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  • N-acetyl D-galactosamine receptor Luo Dehm Raj Luo Attard Ba

    2023-11-20

    Luo, Dehm, Raj. Luo, Attard, Balk, Bevan, Burnstein, Cato, Cherkasov, De Bono, Dong, Gao, Gleave, Heemers, Kanayama, Kittler, Lang, Lee, Logothetis, Matusik, Plymate, Sawyers, Selth, Soule, Tilley, Weigel, Zoubeidi, Dehm, Raj. Luo, Attard, Balk, Bevan, Burnstein, Cato, Cherkasov, De Bono, Dong, Gao, Gleave, Heemers, Kanayama, Kittler, Lang, Lee, Logothetis, Matusik, Plymate, Sawyers, Selth, Soule, Tilley, Weigel, Zoubeidi, Dehm, Raj. Luo, Dehm, Raj. Luo, Attard, Balk, Bevan, Burnstein, Cato, Cherkasov, De Bono, Dong, Gao, Gleave, Heemers, Kanayama, Kittler, Lang, Lee, Logothetis, Matusik, Plymate, Sawyers, Selth, Soule, Tilley, Weigel, Zoubeidi, Dehm, Raj. None. Luo, Dehm, Raj. Luo, Dehm, Raj. None. None. Jun Luo certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject N-acetyl D-galactosamine receptor or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jun Luo has served as a paid consultant/advisor for Sun Pharma, Janssen, and Sanofi; has received research funding to his institution from Orion, Astellas, Sanofi, and Gilead; and is a coinventor of a technology that has been licensed to A&G, Tokai, and Qiagen. Gerhardt Attard received honoraria, speaker fees, and/or research support from and/or has conducted clinical trials for Astellas, Pfizer, Janssen, Sanofi, ESSA, and Arno that have an interest in targeting the androgen receptor in prostate cancer; and is included in the Institute of Cancer Research rewards to inventors list for abiraterone. Laura Cato is an employee at Sanofi-Genzyme. Johann S. De Bono served on advisory boards for multiple pharmaceutical and biotech partners including AstraZeneca, Astellas, Daiichi Sankyo, Genentech, Genmab, GSK, Merck Serono, MSD, Pfizer Oncology, Sanofi-Aventis, and Taiho; and is an employee of the Institute of Cancer Research, a not-for-profit research organization, which has a commercial interest in abiraterone acetate and PARP inhibitors for DNA repair defective cancers. Allen C. Gao has stock and other ownership interests in Pandomedx, Inc. Joshua M. Lang has Salus Discovery and LLC-ownership interest; and is a Sanofi consultant. Richard J. Lee is on the advisory board of Janssen. Christopher J. Logothetis is a coinventor of enzalutamide and entitled to royalties from the University of California. Scott M. Dehm has served as a paid consultant/advisor for Medivation/Astellas and Janssen Research and Development, LLC; and has received research funding from Janssen Research and Development, LLC. Ganesh V. Raj is the founder of C-diagnostics, GaudiumRx and EtiraRx, has received grants from Bayer and Janssen, and serves as a consultant/speaker for Janssen, Medivation/Pfizer, Astellas, Bayer, and Sanofi. Other authors have no disclosure relevant to the subject matter. None. The authors would like to thank Astellas Pharma, Sun Pharma, Janssen Oncology, and Sanofi Genzyme for their unrestricted financial sponsorship of the MARS2 meeting. Introduction As prostate cancer is an androgen-dependent disease, the androgen receptor (AR) is the primary molecular target for systemic prostate cancer therapy. Despite initial robust responses to first-line androgen deprivation therapies (ADTs), nearly all patients with advanced prostate cancer progress to lethal castration-resistant prostate cancer (CRPC). Importantly, in CRPC, the AR continues to be the primary molecular driver, as evidenced by efficacy of novel hormonal therapies, abiraterone and enzalutamide, in CRPC patients [1], [2], [3], [4]. While effective, therapies targeting AR are not curative, due to intrinsic and acquired resistance to first-line ADTs and novel hormonal therapies. Molecular mechanisms of resistance are largely driven by AR aberrations including AR protein overexpression, AR gene amplification, AR gene mutations, and AR variants (AR-Vs) [5].