9. Race and prostate cancer: genomic landscape

Author

Arenas-Gallo, Camilo, Owiredu, Jude, Weinstein, Ilon, Lewicki, Patrick, Basourakos, Spyridon P., Vince, Jr, Randy, Al Hussein Al Awamlh, Bashir, Schumacher, Fredrick R., Spratt, Daniel E., Barbieri, Christopher E., and Shoag, Jonathan E.

Published
2022
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12. Reshaping of the androgen-driven chromatin landscape in normal prostate cells by early cancer drivers and effect on therapeutic sensitivity

Author

Grbesa, Ivana, Augello, Michael A., Liu, Deli, McNally, Dylan R., Gaffney, Christopher D., Huang, Dennis, Lin, Kevin, Ivenitsky, Daria, Goueli, Ramy, Robinson, Brian D., Khani, Francesca, Deonarine, Lesa D., Blattner, Mirjam, Elemento, Olivier, Davicioni, Elai, Sboner, Andrea, and Barbieri, Christopher E.

Published
2021
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13. Diversity in Androgen Receptor Action Among Treatment-naïve Prostate Cancers Is Reflected in Treatment Response Predictions and Molecular Subtypes

Author

Ben-Salem, Salma, Hu, Qiang, Liu, Yang, Alshalalfa, Mohammed, Zhao, Xin, Wang, Irene, Venkadakrishnan, Varadha Balaji, Senapati, Dhirodatta, Kumari, Sangeeta, Liu, Deli, Sboner, Andrea, Barbieri, Christopher E., Feng, Felix, Billaud, Jean-Noel, Davicioni, Elai, Liu, Song, and Heemers, Hannelore V.

Published
2020
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16. Clonal Lineage Tracing with Somatic Delivery of Recordable Barcodes Reveals Migration Histories of Metastatic Prostate Cancer

Author

Serio, R, Scheben, A, Lu, B, Gargiulo, D, Patruno, L, Buckholtz, C, Chaffee, R, Jibilian, M, Persaud, S, Staklinski, S, Hassett, R, Brault, L, Ramazzotti, D, Barbieri, C, Siepel, A, Nowak, D, Serio, Ryan N., Scheben, Armin, Lu, Billy, Gargiulo, Domenic V., Patruno, Lucrezia, Buckholtz, Caroline L., Chaffee, Ryan J., Jibilian, Megan C., Persaud, Steven G., Staklinski, Stephen J., Hassett, Rebecca, Brault, Lise M., Ramazzotti, Daniele, Barbieri, Christopher E., Siepel, Adam C., Nowak, Dawid G., Serio, R, Scheben, A, Lu, B, Gargiulo, D, Patruno, L, Buckholtz, C, Chaffee, R, Jibilian, M, Persaud, S, Staklinski, S, Hassett, R, Brault, L, Ramazzotti, D, Barbieri, C, Siepel, A, Nowak, D, Serio, Ryan N., Scheben, Armin, Lu, Billy, Gargiulo, Domenic V., Patruno, Lucrezia, Buckholtz, Caroline L., Chaffee, Ryan J., Jibilian, Megan C., Persaud, Steven G., Staklinski, Stephen J., Hassett, Rebecca, Brault, Lise M., Ramazzotti, Daniele, Barbieri, Christopher E., Siepel, Adam C., and Nowak, Dawid G.

Abstract

The patterns by which primary tumors spread to metastatic sites remain poorly understood. Here, we define patterns of metastatic seeding in prostate cancer (PCa) using a novel injection-based mouse model — EvoCaP (Evolution in Cancer of the Prostate), featuring aggressive metastatic cancer to bone, liver, lungs, and lymph nodes. To define migration histories between primary and metastatic sites, we used our EvoTraceR pipeline to track distinct tumor clones containing recordable barcodes. We detected widespread intratumoral heterogeneity from the primary tumor in metastatic seeding, with few clonal populations (CPs) instigating most migration. Metastasis-to-metastasis seeding was uncommon, as most cells remained confined within the tissue. Migration patterns in our model were congruent with human PCa seeding topologies. Our findings support the view of metastatic PCa as a systemic disease driven by waves of aggressive clones expanding their niche, infrequently overcoming constraints that otherwise keep them confined in the primary or metastatic site.

Published
2024

17. 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, Cancer, Cancer Genomics, Human Genome, Aging, Prostate Cancer, Urologic Diseases, Genetics, 2.1 Biological and endogenous factors, 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

20. N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer

Author

Berger, Adeline, Brady, Nicholas J., Bareja, Rohan, Robinson, Brian, Conteduca, Vincenza, Augello, Michael A., Puca, Loredana, Ahmed, Adnan, Dardenne, Etienne, Lu, Xiaodong, Hwang, Inah, Bagadion, Alyssa M., Sboner, Andrea, Elemento, Olivier, Paik, Jihye, Yu, Jindan, Barbieri, Christopher E., Dephoure, Noah, Beltran, Himisha, and Rickman, David S.

Subjects
Thermo Fisher Scientific Inc., Analysis, Development and progression, Prognosis, Health aspects, Epigenetic inheritance -- Analysis -- Health aspects, Genes -- Analysis -- Health aspects, Prostate cancer -- Development and progression -- Prognosis -- Analysis -- Health aspects, Scientific equipment industry -- Analysis -- Health aspects, Death, Androgens, Tumors
Abstract

Introduction Lineage plasticity, a process by which differentiated cells lose their identity and acquire an alternative lineage program, has recently been identified as an emerging mechanism of resistance to targeted [...], Despite recent therapeutic advances, prostate cancer remains a leading cause of cancer-related death. A subset of castration-resistant prostate cancers become androgen receptor (AR) signaling independent and develop neuroendocrine prostate cancer (NEPC) features through lineage plasticity. These NEPC tumors, associated with aggressive disease and poor prognosis, are driven, in part, by aberrant expression of N-Myc, through mechanisms that remain unclear. Integrative analysis of the N-Myc transcriptome, cistrome, and interactome using in vivo, in vitro, and ex vivo models (including patient-derived organoids) identified a lineage switch towards a neural identity associated with epigenetic reprogramming. N-Myc and known AR cofactors (e.g., FOXA1 and HOXB13) overlapped, independently of AR, at genomic loci implicated in neural lineage specification. Moreover, histone marks specifically associated with lineage- defining genes were reprogrammed by N-Myc. We also demonstrated that the N-Myc-induced molecular program accurately classifies our cohort of patients with advanced prostate cancer. Finally, we revealed the potential for enhancer of zeste homolog 2 (EZH2) inhibition to reverse the N-Myc-induced suppression of epithelial lineage genes. Altogether, our data provide insights into how N-Myc regulates lineage plasticity and epigenetic reprogramming associated with lineage specification. The N-Myc signature we defined could also help predict the evolution of prostate cancer and thus better guide the choice of future therapeutic strategies.

Published
2019
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23. Supplementary Figure S7 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression

Author

Geng, Chuandong, primary, Zhang, Man-Chao, primary, Manyam, Ganiraju C., primary, Vykoukal, Jody V., primary, Fahrmann, Johannes F., primary, Peng, Shan, primary, Wu, Cheng, primary, Park, Sanghee, primary, Kondraganti, Shakuntala, primary, Wang, Daoqi, primary, Robinson, Brian D., primary, Loda, Massimo, primary, Barbieri, Christopher E., primary, Yap, Timothy A., primary, Corn, Paul G., primary, Hanash, Samir, primary, Broom, Bradley M., primary, Pilié, Patrick G., primary, and Thompson, Timothy C., primary

Published
2023
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24. Supplementary Table S11 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression

Author

Geng, Chuandong, primary, Zhang, Man-Chao, primary, Manyam, Ganiraju C., primary, Vykoukal, Jody V., primary, Fahrmann, Johannes F., primary, Peng, Shan, primary, Wu, Cheng, primary, Park, Sanghee, primary, Kondraganti, Shakuntala, primary, Wang, Daoqi, primary, Robinson, Brian D., primary, Loda, Massimo, primary, Barbieri, Christopher E., primary, Yap, Timothy A., primary, Corn, Paul G., primary, Hanash, Samir, primary, Broom, Bradley M., primary, Pilié, Patrick G., primary, and Thompson, Timothy C., primary

Published
2023
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25. Supplementary Methods S1 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression

Author

Geng, Chuandong, primary, Zhang, Man-Chao, primary, Manyam, Ganiraju C., primary, Vykoukal, Jody V., primary, Fahrmann, Johannes F., primary, Peng, Shan, primary, Wu, Cheng, primary, Park, Sanghee, primary, Kondraganti, Shakuntala, primary, Wang, Daoqi, primary, Robinson, Brian D., primary, Loda, Massimo, primary, Barbieri, Christopher E., primary, Yap, Timothy A., primary, Corn, Paul G., primary, Hanash, Samir, primary, Broom, Bradley M., primary, Pilié, Patrick G., primary, and Thompson, Timothy C., primary

Published
2023
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26. Data from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression

Author

Geng, Chuandong, primary, Zhang, Man-Chao, primary, Manyam, Ganiraju C., primary, Vykoukal, Jody V., primary, Fahrmann, Johannes F., primary, Peng, Shan, primary, Wu, Cheng, primary, Park, Sanghee, primary, Kondraganti, Shakuntala, primary, Wang, Daoqi, primary, Robinson, Brian D., primary, Loda, Massimo, primary, Barbieri, Christopher E., primary, Yap, Timothy A., primary, Corn, Paul G., primary, Hanash, Samir, primary, Broom, Bradley M., primary, Pilié, Patrick G., primary, and Thompson, Timothy C., primary

Published
2023
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33. The long tail of oncogenic drivers in prostate cancer

Author

Armenia, Joshua, Wankowicz, Stephanie A. M., Liu, David, Gao, Jianjiong, Kundra, Ritika, Reznik, Ed, Chatila, Walid K., Chakravarty, Debyani, Han, G. Celine, Coleman, Ilsa, Montgomery, Bruce, Pritchard, Colin, Morrissey, Colm, Barbieri, Christopher E., Beltran, Himisha, Sboner, Andrea, Zafeiriou, Zafeiris, Miranda, Susana, Bielski, Craig M., Penson, Alexander V., Tolonen, Charlotte, Huang, Franklin W., Robinson, Dan, Wu, Yi Mi, Lonigro, Robert, Garraway, Levi A., Demichelis, Francesca, Kantoff, Philip W., Taplin, Mary-Ellen, Abida, Wassim, Taylor, Barry S., Scher, Howard I., Nelson, Peter S., de Bono, Johann S., Rubin, Mark A., Sawyers, Charles L., Chinnaiyan, Arul M., PCF/SU2C International Prostate Cancer Dream Team, Schultz, Nikolaus, and Van Allen, Eliezer M.

Published
2018
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34. SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression

Author

Geng, Chuandong, primary, Zhang, Man-Chao, additional, Manyam, Ganiraju C., additional, Vykoukal, Jody V., additional, Fahrmann, Johannes F., additional, Peng, Shan, additional, Wu, Cheng, additional, Park, Sanghee, additional, Kondraganti, Shakuntala, additional, Wang, Daoqi, additional, Robinson, Brian D., additional, Loda, Massimo, additional, Barbieri, Christopher E., additional, Yap, Timothy A., additional, Corn, Paul G., additional, Hanash, Samir, additional, Broom, Bradley M., additional, Pilié, Patrick G., additional, and Thompson, Timothy C., additional

Published
2023
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36. Tumor subtype defines distinct pathways of molecular and clinical progression in primary prostate cancer

Author

Liu, Deli, Augello, Michael A., Grbesa, Ivana, Prandi, Davide, Liu, Yang, Shoag, Jonathan E., Karnes, R. Jeffrey, Trock, Bruce J., Klein, Eric A., Den, Robert B., Demichelis, Francesca, Davicioni, Elai, Sboner, Andrea, and Barbieri, Christopher E.

Subjects
Identification and classification, Development and progression, Genetic aspects, Prostate cancer -- Development and progression -- Genetic aspects -- Identification and classification
Abstract

Introduction Prostate cancer (PCa) is a clinically and molecularly heterogeneous disease (1-7). Emerging next-generation DNA and RNA sequencing (RNA-seq) data point toward different molecular subclasses of PCa (3, 4, 8, [...], BACKGROUND. Molecular characterization of prostate cancer (PCa) has revealed distinct subclasses based on underlying genomic alterations occurring early in the natural history of the disease. However, how these early alterations influence subsequent molecular events and the course of the disease over its long natural history remains unclear. METHODS. We explored the molecular and clinical progression of different genomic subtypes of PCa using distinct tumor lineage models based on human genomic and transcriptomic data. We developed transcriptional classifiers, and defined "early" and "late" categories of molecular subclasses from 8,158 PCa patients. Molecular subclasses were correlated with clinical outcomes and pathologic characteristics using Kaplan-Meier and logistic regression analyses. RESULTS. We identified PTEN and CHD1 alterations as subtype-specific late progression events specifically in ERG- overexpressing (ERG+) and SPOP-mutant tumors, respectively, and 2 distinct progression models consisting of ERG/PTEN (normal to ERG+ to PTEN-deleted) and SPOP/CHD1 (normal to SPOP-mutated to CHDI- deleted) with shared early tumorigenesis but distinct pathways toward progression. We found that within ERG+ and SPOP-mutant subtypes, late events were associated with worse prognosis. Importantly, the clinical and pathologic features associated with distinct late events at radical prostatectomy were strikingly different; PTEN deletions were associated with increased locoregional stage, while CHD1 deletions were only associated with increased grade, despite equivalent metastatic potential. CONCLUSION. These findings suggest a paradigm in which specific subtypes of PCa follow distinct pathways of progression, at both the molecular and clinical levels. Therefore, the interpretation of common clinical parameters such as locoregional tumor stage may be influenced by the underlying tumor lineage, and potentially influence management decisions. FUNDING. Prostate Cancer Foundation, National Cancer Institute, Urology Care Foundation, Damon Runyon Cancer Research Foundation, US Department of Defense, and the AIRC Foundation.

Published
2021
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37. SPOP mutation drives prostate neoplasia without stabilizing oncogenic transcription factor ERG

Author

Shoag, Jonathan, Liu, Deli, Blattner, Mirjam, Sboner, Andrea, Park, Kyung, Deonarine, Lesa, Robinson, Brian D., Mosquera, Juan Miguel, Chen, Yu, Rubin, Mark A., and Barbieri, Christopher E.

Subjects
Care and treatment, Research, Genetic aspects, Mutation -- Research, Adenocarcinoma -- Care and treatment, Prostate cancer -- Genetic aspects -- Care and treatment
Abstract

Introduction Over the past decade, there has been remarkable progress in the molecular classification of prostate cancer, with the delineation of multiple distinct subclasses defined by recurrent genomic aberrations. Recurrent [...], Nearly 50% of prostate cancers harbor gene fusions that lead to overexpression of the transcription factor ERG, while a mutually exclusive 10% of prostate cancers harbor recurrent mutations in the gene encoding the E3 ubiquitin ligase SPOP. Recent reports suggest that SPOP acts as a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic effector of SPOP mutation. Here, we used human prostate cancer samples and showed that the vast majority of human SPOP-mutant cancers do not express ERG. Comparison of SPOP-mutant and ERG-fusion organoid models showed evidence of divergent, rather than common, transcriptional programs. Furthermore, expression of prostate cancer-associated SPOP mutations in genetically engineered mouse models of SPOP-mutant prostate cancer did not result in the expression of ERG protein in histologically normal prostate glands, high-grade prostatic intraepithelial neoplasia, invasive adenocarcinoma, or prostate organoids. In summary, we found no evidence that ERG is an effector of SPOP mutation in human prostate cancer or mouse models.

Published
2018
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38. MP17-18 PROSTATE CANCER GENETIC ALTERATIONS IN HISPANIC MEN

Author

Arenas-Gallo, Camilo, primary, Rhodes, Stephen, additional, Garcia, Jorge A., additional, Posada, Lina, additional, Weinstein, Ilon, additional, Prunty, Megan, additional, Lewicki, Patrick, additional, Brant, Aaron, additional, Basourakos, Spyridon P., additional, Barbieri, Christopher E., additional, Schumacher, Fredrick R., additional, and Shoag, Jonathan E., additional

Published
2023
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39. Distinct mesenchymal cell states mediate prostate cancer progression

Author

Pakula, Hubert, primary, Omar, Mohamed, additional, Carelli, Ryan, additional, Pederzoli, Filippo, additional, Fanelli, Giuseppe Nicolo, additional, Pannellini, Tania, additional, Van Emmenis, Lucie, additional, Rodrigues, Silvia, additional, Fidalgo-Ribeiro, Caroline, additional, Nuzzo, Pier V., additional, Brady, Nicholas J., additional, Jere, Madhavi, additional, Unkenholz, Caitlin, additional, Alexanderani, Mohammad K., additional, Khani, Francesca, additional, de Almeida, Francisca Nunes, additional, Abate-Shen, Cory, additional, Greenblatt, Matthew B., additional, Rickman, David S., additional, Barbieri, Christopher E., additional, Robinson, Brian D., additional, Marchionni, Luigi, additional, and Loda, Massimo, additional

Published
2023
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40. The Molecular Taxonomy of Primary Prostate Cancer

Author

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., Borges dos Reis, Rodolfo, 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 S.N., 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, Hayes, D. Neil, Heiman, David I., Hess, Julian, Hoadley, Katherine A., Holbrook, Andrea H., Holt, Robert A., Holway, Antonia, Hovens, Christopher M., Hoyle, Alan P., Huang, Mei, Hutter, Carolyn M., Ittmann, Michael, Iype, Lisa, Jefferys, Stuart R., Jones, Corbin D., Jones, Steven J.M., Juhl, Hartmut, Kahles, Andre, Kane, Christopher J., Kasaian, Katayoon, Kerger, Michael, Khurana, Ekta, Kim, Jaegil, Klein, Robert J., Kucherlapati, Raju, Lacombe, Louis, Ladanyi, Marc, Lai, Phillip H., Laird, Peter W., Lander, Eric S., Latour, Mathieu, Lawrence, Michael S., Lau, Kevin, LeBien, Tucker, Lee, Darlene, Lee, Semin, Lehmann, Kjong-Van, Leraas, Kristen M., Leshchiner, Ignaty, Leung, Robert, Libertino, John A., Lichtenberg, Tara M., Lin, Pei, Linehan, W. Marston, Ling, Shiyun, Lippman, Scott M., Liu, Jia, Liu, Wenbin, Lochovsky, Lucas, Loda, Massimo, Logothetis, Christopher, Lolla, Laxmi, Longacre, Teri, Lu, Yiling, Luo, Jianhua, Ma, Yussanne, Mahadeshwar, Harshad S., Mallery, David, Mariamidze, Armaz, Marra, Marco A., Mayo, Michael, McCall, Shannon, McKercher, Ginette, Meng, Shaowu, Mes-Masson, Anne-Marie, Merino, Maria J., Meyerson, Matthew, Mieczkowski, Piotr A., Mills, Gordon B., Shaw, Kenna R. Mills, Minner, Sarah, Moinzadeh, Alireza, Moore, Richard A., Morris, Scott, Morrison, Carl, Mose, Lisle E., Mungall, Andrew J., Murray, Bradley A., Myers, Jerome B., Naresh, Rashi, Nelson, Joel, Nelson, Mark A., Nelson, Peter S., Newton, Yulia, Noble, Michael S., Noushmehr, Houtan, Nykter, Matti, Pantazi, Angeliki, Parfenov, Michael, Park, Peter J., Parker, Joel S., Paulauskis, Joseph, Penny, Robert, Perou, Charles M., Piché, Alain, Pihl, Todd, Pinto, Peter A., Prandi, Davide, Protopopov, Alexei, Ramirez, Nilsa C., Rao, Arvind, Rathmell, W. Kimryn, Rätsch, Gunnar, Ren, Xiaojia, Reuter, Victor E., Reynolds, Sheila M., Rhie, Suhn K., Rieger-Christ, Kimberly, Roach, Jeffrey, Robertson, A. Gordon, Robinson, Brian, Rubin, Mark A., Saad, Fred, Sadeghi, Sara, Saksena, Gordon, Saller, Charles, Salner, Andrew, Sanchez-Vega, Francisco, Sander, Chris, Sandusky, George, Sauter, Guido, Sboner, Andrea, Scardino, Peter T., Scarlata, Eleonora, Schein, Jacqueline E., Schlomm, Thorsten, Schmidt, Laura S., Schultz, Nikolaus, Schumacher, Steven E., Seidman, Jonathan, Neder, Luciano, Seth, Sahil, Sharp, Alexis, Shelton, Candace, Shelton, Troy, Shen, Hui, Shen, Ronglai, Sherman, Mark, Sheth, Margi, Shi, Yan, Shih, Juliann, Shmulevich, Ilya, Simko, Jeffry, Simon, Ronald, Simons, Janae V., Sipahimalani, Payal, Skelly, Tara, Sofia, Heidi J., Soloway, Matthew G., Song, Xingzhi, Sorcini, Andrea, Sougnez, Carrie, Stepa, Serghei, Stewart, Chip, Stewart, John, Stuart, Joshua M., Sullivan, Travis B., Sun, Charlie, Sun, Huandong, Tam, Angela, Tan, Donghui, Tang, Jiabin, Tarnuzzer, Roy, Tarvin, Katherine, Taylor, Barry S., Teebagy, Patrick, Tenggara, Imelda, Têtu, Bernard, Tewari, Ashutosh, Thiessen, Nina, Thompson, Timothy, Thorne, Leigh B., Tirapelli, Daniela P., Tomlins, Scott A., Trevisan, Felipe Amstalden, Troncoso, Patricia, True, Lawrence D., Tsourlakis, Maria Christina, Tyekucheva, Svitlana, Van Allen, Eliezer, Van Den Berg, David J., Veluvolu, Umadevi, Verhaak, Roel, Vocke, Cathy D., Voet, Doug, Wan, Yunhu, Wang, Qingguo, Wang, Wenyi, Wang, Zhining, Weinhold, Nils, Weinstein, John N., Weisenberger, Daniel J., Wilkerson, Matthew D., Wise, Lisa, Witte, John, Wu, Chia-Chin, Wu, Junyuan, Wu, Ye, Xu, Andrew W., Yadav, Shalini S., Yang, Liming, Yang, Lixing, Yau, Christina, Ye, Huihui, Yena, Peggy, Zeng, Thomas, Zenklusen, Jean C., Zhang, Hailei, Zhang, Jianhua, Zhang, Jiashan, Zhang, Wei, Zhong, Yi, Zhu, Kelsey, and Zmuda, Erik

Published
2015
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41. Prostate cancer-associated SPOP mutations confer resistance to BET inhibitors through stabilization of BRD4

Author

Dai, Xiangpeng, Gan, Wenjian, Li, Xiaoning, Wang, Shangqian, Zhang, Wei, Huang, Ling, Liu, Shengwu, Zhong, Qing, Guo, Jianping, Zhang, Jinfang, Chen, Ting, Shimizu, Kouhei, Beca, Francisco, Blattner, Mirjam, Vasudevan, Divya, Buckley, Dennis L, Qi, Jun, Buser, Lorenz, Liu, Pengda, Inuzuka, Hiroyuki, Beck, Andrew H, Wang, Liewei, Wild, Peter J, Garraway, Levi A, Rubin, Mark A, Barbieri, Christopher E, Wong, Kwok-Kin, Muthuswamy, Senthil K, Huang, Jiaoti, Chen, Yu, Bradner, James E, and Wei, Wenyi

Subjects
Drug therapy, Physiological aspects, Genetic aspects, Research, Gene mutation -- Physiological aspects -- Research, Drug resistance -- Genetic aspects -- Research, Prostate cancer -- Genetic aspects -- Drug therapy -- Research
Abstract

Author(s): Xiangpeng Dai [1]; Wenjian Gan [1]; Xiaoning Li [1, 2]; Shangqian Wang [3]; Wei Zhang [4, 5]; Ling Huang [6]; Shengwu Liu [7, 8]; Qing Zhong [9]; Jianping Guo [...]

Published
2017
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45. Supplementary Figure 2 from SPOP-Mutated/CHD1-Deleted Lethal Prostate Cancer and Abiraterone Sensitivity

Author

Boysen, Gunther, primary, Rodrigues, Daniel N., primary, Rescigno, Pasquale, primary, Seed, George, primary, Dolling, David, primary, Riisnaes, Ruth, primary, Crespo, Mateus, primary, Zafeiriou, Zafeiris, primary, Sumanasuriya, Semini, primary, Bianchini, Diletta, primary, Hunt, Joanne, primary, Moloney, Deirdre, primary, Perez-Lopez, Raquel, primary, Tunariu, Nina, primary, Miranda, Susana, primary, Figueiredo, Inês, primary, Ferreira, Ana, primary, Christova, Rossitza, primary, Gil, Veronica, primary, Aziz, Sara, primary, Bertan, Claudia, primary, de Oliveira, Flavia M., primary, Atkin, Mark, primary, Clarke, Matthew, primary, Goodall, Jane, primary, Sharp, Adam, primary, MacDonald, Theresa, primary, Rubin, Mark A., primary, Yuan, Wei, primary, Barbieri, Christopher E., primary, Carreira, Suzanne, primary, Mateo, Joaquin, primary, and de Bono, Johann S., primary

Published
2023
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46. Supplemental Table 1 from Vasectomy and Risk of Prostate Cancer in a Screening Trial

Author

Shoag, Jonathan, primary, Savenkov, Oleksander, primary, Christos, Paul J., primary, Mittal, Sameer, primary, Halpern, Joshua A., primary, Askin, Gulce, primary, Shoag, Daniel, primary, Golan, Ron, primary, Lee, Daniel J., primary, O'Malley, Padraic, primary, Najari, Bobby, primary, Eisner, Brian, primary, Hu, Jim C., primary, Scherr, Douglas, primary, Schlegel, Peter, primary, and Barbieri, Christopher E., primary

Published
2023
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47. Data Supplement from Evidence for Molecular Differences in Prostate Cancer between African American and Caucasian Men

Author

Khani, Francesca, primary, Mosquera, Juan Miguel, primary, Park, Kyung, primary, Blattner, Mirjam, primary, O'Reilly, Catherine, primary, MacDonald, Theresa Y., primary, Chen, Zhengming, primary, Srivastava, Abhishek, primary, Tewari, Ashutosh K., primary, Barbieri, Christopher E., primary, Rubin, Mark A., primary, and Robinson, Brian D., primary

Published
2023
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48. Supplementary Figure 3 from SPOP-Mutated/CHD1-Deleted Lethal Prostate Cancer and Abiraterone Sensitivity

Author

Boysen, Gunther, primary, Rodrigues, Daniel N., primary, Rescigno, Pasquale, primary, Seed, George, primary, Dolling, David, primary, Riisnaes, Ruth, primary, Crespo, Mateus, primary, Zafeiriou, Zafeiris, primary, Sumanasuriya, Semini, primary, Bianchini, Diletta, primary, Hunt, Joanne, primary, Moloney, Deirdre, primary, Perez-Lopez, Raquel, primary, Tunariu, Nina, primary, Miranda, Susana, primary, Figueiredo, Inês, primary, Ferreira, Ana, primary, Christova, Rossitza, primary, Gil, Veronica, primary, Aziz, Sara, primary, Bertan, Claudia, primary, de Oliveira, Flavia M., primary, Atkin, Mark, primary, Clarke, Matthew, primary, Goodall, Jane, primary, Sharp, Adam, primary, MacDonald, Theresa, primary, Rubin, Mark A., primary, Yuan, Wei, primary, Barbieri, Christopher E., primary, Carreira, Suzanne, primary, Mateo, Joaquin, primary, and de Bono, Johann S., primary

Published
2023
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49. Supplementary Table 1 from SPOP-Mutated/CHD1-Deleted Lethal Prostate Cancer and Abiraterone Sensitivity

Author

Boysen, Gunther, primary, Rodrigues, Daniel N., primary, Rescigno, Pasquale, primary, Seed, George, primary, Dolling, David, primary, Riisnaes, Ruth, primary, Crespo, Mateus, primary, Zafeiriou, Zafeiris, primary, Sumanasuriya, Semini, primary, Bianchini, Diletta, primary, Hunt, Joanne, primary, Moloney, Deirdre, primary, Perez-Lopez, Raquel, primary, Tunariu, Nina, primary, Miranda, Susana, primary, Figueiredo, Inês, primary, Ferreira, Ana, primary, Christova, Rossitza, primary, Gil, Veronica, primary, Aziz, Sara, primary, Bertan, Claudia, primary, de Oliveira, Flavia M., primary, Atkin, Mark, primary, Clarke, Matthew, primary, Goodall, Jane, primary, Sharp, Adam, primary, MacDonald, Theresa, primary, Rubin, Mark A., primary, Yuan, Wei, primary, Barbieri, Christopher E., primary, Carreira, Suzanne, primary, Mateo, Joaquin, primary, and de Bono, Johann S., primary

Published
2023
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50. Supplementary Figure 1 from SPOP-Mutated/CHD1-Deleted Lethal Prostate Cancer and Abiraterone Sensitivity

Author

Boysen, Gunther, primary, Rodrigues, Daniel N., primary, Rescigno, Pasquale, primary, Seed, George, primary, Dolling, David, primary, Riisnaes, Ruth, primary, Crespo, Mateus, primary, Zafeiriou, Zafeiris, primary, Sumanasuriya, Semini, primary, Bianchini, Diletta, primary, Hunt, Joanne, primary, Moloney, Deirdre, primary, Perez-Lopez, Raquel, primary, Tunariu, Nina, primary, Miranda, Susana, primary, Figueiredo, Inês, primary, Ferreira, Ana, primary, Christova, Rossitza, primary, Gil, Veronica, primary, Aziz, Sara, primary, Bertan, Claudia, primary, de Oliveira, Flavia M., primary, Atkin, Mark, primary, Clarke, Matthew, primary, Goodall, Jane, primary, Sharp, Adam, primary, MacDonald, Theresa, primary, Rubin, Mark A., primary, Yuan, Wei, primary, Barbieri, Christopher E., primary, Carreira, Suzanne, primary, Mateo, Joaquin, primary, and de Bono, Johann S., primary

Published
2023
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