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1. Body composition in recurrent prostate cancer and the role of steroidogenic genotype.

Author

Venkatesh, Neha, Tidwell, Rebecca S., Yao Yu, Aparicio, Ana, Zurita, Amado J., Subudhi, Sumit K., Siddiqui, Bilal A., Mukhida, Sagar S., Gregg, Justin R., Corn, Paul G., Koutroumpakis, Efstratios, McQuade, Jennifer L., Frigo, Daniel E., Pilie, Patrick G., Huff, Chad, Logothetis, Christopher J., and Hahn, Andrew W.

Abstract

Hormone therapy (HT) to treat prostate cancer is reported to cause adverse changes in body composition. Clinically, interpatient body composition changes are heterogeneous, but the biological and clinical determinants of body composition toxicity are unknown. Herein, we test the hypothesis that inherited polymorphisms in steroidogenic genes are associated with differential changes in body composition after HT. Men with biochemically recurrent prostate cancer (BCR) who received 8 months of LHRH analog (LHRHa) +/- abiraterone acetate (AAP) were eligible if they had: i) CT imaging of L3 prior to and after treatment; and ii) nucleated cells collected. Cardiometabolic co-morbidities were retrospectively extracted. Body composition was measured using an AI-based segmentation tool. Germline DNA whole exome or genome sequencing was performed. In 162 men treated with 8 months of HT, median skeletal muscle mass (SMMi) loss was 6.6% and subcutaneous adipose gain was 12.3%. Men with type 2 diabetes had higher losses of SMMi after treatment (-11.1% vs -6.3%, P = 0.003). For the 150 men with germline NGS, SRD5A2 rs523349 genotype was associated with differential loss in skeletal muscle density after HT, (-1.3% vs -7.1%, P = 0.04). In addition, the HSD3B1 rs104703 genotype was associated with decreased baseline visceral adipose tissue (63.0 cm2/m2 vs 77.9, P = 0.05). In men with BCR, HT induced notable loss of skeletal muscle and increased subcutaneous adipose tissue. An inherited polymorphism in SRD5A2 and T2DM was associated with differential skeletal muscle toxicity. These findings suggest that inherited polymorphisms may contribute to the body composition toxicity observed with HT. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Niraparib in patients with metastatic castration-resistant prostate cancer and DNA repair gene defects (GALAHAD): a multicentre, open-label, phase 2 trial

Author

Parnis, Francis, Joshua, Anthony M., Horvath, Lisa G., Steer, Christopher, Marx, Gavin, Sandhu, Shahneen, Gurney, Howard, Ferguson, Thomas, Van Bruwaene, Siska, Luyten, Daisy, Schatteman, Peter, Lumen, Nicolaas, Dirix, Luc, Goeminne, Jean-Charles, Gil, Thierry, Seront, Emmanuel, Vulsteke, Christof, Kussumoto, Celio, Franke, Fabio A., Martinelli de Oliveira, Fabricio Augusto, Pereira de Santana Gomes, Andrea Juliana, Pinczowski, Hélio, Preto, Daniel D'Almeida, Zucca, Luis Eduardo, Borges, Giuliano Santos, Murad, Andre M., Saad, Fred, Chi, Kim N., Fradet, Yves, Fleshner, Neil E., Emmenegger, Urban, Brasso, Klaus, Fizazi, Karim, Culine, Stephane, Thiery-Vuillemin, Antoine, Joly, Florence, Fléchon, Aude, Hilgers, Werner, Eymard, Jean-Christophe, Borchiellini, Delphine, Barthélémy, Philippe, Berger, Raanan, Leibowitz-Amit, Raya, Mermershtain, Wilmosh, Rouvinov, Keren, Peer, Avivit, Kovel, Svetlana, Sella, Avishay, Lolkema, Martijn P., van den Eertwegh, Alfonsus J.M., Voortman, Johannes, Aarts, Maureen J., Gietema, Jourik A., Kim, Choung-Soo, Choi, Young-Deuk, Chung, Byung-Ha, Gafanov, Rustem A., Kopyltsov, Evgeniy, Usynin, Evgeny A., Carles, Joan, Mellado, Begoña, Maroto, José Pablo, García-Donás, Jesús, Rodríguez Moreno, Juan Francisco, Durán, Ignacio, Pérez-Valderrama, Begoña, Castro, Elena, Olmos, David, Méndez-Vidal, María José, Estellés, David Lorente, Sarrió, Regina Gironés, Muñoz-Langa, José, Herranz, Urbano Anido, Puente Vázquez, Javier, Castellanos, Enrique, Hellström, Martin, Widmark, Anders, Lissbrant, Ingela Franck, Jellvert, Åsa, Külich, Cecilia, Blom, René, Ståhl, Olof, Chiang, Po-Hui, Kang, Chih-Hsiung, Ou, Yen-Chuan, Wang, Shian-Shiang, Wu, Hsi-Chin, Lu, Yu-Chuan, Attard, Gerhardt, Khoo, Vincent, Bahl, Amit, Kellati, Prasad, Parikh, Omi, Srinivasan, Rajaguru, Lester, Jason F., Staffurth, John N., Cheng, Heather H., Efstathiou, Eleni, Pilié, Patrick G., George, Daniel J., Karsh, Lawrence I., Kelly, W. Kevin, Danila, Daniel C., Sieber, Paul R., Smith, Matthew R., Heath, Elisabeth I., Vaishampayan, Ulka N., Flaig, Thomas W., Emamekhoo, Hamid, Pinski, Jacek K., Kalebasty, Arash Rezazadeh, Maly, Joseph J., Moon, Helen, Smith, Matthew R, Scher, Howard I, Lara, Primo N, Jr, Yu, Evan Y, George, Daniel J, Chi, Kim N, Danila, Daniel C, Mason, Gary E, Espina, Byron M, Zhao, Xin, Urtishak, Karen A, Francis, Peter, and Lopez-Gitlitz, Angela

Published
2022
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5. Comprehensive Molecular Characterization Identifies Distinct Genomic and Immune Hallmarks of Renal Medullary Carcinoma

Author

Msaouel, Pavlos, Malouf, Gabriel G., Su, Xiaoping, Yao, Hui, Tripathi, Durga N., Soeung, Melinda, Gao, Jianjun, Rao, Priya, Coarfa, Cristian, Creighton, Chad J., Bertocchio, Jean-Philippe, Kunnimalaiyaan, Selvi, Multani, Asha S., Blando, Jorge, He, Rong, Shapiro, Daniel D., Perelli, Luigi, Srinivasan, Sanjana, Carbone, Federica, Pilié, Patrick G., Karki, Menuka, Seervai, Riyad N.H., Vokshi, Bujamin H., Lopez-Terrada, Dolores, Cheng, Emily H., Tang, Ximing, Lu, Wei, Wistuba, Ignacio I., Thompson, Timothy C., Davidson, Irwin, Giuliani, Virginia, Schlacher, Katharina, Carugo, Alessandro, Heffernan, Timothy P., Sharma, Padmanee, Karam, Jose A., Wood, Christopher G., Walker, Cheryl L., Genovese, Giannicola, and Tannir, Nizar M.

Published
2020
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6. Ataxia-Telangiectasia Mutated (ATM) loss of function displays variant and tissue-specific differences across tumor types

Author

Pilie, Patrick G., primary, Giuliani, Virginia, additional, Wang, Wei-Lien, additional, McGrail, Daniel J., additional, Bristow, Christopher A., additional, Ngoi, Natalie Y.L., additional, Kyewalabye, Keith, additional, Wani, Khalida M., additional, Le, Hung, additional, Campbell, Erick, additional, Sánchez, Nora S., additional, Yang, Dong, additional, Gheeya, Jinesh S., additional, Goswamy, Rohit Vivek., additional, Holla, Vijaykumar, additional, Shaw, Kenna Rael., additional, Meric-Bernstam, Funda, additional, Liu, Chiu-Yi, additional, Ma, XiaoYan, additional, Feng, Ningping, additional, Machado, Annette A., additional, Bardenhagen, Jennifer P., additional, Vellano, Christopher P., additional, Marszalek, Joseph R., additional, Rajendra, Eeson, additional, Piscitello, Desiree, additional, Johnson, Timothy I., additional, Likhatcheva, Maria, additional, Elinati, Elias, additional, Majithiya, Jayesh, additional, Neves, Joana, additional, Grinkevich, Vera, additional, Ranzani, Marco, additional, Roy-Luzarraga, Marina, additional, Boursier, Marie, additional, Armstrong, Lucy, additional, Geo, Lerin, additional, Lillo, Giorgia, additional, Tse, Wai Yiu, additional, Lazar, Alexander J., additional, Kopetz, Scott E., additional, Geck Do, Mary K., additional, Lively, Sarah, additional, Johnson, Michael G., additional, Robinson, Helen M.R., additional, Smith, Graeme C.M., additional, Carroll, Christopher L., additional, Di Francesco, M. Emilia, additional, Jones, Philip, additional, Heffernan, Timothy P., additional, and Yap, Timothy A., additional

Published
2024
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7. Evaluation of the Aggressive-Variant Prostate Cancer Molecular Signature in Clinical Laboratory Improvement Amendments (CLIA) Environments

Author

Viscuse, Paul V., primary, Slack-Tidwell, Rebecca S., additional, Zhang, Miao, additional, Rohra, Prih, additional, Zhu, Keyi, additional, San Lucas, F. Anthony, additional, Konnick, Eric, additional, Pilie, Patrick G., additional, Siddiqui, Bilal, additional, Logothetis, Christopher J., additional, Corn, Paul, additional, Subudhi, Sumit K., additional, Pritchard, Colin C., additional, Soundararajan, Rama, additional, and Aparicio, Ana, additional

Published
2023
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8. Supplementary Data 1 from SETD2 Loss and ATR Inhibition Synergize to Promote cGAS Signaling and Immunotherapy Response in Renal Cell Carcinoma

Author

Liu, Xian-De, primary, Zhang, Yan-Ting, primary, McGrail, Daniel J., primary, Zhang, Xuesong, primary, Lam, Truong, primary, Hoang, Anh, primary, Hasanov, Elshad, primary, Manyam, Ganiraju, primary, Peterson, Christine B., primary, Zhu, Haifeng, primary, Kumar, Shwetha V., primary, Akbani, Rehan, primary, Pilie, Patrick G., primary, Tannir, Nizar M., primary, Peng, Guang, primary, and Jonasch, Eric, primary

Published
2023
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9. Data from SETD2 Loss and ATR Inhibition Synergize to Promote cGAS Signaling and Immunotherapy Response in Renal Cell Carcinoma

Author

Liu, Xian-De, primary, Zhang, Yan-Ting, primary, McGrail, Daniel J., primary, Zhang, Xuesong, primary, Lam, Truong, primary, Hoang, Anh, primary, Hasanov, Elshad, primary, Manyam, Ganiraju, primary, Peterson, Christine B., primary, Zhu, Haifeng, primary, Kumar, Shwetha V., primary, Akbani, Rehan, primary, Pilie, Patrick G., primary, Tannir, Nizar M., primary, Peng, Guang, primary, and Jonasch, Eric, primary

Published
2023
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11. SETD2 Loss and ATR Inhibition Synergize to Promote cGAS Signaling and Immunotherapy Response in Renal Cell Carcinoma

Author

Liu, Xian-De, primary, Zhang, Yan-Ting, additional, McGrail, Daniel J., additional, Zhang, Xuesong, additional, Lam, Truong, additional, Hoang, Anh, additional, Hasanov, Elshad, additional, Manyam, Ganiraju, additional, Peterson, Christine B., additional, Zhu, Haifeng, additional, Kumar, Shwetha V., additional, Akbani, Rehan, additional, Pilie, Patrick G., additional, Tannir, Nizar M., additional, Peng, Guang, additional, and Jonasch, Eric, additional

Published
2023
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13. Morphologically Normal-Appearing Mammary Epithelial Cells Obtained from High-Risk Women Exhibit Methylation Silencing of INK4a/ARF

Author

Bean, Gregory R, Bryson, Andrew D, Pilie, Patrick G, Goldenberg, Vanessa, Baker, Joseph C, Ibarra, Catherine, Brander, Danielle MU, Paisie, Carolyn, Case, Natalie R, Gauthier, Mona, Reynolds, Paul A, Dietze, Eric, Ostrander, Julie, Scott, Victoria, Wilke, Lee G, Yee, Lisa, Kimler, Bruce F, Fabian, Carol J, Zalles, Carola M, Broadwater, Gloria, Tlsty, Thea D, and Seewaldt, Victoria L

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Aging, Genetics, Breast Cancer, Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Adult, Aged, Breast Neoplasms, Cyclin-Dependent Kinase Inhibitor p16, DNA Methylation, Epithelial Cells, Female, Gene Silencing, Humans, Mammary Glands, Human, Middle Aged, Promoter Regions, Genetic, Risk, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

Purposep16(INK4a) has been appreciated as a key regulator of cell cycle progression and senescence. Cultured human mammary epithelial cells that lack p16(INK4a) activity have been shown to exhibit premalignant phenotypes, such as telomeric dysfunction, centrosomal dysfunction, a sustained stress response, and, most recently, a dysregulation of chromatin remodeling and DNA methylation. These data suggest that cells that lack p16(INK4a) activity would be at high risk for breast cancer development and may exhibit an increased frequency of DNA methylation events in early cancer.Experimental designTo test this hypothesis, the frequencies of INK4a/ARF promoter hypermethylation, as well as four additional selected loci, were tested in the initial random periareolar fine needle aspiration samples from 86 asymptomatic women at high risk for development of breast cancer, stratified using the Masood cytology index.ResultsINK4a/ARF promoter hypermethylation was observed throughout all early stages of intraepithelial neoplasia and, importantly, in morphologically normal-appearing mammary epithelial cells; 29 of 86 subjects showed INK4a/ARF promoter hypermethylation in at least one breast. Importantly, INK4a/ARF promoter hypermethylation was not associated with atypia, and the frequency of hypermethylation did not increase with increasing Masood cytology score. The frequency of INK4a/ARF promoter hypermethylation was associated with the combined frequency of promoter hypermethylation of retinoic acid receptor-beta2, estrogen receptor-alpha, and breast cancer-associated 1 genes (P = 0.001).ConclusionsBecause INK4a/ARF promoter hypermethylation does not increase with age but increases with the frequency of other methylation events, we predict that INK4a/ARF promoter hypermethylation may serve as a marker of global methylation dysregulation.

Published
2007

15. Abstract 3432: Ataxia-telangiectasia mutated loss of function displays variant and tissue specific differences across tumor types

Author

Pilie, Patrick G., primary, Mcgrail, Daniel, additional, Wang, Wei-Lien, additional, Ngoi, Natalie, additional, Kyewalabye, Keith, additional, Wani, Khalida, additional, Le, Hung, additional, Campbell, Erick, additional, Holla, Vijaykumar, additional, Shaw, Kenna R., additional, Meric-Bernstam, Funda, additional, Lazar, Alexander J., additional, Giuliani, Virginia, additional, Heffernan, Timothy, additional, and Yap, Timothy A., additional

Published
2023
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16. Body composition as a determinant of the therapeutic index with androgen signaling inhibition

Author

Hahn, Andrew W., Tidwell, Rebecca S., Pilie, Patrick G., Yu, Yao, Liu, Jingjing, Surasi, Devaki Shilpa, Titus, Mark, Zhang, Jianhua, Venkatesh, Neha, Panaretakis, Theocharis, Gregg, Justin R., Zurita, Amado J., Siddiqui, Bilal A., Corn, Paul G., Subudhi, Sumit K., Msaouel, Pavlos, Koutroumpakis, Efstratios, Huff, Chad D., Aparicio, Ana, McQuade, Jennifer L., Frigo, Daniel E., and Logothetis, Christopher J.

Abstract

Background: Androgen signaling is central to prostate cancer and men’s health. Prior data indicates that increasing body fat is unfavorable in the localized setting yet associated with favorable outcomes in men with metastatic disease. Understanding the biological links between adiposity and prostate cancer may optimize the therapeutic index with ASI. We hypothesized that host adiposity and androgen synthesis are linked to the efficacy and toxicity of ASI for men with metastatic castration-resistant prostate cancer (mCRPC). Methods: A post-hoc analysis was done of NCT02703623 where men with mCRPC (n= 186) were treated for 8 weeks with abiraterone acetate, prednisone, and apalutamide (AAPA), and a satisfactory response was defined as a PSA decline >50%. Body composition was measured on baseline CT scans. Germline DNA WES was performed with a focus on variants in steroidogenic genes. Adipokine levels were measured in pre-treatment plasma. Results: Germline polymorphisms in 3 genes involved in androgen synthesis (AKR1C3rs12529, CYP17A1rs6162, SRD5A2rs523349) were associated with differences in body composition at baseline on ADT alone (prior to receipt of AAPA). Elevated subcutaneous adipose tissue index (SATi, p= 0.02), visceral adipose tissue index (VATi, p= 0.03), and BMI (p= 0.04) were associated with satisfactory response to AAPA. Leptin had positive correlation with VATi (r= 0.47) and SATi (r= 0.48). Conclusion: Inherited polymorphisms in androgen synthesis correlated with differences in body composition after exposure to ADT and warrant further investigation as candidate markers for body composition toxicity. Elevated subcutaneous and visceral adiposity were associated with improved response to ASI.

Published
2024
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19. Pilot and feasibility study: prospective proteomic profiling of mammary epithelial cells from high-risk women provides evidence of activation of pro-survival pathways

Author

Ibarra-Drendall, Catherine, Troch, Michelle M., Barry, William T., Broadwater, Gloria, Petricoin, III, Emanuel F., Wulfkuhle, Julia, Liotta, Lance A., Lem, Siya, Baker, Jr., Joseph C., Ford, Anne C., Wilke, Lee G., Zalles, Carola, Kuderer, Nicole M., Hoffman, Abigail W., Shivraj, Melanie, Mehta, Priya, Williams, Jamila, Tolbert, Nora, Lee, Laurie W., Pilie, Patrick G., Yu, Dihua, and Seewaldt, Victoria L.

Published
2012
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23. Erratum to: Pilot and feasibility study: prospective proteomic profiling of mammary epithelial cells from high-risk women provides evidence of activation of pro-survival pathways

Author

Ibarra-Drendall, Catherine, Troch, Michelle M., Barry, William T., Broadwater, Gloria, Petricoin, III, Emanuel F., Wulfkuhle, Julia, Liotta, Lance A., Lem, Siya, Baker, Jr., Joseph C., Ford, Anne C., Wilke, Lee G., Zalles, Carola, Kuderer, Nicole M., Hoffman, Abigail W., Shivraj, Melanie, Mehta, Priya, Williams, Jamila, Tolbert, Nora, Lee, Laurie W., Pilie, Patrick G., Yu, Dihua, and Seewaldt, Victoria L.

Published
2012
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24. HOXB13 and other high penetrant genes for prostate cancer.

Author

Pilie, Patrick G, Giri, Veda N., Cooney, Kathleen A., Pilie, Patrick G, Giri, Veda N., and Cooney, Kathleen A.

Abstract

Cancer initiation and progression is the result of an accumulation of mutations in key tumor suppressor genes, mismatch repair genes, or oncogenes, which impact cancer cell growth, death, and differentiation. Mutations occurring in cancer tissue are termed somatic; whereas, heritable mutations that may be passed onto subsequent generations occur in germline DNA. It is these germline mutations that can lead to cancer family syndromes whereby family members carrying a deleterious germline mutation have an increased susceptibility to certain cancer phenotypes. Common features of hereditary cancer syndromes include early age-of-onset, multiple affected generations, rare tumor types, and/or multiple primary malignancies. Approximately, 5%-10% of all common cancers, including prostate cancer, have a hereditary component and are attributable to highly penetrant germline mutations.1 Across all cancer types, known cancer susceptibility syndromes number >100; however, it is important to note that mutations in high-penetrance genes explain only a fraction of heritable cancers.2 Well-known examples of hereditary cancer syndromes include Lynch (HNPCC), Cowden (PHTS), Li-Fraumeni, and Hereditary Breast and Ovarian Cancer (HBOC) syndromes, which are attributable to mutations in mismatch repair genes, PTEN, p53, and BRCA1/2, respectively.

Published
2016

25. Pilot and feasibility study: prospective proteomic profiling of mammary epithelial cells from high-risk women provides evidence of activation of pro-survival pathways

Author

Ibarra-Drendall, Catherine, primary, Troch, Michelle M., additional, Barry, William T., additional, Broadwater, Gloria, additional, Petricoin, Emanuel F., additional, Wulfkuhle, Julia, additional, Liotta, Lance A., additional, Lem, Siya, additional, Baker, Joseph C., additional, Ford, Anne C., additional, Wilke, Lee G., additional, Zalles, Carola, additional, Kuderer, Nicole M., additional, Hoffman, Abigail W., additional, Shivraj, Melanie, additional, Mehta, Priya, additional, Williams, Jamila, additional, Tolbert, Nora, additional, Lee, Laurie W., additional, Pilie, Patrick G., additional, Yu, Dihua, additional, and Seewaldt, Victoria L., additional

Published
2011
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26. Protein Microarray Analysis of Mammary Epithelial Cells from Obese and Nonobese Women at High Risk for Breast Cancer: Feasibility Data

Author

Pilie, Patrick G., primary, Ibarra-Drendall, Catherine, additional, Troch, Michelle M., additional, Broadwater, Gloria, additional, Barry, William T., additional, Petricoin, Emanuel F., additional, Wulfkuhle, Julia D., additional, Liotta, Lance A., additional, Lem, Siya, additional, Baker, Joseph C., additional, Stouder, April, additional, Ford, Anne C., additional, Wilke, Lee G., additional, Zalles, Carola M., additional, Mehta, Priya, additional, Williams, Jamila, additional, Shivraj, Melanie, additional, Su, Zuowei, additional, Geradts, Joseph, additional, Yu, Dihua, additional, and Seewaldt, Victoria L., additional

Published
2011
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28. CpG Island Tumor Suppressor Promoter Methylation in Non-BRCA-Associated Early Mammary Carcinogenesis

Author

Vasilatos, Shauna N., primary, Broadwater, Gloria, additional, Barry, William T., additional, Baker, Joseph C., additional, Lem, Siya, additional, Dietze, Eric C., additional, Bean, Gregory R., additional, Bryson, Andrew D., additional, Pilie, Patrick G., additional, Goldenberg, Vanessa, additional, Skaar, David, additional, Paisie, Carolyn, additional, Torres-Hernandez, Alejandro, additional, Grant, Tracey L., additional, Wilke, Lee G., additional, Ibarra-Drendall, Catherine, additional, Ostrander, Julie H., additional, D'Amato, Nicholas C., additional, Zalles, Carola, additional, Jirtle, Randy, additional, Weaver, Valerie M., additional, and Seewaldt, Victoria L., additional

Published
2009
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29. ESR1 Promoter Hypermethylation Does Not Predict Atypia in RPFNA nor Persistent Atypia after 12 Months Tamoxifen Chemoprevention

Author

Baker, Joseph C., primary, Ostrander, Julie H., additional, Lem, Siya, additional, Broadwater, Gloria, additional, Bean, Gregory R., additional, D'Amato, Nicholas C., additional, Goldenberg, Vanessa K., additional, Rowell, Craig, additional, Ibarra-Drendall, Catherine, additional, Grant, Tracey, additional, Pilie, Patrick G., additional, Vasilatos, Shauna N., additional, Troch, Michelle M., additional, Scott, Victoria, additional, Wilke, Lee G., additional, Paisie, Carolyn, additional, Rabiner, Sarah M., additional, Torres-Hernandez, Alejandro, additional, Zalles, Carola M., additional, and Seewaldt, Victoria L., additional

Published
2008
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