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2. Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Author

Gusev, A, Shi, H, Kichaev, G, Pomerantz, M, Li, F, Long, HW, Ingles, SA, Kittles, RA, Strom, SS, Rybicki, BA, Nemesure, B, Isaacs, WB, Zheng, W, Pettaway, CA, Yeboah, ED, Tettey, Y, Biritwum, RB, Adjei, AA, Tay, E, Truelove, A, Niwa, S, Chokkalingam, AP, John, EM, Murphy, AB, Signorello, LB, Carpten, J, Leske, MC, Wu, S-Y, Hennis, AJM, Neslund-Dudas, C, Hsing, AW, Chu, L, Goodman, PJ, Klein, EA, Witte, JS, Casey, G, Kaggwa, S, Cook, MB, Stram, DO, Blot, WJ, Eeles, RA, Easton, D, Kote-Jarai, Z, Al Olama, AA, Benlloch, S, Muir, K, Giles, GG, Southey, MC, Fitzgerald, LM, Gronberg, H, Wiklund, F, Aly, M, Henderson, BE, Schleutker, J, Wahlfors, T, Tammela, TLJ, Nordestgaard, BG, Key, TJ, Travis, RC, Neal, DE, Donovan, JL, Hamdy, FC, Pharoah, P, Pashayan, N, Khaw, K-T, Stanford, JL, Thibodeau, SN, McDonnell, SK, Schaid, DJ, Maier, C, Vogel, W, Luedeke, M, Herkommer, K, Kibel, AS, Cybulski, C, Wokolorczyk, D, Kluzniak, W, Cannon-Albright, L, Teerlink, C, Brenner, H, Dieffenbach, AK, Arndt, V, Park, JY, Sellers, TA, Lin, H-Y, Slavov, C, Kaneva, R, Mitev, V, Batra, J, Spurdle, A, Clements, JA, Teixeira, MR, Pandha, HS, Michael, A, Paulo, P, Maia, S, Kierzek, A, Conti, DV, Albanes, D, Berg, C, Berndt, SI, Campa, D, Crawford, ED, Diver, WR, Gapstur, SM, Gaziano, JM, Giovannucci, E, Hoover, R, Hunter, DJ, Johansson, M, Kraft, P, Le Marchand, L, Lindstrom, S, Navarro, C, Overvad, K, Riboli, E, Siddiq, A, Stevens, VL, Trichopoulos, D, Vineis, P, Yeager, M, Trynka, G, Raychaudhuri, S, Schumacher, FR, Price, AL, Freedman, ML, Haiman, CA, Pasaniuc, B, Cook, M, Guy, M, Govindasami, K, Leongamornlert, D, Sawyer, EJ, Wilkinson, R, Saunders, EJ, Tymrakiewicz, M, Dadaev, T, Morgan, A, Fischer, C, Hazel, S, Livni, N, Lophatananon, A, Pedersen, J, Hopper, JL, Adolfson, J, Stattin, P, Johansson, J-E, Cavalli-Bjoerkman, C, Karlsson, A, Broms, M, Auvinen, A, Kujala, P, Maeaettaenen, L, Murtola, T, Taari, K, Weischer, M, Nielsen, SF, Klarskov, P, Roder, A, Iversen, P, Wallinder, H, Tillmans, L, Riska, S, Wang, L, Rinckleb, A, Lubiski, J, Stegmaier, C, Pow-Sang, J, Park, H, Radlein, S, Rincon, M, Haley, J, Zachariah, B, Kachakova, D, Popov, E, Mitkova, A, Vlahova, A, Dikov, T, Christova, S, Heathcote, P, Wood, G, Malone, G, Saunders, K, Eckert, A, Yeadon, T, Kerr, K, Collins, A, Turner, M, Srinivasan, S, Kedda, M-A, Alexander, K, Omara, T, Wu, H, Henrique, R, Pinto, P, Santos, J, Barros-Silva, J, Pharoah, Paul [0000-0001-8494-732X], Trynka, Gosia [0000-0002-6955-9529], Apollo - University of Cambridge Repository, Clinicum, Department of Surgery, Urologian yksikkö, and University of Helsinki

Subjects
0301 basic medicine, Male, Genetics and Molecular Biology (all), Linkage disequilibrium, Inheritance Patterns, COMMON DISEASES, General Physics and Astronomy, Genome-wide association study, urologic and male genital diseases, Biochemistry, Linkage Disequilibrium, Epigenesis, Genetic, Histones, Prostate cancer, Genotype, ELEMENTS, genetics, SNPS, ENCODE, RISK, PITFALLS, Genetics, African Americans, Multidisciplinary, Tumor, biological sciences, Chemistry (all), Acetylation, Single Nucleotide, 3. Good health, Centre for Surgical Research, SUSCEPTIBILITY LOCI, Science, 3122 Cancers, European Continental Ancestry Group, Single-nucleotide polymorphism, Biology, Polymorphism, Single Nucleotide, PRACTICAL consortium, General Biochemistry, Genetics and Molecular Biology, White People, Article, Cell Line, RC0254, 03 medical and health sciences, Physics and Astronomy (all), Atlases as Topic, Genetic, Cell Line, Tumor, MD Multidisciplinary, medicine, SNP, Humans, cancer, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Polymorphism, Genetic association, Cancer och onkologi, COMPLEX TRAITS, Prostatic Neoplasms, General Chemistry, Heritability, ta3122, 3126 Surgery, anesthesiology, intensive care, radiology, medicine.disease, Black or African American, ENHANCERS, 030104 developmental biology, Genetic Loci, Genome-Wide Association Study, Biochemistry, Genetics and Molecular Biology (all), Cancer and Oncology, 3111 Biomedicine, Epigenesis
Abstract

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa., Over one hundred loci have been identified to be associated with the familial risk of prostate cancer but the functional effects are poorly understood. Here the authors use single-nucleotide variant and epigentic data to show an underlying genetic architecture marked by histone modification.

Published
2016

3. Genome-Wide Meta-Analyses of Breast, Ovarian, and Prostate Cancer Association Studies Identify Multiple New Susceptibility Loci Shared by at Least Two Cancer Types

Author

Kar, S. P., Beesley, J., Amin Al Olama, A., Michailidou, K., Tyrer, J., Kote-Jarai, Z., Lawrenson, K., Lindstrom, S., Ramus, S. J., Thompson, D. J., Kibel, Adam Stuart, Dansonka-Mieszkowska, A., Michael, A., Dieffenbach, A. K., Gentry-Maharaj, A., Whittemore, A. S., Wolk, A., Monteiro, A., Peixoto, A., Kierzek, A., Cox, A., Rudolph, A., Gonzalez-Neira, A., Wu, A. H., Lindblom, A., Swerdlow, A., Ziogas, A., Ekici, A. B., Burwinkel, B., Karlan, B. Y., Nordestgaard, B. G., Blomqvist, C., Phelan, C., McLean, C., Pearce, C. L., Vachon, C., Cybulski, C., Slavov, C., Stegmaier, C., Maier, C., Ambrosone, C. B., Hogdall, C. K., Teerlink, C. C., Kang, D., Tessier, D. C., Schaid, D. J., Stram, D. O., Cramer, Daniel William, Neal, D. E., Eccles, D., Flesch-Janys, D., Edwards, D. R. V., Wokozorczyk, D., Levine, D. A., Yannoukakos, D., Sawyer, E. J., Bandera, E. V., Poole, Elizabeth M., Goode, E. L., Khusnutdinova, E., Hogdall, E., Song, F, Bruinsma, F., Heitz, F., Modugno, F., Hamdy, F. C., Wiklund, F., Giles, G. G., Olsson, H., Wildiers, H., Ulmer, H.-U., Pandha, H., Risch, H. A., Darabi, H., Salvesen, H. B., Nevanlinna, H., Gronberg, H., Brenner, H., Brauch, H., Anton-Culver, H., Song, H., Lim, H.-Y., McNeish, I., Campbell, I., Vergote, I., Gronwald, J., Lubinski, J., Stanford, J. L., Benitez, J., Doherty, J. A., Permuth, J. B., Chang-Claude, J., Donovan, J. L., Dennis, J., Schildkraut, J. M., Schleutker, J., Hopper, J. L., Kupryjanczyk, J., Park, J. Y., Figueroa, J., Clements, J. A., Knight, J. A., Peto, J., Cunningham, J. M., Pow-Sang, J., Batra, J., Czene, K., Lu, K. H., Herkommer, K., Khaw, K.-T., Matsuo, K., Muir, K., Offitt, K., Chen, K., Moysich, K. B., Aittoma ki, K., Odunsi, K., Kiemeney, L. A., Massuger, L. F. A. G., Fitzgerald, L. M., Cook, L. S., Cannon-Albright, L., Hooning, M. J., Pike, M. C., Bolla, M. K., Luedeke, M., Teixeira, M. R., Goodman, M. T., Schmidt, M. K., Riggan, M., Aly, M., Rossing, M. A., Beckmann, M. W., Moisse, M., Sanderson, M., Southey, M. C., Jones, M., Lush, M., Hildebrandt, M. A. T., Hou, M.-F., Schoemaker, M. J., Garcia-Closas, M., Bogdanova, N., Rahman, N., Le, N. D., Orr, N., Wentzensen, N., Pashayan, N., Peterlongo, P., Guenel, P., Brennan, P., Paulo, P., Webb, P. M., Broberg, P., Fasching, P. A., Devilee, P., Wang, Q., Cai, Q., Li, Q., Kaneva, R., Butzow, R., Kopperud, R. K., Schmutzler, R. K., Stephenson, R. A., MacInnis, R. J., Hoover, R. N., Winqvist, R., Ness, R., Milne, R. L., Travis, R. C., Benlloch, S., Olson, S. H., McDonnell, S. K., Tworoger, Shelley Slate, Maia, S., Berndt, S., Lee, S. C., Teo, S.-H., Thibodeau, S. N., Bojesen, S. E., Gapstur, S. M., Kjaer, S. K., Pejovic, T., Tammela, T. L. J., Do rk, T., Bru ning, T., Wahlfors, T., Key, T. J., Edwards, T. L., Menon, U., Hamann, U., Mitev, V., Kosma, V.-M., Setiawan, V. W., Kristensen, V., Arndt, V., Vogel, W., Zheng, W., Sieh, W., Blot, W. J., Kluzniak, W., Shu, X.-O., Gao, Y.-T., Schumacher, F., Freedman, M. L., Berchuck, A., Dunning, A. M., Simard, J., Haiman, C. A., Spurdle, A., Sellers, T. A., Hunter, David J., Henderson, B. E., Kraft, Peter Elias, Chanock, S. J., Couch, F. J., Hall, P., Gayther, S. A., Easton, D. F., Chenevix-Trench, G., Eeles, R., Pharoah, P. D. P., Lambrechts, D., and undefined, undefined

Subjects
breast cancer, ovarian cancer, prostate cancer, genome-wide association studies, pleiotropy
Abstract

Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P < 10(-8) seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type-specific expression quantitative trait locus and enhancer-gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P < 10(-5) in the three-cancer meta-analysis., Other Research Unit

Published
2016
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4. Combination of Nivolumab Immunotherapy with Radiation Therapy and Androgen Deprivation Therapy in the Management of Gleason Group 5 Prostate Cancer: Final Analysis of a Phase 2 Trial.

Author

Bryant, J.M., Sandoval, M.L., Putney, R., Caslini, C., Katende, E., Fink, A., Trivedi, P., Naqvi, S.M., Kim, Y., Zhang, J., Park, J., Serna, A., Lam, N.B., Pow-Sang, J., Poch, M., Li, R., Manley, B., Naghavi, A.O., Torres-Roca, J.F., and Grass, D.

Subjects
*ANDROGEN deprivation therapy, *IMMUNOMODULATORS, *AUTOIMMUNE hepatitis, *THERAPEUTICS, *RADIOTHERAPY, *PROSTATE cancer
Abstract

Survival outcomes of grade group 5 (GG5) prostate cancer (PCa) after standard of care therapy (SOC) remain poor. Evidence suggests that high-dose rate brachytherapy (HDR) and androgen deprivation therapy (ADT) can serve as immune modulators. We determine whether the addition of a checkpoint inhibitor (ICI) to SOC would synergize to improve disease control for GG5 PCa patients with or without oligometastatic disease. The single-arm phase 2 trial accrued 34 patients between September 2018 and April 2021 with a data cutoff date of December 6, 2023. Patients had to have GG5 PCa with > 30% positive cores and receive ICI plus SOC regimen (ADT, HDR, and external beam RT [EBRT]). ICI (240 mg) was given every 2 weeks for 4 doses beginning 4 weeks prior to HDR. HDR consisted of 2 implants (1150 cGy). EBRT (4500 cGy/25 fractions) followed HDR. Biopsies were taken at time of diagnosis, HDR, and 1-month post HDR. Biopsy tumor samples underwent transcriptome profiling using the Decipher® Affymetrix platform. Major pathologic response (MPR) was defined as ≤ 1 positive cores. The primary endpoint was a 2-year freedom from biochemical recurrence (FFBR; as defined by NCCN) improvement to ≥ 90% from 75% with a one-sided alpha of 0.05 (binomial exact test). A separate contemporary control cohort consisted of all GG5 patients treated with trimodality between January 2013 and April 2021 that met study enrollment criteria. Additional statistical analyses consisted of Wilcoxon tests for transcriptome data, and Kaplan Meier log-rank (KM) and Cox univariable (UVA)/multivariable (MVA) analysis for clinical data. The primary endpoint was reached with a 2-year FFBR of 90.3% (P = 0.031). Median follow up and ADT length was 38 and 18 months, respectively. The addition of nivolumab resulted in a median KM FFBR of 58.6 months (95% CI not reached) and there were no disease or treatment related deaths. Compared to contemporary controls (n = 45), nivolumab demonstrated a 21.6% improvement in 3-year FFBR (90.4% vs. 68.8%, P = 0.032). Nivolumab (P = 0.009), > 18 months of ADT (0.037), and stage IVB (P = 0.030) were significant on 3-year FFBR MVA with control cohort. A higher Decipher® Ricketts Immunosuppression biomarker was associated with both early MPR (P = 0.012) and 3-month radiographic response (P = 0.021) for patients with intermediate/high Decipher® scores. Two patients (6.3%) experienced an acute grade 3 (autoimmune hepatitis and QT prolongation) toxicity related to nivolumab. Nivolumab plus SOC for GG5 PCa demonstrated an improvement in 2-year FFBR to historic rate and was well tolerated. It was also associated with a 3-year FFBR improvement over a strictly defined external control cohort. Ricketts Immunosuppression was identified as a potential biomarker to predict favorable treatment response, contributing to the ongoing effort to optimize patient selection for ICI-based approaches. Our findings support further investigation with a larger randomized phase 2/3 study. Trial information: NCT03543189. [ABSTRACT FROM AUTHOR]

Published
2024
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5. PCN21 AFRICAN AMERICAN MEN WITH LOW RISK PROSTATE CANCER IN MIDLIFE ARE ASSOCIATED WITH HIGHER RISK OF GLEASON UPGRADING.

Author

Awasthi, S., Mahal, B., Creed, J., Williams, V., Fink, A.K., Zgibor, J., Pow-Sang, J., Park, J., Gerke, T., and Yamoah, K.

Subjects
*GLEASON grading system, *AFRICAN American men, *ANDROGEN drugs, *PROSTATE cancer
Abstract

Low risk prostate cancer (PCa) offers a favorable prognosis, which is associated with minimal risk of adverse oncologic outcomes. However, African American Men (AAM) with low risk PCa have been shown to experience disparate pathologic and survival outcomes compared to their white counterparts. [Extracted from the article]

Published
2020
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