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4. Characterizing prostate cancer risk through multi-ancestry genome-wide discovery of 187 novel risk variants.

Author

Wang, Anqi, Shen, Jiayi, Rodriguez, Alex, Saunders, Edward, Chen, Fei, Janivara, Rohini, Darst, Burcu, Sheng, Xin, Xu, Yili, Chou, Alisha, Benlloch, Sara, Dadaev, Tokhir, Brook, Mark, Plym, Anna, Sahimi, Ali, Hoffman, Thomas, Takahashi, Atushi, Matsuda, Koichi, Momozawa, Yukihide, Fujita, Masashi, Laisk, Triin, Figuerêdo, Jéssica, Muir, Kenneth, Ito, Shuji, Liu, Xiaoxi, Uchio, Yuji, Kubo, Michiaki, Kamatani, Yoichiro, Lophatananon, Artitaya, Wan, Peggy, Andrews, Caroline, Lori, Adriana, Choudhury, Parichoy, Schleutker, Johanna, Tammela, Teuvo, Sipeky, Csilla, Auvinen, Anssi, Giles, Graham, Southey, Melissa, MacInnis, Robert, Cybulski, Cezary, Wokolorczyk, Dominika, Lubinski, Jan, Rentsch, Christopher, Cho, Kelly, Mcmahon, Benjamin, Neal, David, Donovan, Jenny, Hamdy, Freddie, Martin, Richard, Nordestgaard, Borge, Nielsen, Sune, Weischer, Maren, Bojesen, Stig, Røder, Andreas, Stroomberg, Hein, Batra, Jyotsna, Chambers, Suzanne, Horvath, Lisa, Clements, Judith, Tilly, Wayne, Risbridger, Gail, Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordstrom, Tobias, Pashayan, Nora, Dunning, Alison, Ghoussaini, Maya, Travis, Ruth, Key, Tim, Riboli, Elio, Park, Jong, Sellers, Thomas, Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie, Cook, Michael, Mucci, Lorelei, Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David, Penney, Kathryn, Turman, Constance, Tangen, Catherine, Goodman, Phyllis, Thompson, Ian, Hamilton, Robert, Fleshner, Neil, Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet, Ostrander, Elaine, Koutros, Stella, Beane Freeman, Laura, Stampfer, Meir, Wolk, Alicja, and Håkansson, Niclas

Subjects
Humans, Male, Black People, Genetic Predisposition to Disease, Genome-Wide Association Study, Hispanic or Latino, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Risk Factors, White People, Asian People
Abstract

The transferability and clinical value of genetic risk scores (GRSs) across populations remain limited due to an imbalance in genetic studies across ancestrally diverse populations. Here we conducted a multi-ancestry genome-wide association study of 156,319 prostate cancer cases and 788,443 controls of European, African, Asian and Hispanic men, reflecting a 57% increase in the number of non-European cases over previous prostate cancer genome-wide association studies. We identified 187 novel risk variants for prostate cancer, increasing the total number of risk variants to 451. An externally replicated multi-ancestry GRS was associated with risk that ranged from 1.8 (per standard deviation) in African ancestry men to 2.2 in European ancestry men. The GRS was associated with a greater risk of aggressive versus non-aggressive disease in men of African ancestry (P = 0.03). Our study presents novel prostate cancer susceptibility loci and a GRS with effective risk stratification across ancestry groups.

Published
2023

5. Association between Outdoor Light at Night and Prostate Cancer in the Health Professionals Follow-up Study.

Author

Iyer, Hari, Wilt, Grete, Booker, Benjamin, Nethery, Rachel, Laden, Francine, Mucci, Lorelei, Markt, Sarah, Chowdhury-Paulino, Ilkania, Hart, Jaime, and James, Peter

Subjects
Male, Humans, Lighting, Follow-Up Studies, Longitudinal Studies, Circadian Rhythm, Risk Factors, Prostatic Neoplasms
Abstract

BACKGROUND: Circadian disruption is a potential risk factor for advanced prostate cancer, and light at night (LAN) exposure may disrupt circadian rhythms. We evaluated whether outdoor LAN increases the risk of prostate cancer. METHODS: We prospectively followed 49,148 participants in the Health Professionals Follow-up Study from 1986 through 2016. We estimated baseline and cumulative time-varying outdoor LAN with ∼1 km2 resolution using data from the US Defense Meteorological Satellite Programs Operational Linescan System, which was assigned to participants geocoded addresses. Participants reside in all 50 U.S. states and reported a work or home address. We used multivariable Cox models to estimate HRs and 95% confidence intervals (CI) for the association between outdoor LAN and risk of overall (7,175 cases) and fatal (915 cases) prostate cancer adjusting for individual and contextual factors. RESULTS: There was no association between the interquartile range increase in cumulative LAN and total (HR, 1.02; 95% CI, 0.98-1.06) or fatal (HR, 1.05; 95% CI, 0.96-1.15) prostate cancer in adjusted models. However, there was a positive association between baseline LAN and total prostate cancer among non-movers (HR, 1.06; 95% CI, 1.00-1.14) including among highly screened participants (HR, 1.11; 95% CI, 1.01-1.23). CONCLUSIONS: There was a suggestive positive association between baseline outdoor LAN and total prostate cancer. Additional studies with different measures of outdoor LAN and in more diverse populations are necessary. IMPACT: To our knowledge, this is the first longitudinal cohort study exploring the relationship between outdoor LAN and prostate cancer.

Published
2023

6. Influence of Neighborhood Social and Natural Environment on Prostate Tumor Histology in a Cohort of Male Health Professionals.

Author

Iyer, Hari, Vaselkiv, Jane, Stopsack, Konrad, Roscoe, Charlotte, DeVille, Nicole, Zhang, Yiwen, Penney, Kathryn, Balk, Steven, Fiorentino, Michelangelo, Hart, Jaime, De Vivo, Immaculata, Mucci, Lorelei, Laden, Francine, Rebbeck, Timothy, and James, Peter

Subjects
atrophy, inflammation, neighborhood, prostate cancer, prostatic neoplasms, residence characteristics, socioeconomic factors, Humans, Male, Environment, Follow-Up Studies, Inflammation, Prostatic Neoplasms, Residence Characteristics, Social Class, Socioeconomic Factors
Abstract

Adverse neighborhood social and natural (green space) environments may contribute to the etiology of prostate cancer (CaP), but mechanisms are unclear. We examined associations between neighborhood environment and prostate intratumoral inflammation in 967 men diagnosed with CaP with available tissue samples from 1986-2009 in the Health Professionals Follow-up Study. Exposures were linked to work or residential addresses in 1988. We estimated indices of neighborhood socioeconomic status (nSES) and segregation (Index of Concentration at the Extremes (ICE)) using US Census tract-level data. Surrounding greenness was estimated using seasonal averaged Normalized Difference Vegetation Index (NDVI) data. Surgical tissue underwent pathological review for acute and chronic inflammation, corpora amylacea, and focal atrophic lesions. Adjusted odds ratios (aORs) for inflammation (ordinal) and focal atrophy (binary) were estimated using logistic regression. No associations were observed for acute or chronic inflammation. Each interquartile-range increase in NDVI within 1,230 m of the participants work or home address (aOR = 0.74, 95% confidence interval (CI): 0.59, 0.93), in ICE-income (aOR = 0.79, 95% CI: 0.61, 1.04), and in ICE-race/income (aOR = 0.79, 95% CI: 0.63, 0.99) was associated with lower odds of postatrophic hyperplasia. Interquartile-range increases in nSES (aOR = 0.76, 95% CI: 0.57, 1.02) and ICE-race/income (aOR = 0.73, 95% CI: 0.54, 0.99) were associated with lower odds of tumor corpora amylacea. Histopathological inflammatory features of prostate tumors may be influenced by neighborhood.

Published
2023

7. Associations between Etiologic or Prognostic Tumor Tissue Markers and Neighborhood Contextual Factors in Male Health Professionals Diagnosed with Prostate Cancer.

Author

Iyer, Hari, Kensler, Kevin, Vaselkiv, Jane, Stopsack, Konrad, Roscoe, Charlotte, Bandera, Elisa, Qin, Bo, Jang, Thomas, Lotan, Tamara, Hart, Jaime, Mucci, Lorelei, Laden, Francine, Rebbeck, Timothy, and James, Peter

Subjects
Humans, Male, Prognosis, Follow-Up Studies, Prospective Studies, Transcriptional Regulator ERG, Trypsin Inhibitor, Kazal Pancreatic, Tumor Suppressor Protein p53, Prostatic Neoplasms, Biomarkers, Tumor, Residence Characteristics
Abstract

BACKGROUND: There is growing evidence that unfavorable neighborhood contexts may influence prostate cancer progression. Whether these associations may be explained in part by differences in tumor-level somatic alterations remain unclear. METHODS: Data on tumor markers (PTEN, p53, ERG, and SPINK1) were obtained from 1,157 participants with prostate cancer in the Health Professionals Follow-up Study. Neighborhood greenness, socioeconomic status, and the income Index of Concentration at Extremes were obtained from satellite and census data and linked to participants address at diagnosis and at study enrollment. Exposures were scaled to an interquartile range and modeled as tertiles. Bivariate associations between tertiles of neighborhood factors and tumor markers were assessed in covariate adjusted logistic regression models to estimate ORs and 95% confidence intervals. RESULTS: There was no association between any of the neighborhood contextual factors and PTEN, p53, ERG, or SPINK1 in bivariate or multivariable adjusted models. Results were generally consistent when modeling exposure using exposure at diagnosis or at study enrollment. CONCLUSIONS: In this multilevel study of men with prostate cancer, we found no evidence of associations between neighborhood context and tumor tissue markers. IMPACT: Our results provide some of the first empirical data in support of the hypothesis that prostate cancer risk conferred by tumor tissue markers may arise independently of underlying neighborhood context. Prospective studies in more diverse populations are needed to confirm these findings.

Published
2023

8. Impact of individual level uncertainty of lung cancer polygenic risk score (PRS) on risk stratification

Author

Wang, Xinan, Zhang, Ziwei, Ding, Yi, Chen, Tony, Mucci, Lorelei, Albanes, Demetrios, Landi, Maria Teresa, Caporaso, Neil E., Lam, Stephen, Tardon, Adonina, Chen, Chu, Bojesen, Stig E., Johansson, Mattias, Risch, Angela, Bickeböller, Heike, Wichmann, H-Erich, Rennert, Gadi, Arnold, Susanne, Brennan, Paul, McKay, James D., Field, John K., Shete, Sanjay S., Le Marchand, Loic, Liu, Geoffrey, Andrew, Angeline S., Kiemeney, Lambertus A., Zienolddiny-Narui, Shan, Behndig, Annelie, Johansson, Mikael, Cox, Angie, Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Hung, Rayjean J., Amos, Christopher I., Lin, Xihong, and Christiani, David C.

Published
2024
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9. Transcriptomes of Prostate Cancer with TMPRSS2:ERG and Other ETS Fusions.

Author

Stopsack, Konrad H, Su, Xiaofeng A, Vaselkiv, J Bailey, Graff, Rebecca E, Ebot, Ericka M, Pettersson, Andreas, Lis, Rosina T, Fiorentino, Michelangelo, Loda, Massimo, Penney, Kathryn L, Lotan, Tamara L, and Mucci, Lorelei A

Subjects
Clinical Research, Genetics, Prostate Cancer, Human Genome, Urologic Diseases, Cancer, Aetiology, 2.1 Biological and endogenous factors, Male, Humans, Transcriptome, Oncogene Proteins, Fusion, Proto-Oncogene Proteins c-ets, Prostatic Neoplasms, Gene Expression Profiling, Transcriptional Regulator ERG, Serine Endopeptidases, Oncology and Carcinogenesis, Developmental Biology, Oncology & Carcinogenesis
Abstract

The most common somatic event in primary prostate cancer is a fusion between the androgen-related TMPRSS2 gene and the ERG oncogene. Tumors with these fusions, which occur early in carcinogenesis, have a distinctive etiology. A smaller subset of other tumors harbor fusions between TMPRSS2 and members of the ETS transcription factor family other than ERG. To assess the genomic similarity of tumors with non-ERG ETS fusions and those with fusions involving ERG, this study derived a transcriptomic signature of non-ERG ETS fusions and assessed this signature and ERG-related gene expression in 1,050 men with primary prostate cancer from three independent population-based and hospital-based studies. Although non-ERG ETS fusions involving ETV1, ETV4, ETV5, or FLI1 were individually rare, they jointly accounted for one in seven prostate tumors. Genes differentially regulated between non-ERG ETS tumors and tumors without ETS fusions showed similar differential expression when ERG tumors and tumors without ETS fusions were compared (differences explained: R2 = 69-77%), including ETS-related androgen receptor (AR) target genes. Differences appeared to result from similarities among ETS tumors rather than similarities among non-ETS tumors. Gene sets associated with ERG fusions were consistent with gene sets associated with non-ERG ETS fusions, including fatty acid and amino acid metabolism, an observation that was robust across cohorts.ImplicationsConsidering ETS fusions jointly may be useful for etiologic studies on prostate cancer, given that the transcriptome is profoundly impacted by ERG and non-ERG ETS fusions in a largely similar fashion, most notably genes regulating metabolic pathways.

Published
2023

11. Quality of life in the year after new diagnosis with advanced prostate cancer for Black and White individuals living in the US

Author

Rencsok, Emily M., Slopen, Natalie, Autio, Karen, Morgans, Alicia, McSwain, Lawrence, Barata, Pedro, Cheng, Heather H., Dreicer, Robert, Heath, Elisabeth, McKay, Rana R., Pomerantz, Mark, Rathkopf, Dana, Tagawa, Scott, Whang, Young E., Ragin, Camille, Odedina, Folakemi T., George, Daniel J., Kantoff, Philip W., Vinson, Jacob, Villanti, Paul, Haneuse, Sebastien, and Mucci, Lorelei A.

Published
2023
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12. Prostate cancer risk stratification improvement across multiple ancestries with new polygenic hazard score

Author

Huynh-Le, Minh-Phuong, Karunamuni, Roshan, Fan, Chun Chieh, Asona, Lui, Thompson, Wesley K, Martinez, Maria Elena, Eeles, Rosalind A, Kote-Jarai, Zsofia, Muir, Kenneth R, Lophatananon, Artitaya, Schleutker, Johanna, Pashayan, Nora, Batra, Jyotsna, Grönberg, Henrik, Neal, David E, Nordestgaard, Børge G, Tangen, Catherine M, MacInnis, Robert J, Wolk, Alicja, Albanes, Demetrius, Haiman, Christopher A, Travis, Ruth C, Blot, William J, Stanford, Janet L, Mucci, Lorelei A, West, Catharine ML, Nielsen, Sune F, Kibel, Adam S, Cussenot, Olivier, Berndt, Sonja I, Koutros, Stella, Sørensen, Karina Dalsgaard, Cybulski, Cezary, Grindedal, Eli Marie, Menegaux, Florence, Park, Jong Y, Ingles, Sue A, Maier, Christiane, Hamilton, Robert J, Rosenstein, Barry S, Lu, Yong-Jie, Watya, Stephen, Vega, Ana, Kogevinas, Manolis, Wiklund, Fredrik, Penney, Kathryn L, Huff, Chad D, Teixeira, Manuel R, Multigner, Luc, Leach, Robin J, Brenner, Hermann, John, Esther M, Kaneva, Radka, Logothetis, Christopher J, Neuhausen, Susan L, De Ruyck, Kim, Ost, Piet, Razack, Azad, Newcomb, Lisa F, Fowke, Jay H, Gamulin, Marija, Abraham, Aswin, Claessens, Frank, Castelao, Jose Esteban, Townsend, Paul A, Crawford, Dana C, Petrovics, Gyorgy, van Schaik, Ron HN, Parent, Marie-Élise, Hu, Jennifer J, Zheng, Wei, Mills, Ian G, Andreassen, Ole A, Dale, Anders M, and Seibert, Tyler M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Prostate Cancer, Cancer, Urologic Diseases, Prevention, Genetics, Good Health and Well Being, Male, Humans, Prostate-Specific Antigen, Prostatic Neoplasms, Early Detection of Cancer, Polymorphism, Single Nucleotide, Risk Factors, Risk Assessment, Genetic Predisposition to Disease, UKGPCS collaborators, APCB, NC-LA PCaP Investigators, IMPACT Study Steering Committee and Collaborators, Canary PASS Investigators, Profile Study Steering Committee, PRACTICAL Consortium, Urology & Nephrology, Clinical sciences, Oncology and carcinogenesis
Abstract

BackgroundProstate cancer risk stratification using single-nucleotide polymorphisms (SNPs) demonstrates considerable promise in men of European, Asian, and African genetic ancestries, but there is still need for increased accuracy. We evaluated whether including additional SNPs in a prostate cancer polygenic hazard score (PHS) would improve associations with clinically significant prostate cancer in multi-ancestry datasets.MethodsIn total, 299 SNPs previously associated with prostate cancer were evaluated for inclusion in a new PHS, using a LASSO-regularized Cox proportional hazards model in a training dataset of 72,181 men from the PRACTICAL Consortium. The PHS model was evaluated in four testing datasets: African ancestry, Asian ancestry, and two of European Ancestry-the Cohort of Swedish Men (COSM) and the ProtecT study. Hazard ratios (HRs) were estimated to compare men with high versus low PHS for association with clinically significant, with any, and with fatal prostate cancer. The impact of genetic risk stratification on the positive predictive value (PPV) of PSA testing for clinically significant prostate cancer was also measured.ResultsThe final model (PHS290) had 290 SNPs with non-zero coefficients. Comparing, for example, the highest and lowest quintiles of PHS290, the hazard ratios (HRs) for clinically significant prostate cancer were 13.73 [95% CI: 12.43-15.16] in ProtecT, 7.07 [6.58-7.60] in African ancestry, 10.31 [9.58-11.11] in Asian ancestry, and 11.18 [10.34-12.09] in COSM. Similar results were seen for association with any and fatal prostate cancer. Without PHS stratification, the PPV of PSA testing for clinically significant prostate cancer in ProtecT was 0.12 (0.11-0.14). For the top 20% and top 5% of PHS290, the PPV of PSA testing was 0.19 (0.15-0.22) and 0.26 (0.19-0.33), respectively.ConclusionsWe demonstrate better genetic risk stratification for clinically significant prostate cancer than prior versions of PHS in multi-ancestry datasets. This is promising for implementing precision-medicine approaches to prostate cancer screening decisions in diverse populations.

Published
2022

13. Post-diagnostic health behaviour scores in relation to fatal prostate cancer.

Author

Graff, Rebecca E, Langlais, Crystal S, Van Blarigan, Erin L, Pernar, Claire H, Stampfer, Meir J, Giovannucci, Edward L, Mucci, Lorelei A, Chan, June M, and Kenfield, Stacey A

Subjects
Humans, Prostatic Neoplasms, Proportional Hazards Models, Risk Factors, Follow-Up Studies, Prospective Studies, Health Behavior, Male, Aging, Prostate Cancer, Urologic Diseases, Cancer, Prevention, Good Health and Well Being, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundIndividual health behaviours have been associated with fatal prostate cancer (PCa). Their combined association with fatal PCa after diagnosis is unknown.MethodsThis prospective cohort included 4518 men diagnosed with nonmetastatic PCa from the Health Professionals Follow-up Study. Exposures included a three-factor score integrating post-diagnostic fatal PCa risk factors ("2021 PCa Behaviour Score"), six-factor score integrating incident aggressive PCa risk factors ("2015 PCa Behaviour Score"), and two scores integrating recommendations for cancer prevention and survival, respectively. Multivariable Cox models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for fatal PCa.ResultsOver a median 10.2 years, we observed 219 PCa deaths. Each additional point of one of the PCa-specific health behaviour scores (2015 PCa Behaviour Score) was associated with a 19% reduced fatal PCa risk (HR: 0.81, 95%CI: 0.68-0.97). The 2021 PCa Behaviour Score and scores integrating national recommendations were not associated with fatal PCa.ConclusionsWhile a PCa-specific health behaviour score was associated with a reduced risk of fatal PCa, we did not otherwise observe strong evidence of associations between post-diagnostic scores and fatal PCa. Avoiding tobacco, healthy body size, and physical activity may decrease PCa death risk, but further research is needed to inform cancer survivorship recommendations.

Published
2022

16. Impact of neighborhood socioeconomic status, income segregation, and greenness on blood biomarkers of inflammation.

Author

Iyer, Hari, Hart, Jaime, James, Peter, Elliott, Elise, DeVille, Nicole, Holmes, Michelle, De Vivo, Immaculata, Mucci, Lorelei, Laden, Francine, and Rebbeck, Timothy

Subjects
Biomarkers, Disparities, Health behavior, Inflammation, Residence characteristics, Socioeconomic factors, Biomarkers, Female, Humans, Inflammation, Male, Prospective Studies, Residence Characteristics, Social Class, Socioeconomic Factors
Abstract

BACKGROUND: Neighborhood deprivation is linked with inflammation, which may explain poorer health across populations. Behavioral risk factors are assumed to largely mediate these relationships, but few studies have examined this. We examined three neighborhood contextual factors that could exert direct effects on inflammation: (1) neighborhood socioeconomic status, (2) an index of concentration at extremes (that measures segregation), and (3) surrounding vegetation (greenness). METHODS: Using blood samples and addresses collected from prospective cohorts of 7,930 male (1990-1994) and 16,183 female (1986-1990) health professionals with at least one inflammatory marker, we prospectively linked neighborhood contextual factors to inflammatory biomarkers (adiponectin, C-reactive protein, interleukin-6, soluble tumor necrosis factor receptor-2). Log-transformed, z-scaled component measures were used to calculate an inflammation score. Neighborhood socioeconomic status and index of concentration of extremes were obtained from the 1990 decennial census and linked to participant addresses. Surrounding greenness was assessed from satellite data and focal statistics were applied to generate exposures within 270 m and 1230 m of the participants address. We fit multiple linear regression models adjusting for demographic, clinical, and behavioral risk factors. RESULTS: Higher neighborhood socioeconomic status was associated with lower inflammation score in women (β for interquartile range increase = -27.7%, 95% CI: -34.9%, -19.8%) and men (β = -21.2%, 95% CI: -31.0%, -10.1%). Similarly, participants in neighborhoods with higher concentrations of high-income households were associated with lower inflammation score in women (β = -27.8%, 95% CI: -35.8%, -18.7%) and men (β = -16.4%, 95% CI: -29.7%, -0.56%). Surrounding greenness within 270 m of each participants address was associated with lower inflammation score in women (β = -18.9%, 95% CI: -28.9%, -7.4%) but not men. Results were robust to sensitivity analyses to assess unmeasured confounding and selection bias. DISCUSSION: Our findings support the hypothesis that adverse neighborhood environments may contribute to inflammation through pathways independent of behavioral risk factors, including psychosocial stress and toxic environments.

Published
2022

19. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis

Author

Landi, Maria Teresa, Stevens, Victoria, Wang, Ying, Albanes, Demetrios, Caporaso, Neil, Brennan, Paul, Amos, Christopher I., Shete, Sanjay, Hung, Rayjean J., Bickeböller, Heike, Risch, Angela, Houlston, Richard, Lam, Stephen, Tardon, Adonina, Chen, Chu, Bojesen, Stig E., Johansson, Mattias, Wichmann, H-Erich, Christiani, David, Rennert, Gadi, Arnold, Susanne, Field, John K., Le Marchand, Loic, Melander, Olle, Brunnström, Hans, Liu, Geoffrey, Andrew, Angeline, Kiemeney, Lambertus A., Shen, Hongbing, Zienolddiny, Shan, Grankvist, Kjell, Johansson, Mikael, Teare, M. Dawn, Hong, Yun-Chul, Yuan, Jian-Min, Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Al Olama, Ali Amin, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Chanock, Stephen, Tangen, Catherine M., Batra, Jyotsna, Clements, Judith A., Grönberg, Henrik, Pashayan, Nora, Schleutker, Johanna, Albanes, Demetrius, Weinstein, Stephanie J., Wolk, Alicja, West, Catharine M.L., Mucci, Lorelei A., Cancel-Tassin, Géraldine, Koutros, Stella, Sørensen, Karina Dalsgaard, Grindedal, Eli Marie, Neal, David E., Hamdy, Freddie C., Donovan, Jenny L., Travis, Ruth C., Hamilton, Robert J., Ingles, Sue Ann, Rosenstein, Barry S., Lu, Yong-Jie, Giles, Graham G., MacInnis, Robert J., Kibel, Adam S., Vega, Ana, Kogevinas, Manolis, Penney, Kathryn L., Park, Jong Y., Stanfrod, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Logothetis, Christopher J., John, Esther M., Teixeira, Manuel R., Neuhausen, Susan L., De Ruyck, Kim, Razack, Azad, Newcomb, Lisa F., Lessel, Davor, Kaneva, Radka, Usmani, Nawaid, Claessens, Frank, Townsend, Paul A., Castelao, Jose Esteban, Roobol, Monique J., Menegaux, Florence, Khaw, Kay-Tee, Cannon-Albright, Lisa, Pandha, Hardev, Thibodeau, Stephen N., Hunter, David J., Kraft, Peter, Blot, William J., Riboli, Elio, Yarmolinsky, James, Robinson, Jamie W., Mariosa, Daniela, Karhunen, Ville, Huang, Jian, Dimou, Niki, Murphy, Neil, Burrows, Kimberley, Bouras, Emmanouil, Smith-Byrne, Karl, Lewis, Sarah J., Galesloot, Tessel E., Vermeulen, Sita, Martin, Paul, Hou, Lifang, Newcomb, Polly A., White, Emily, Wu, Anna H., Le Marchand, Loïc, Phipps, Amanda I., Buchanan, Daniel D., Zhao, Sizheng Steven, Gill, Dipender, Chanock, Stephen J., Purdue, Mark P., Davey Smith, George, Herzig, Karl-Heinz, Järvelin, Marjo-Riitta, Amos, Chris I., Dehghan, Abbas, Gunter, Marc J., Tsilidis, Kostas K., and Martin, Richard M.

Published
2024
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21. Additional SNPs improve risk stratification of a polygenic hazard score for prostate cancer.

Author

Karunamuni, Roshan A, Huynh-Le, Minh-Phuong, Fan, Chun C, Thompson, Wesley, Eeles, Rosalind A, Kote-Jarai, Zsofia, Muir, Kenneth, Lophatananon, Artitaya, UKGPCS collaborators, Schleutker, Johanna, Pashayan, Nora, Batra, Jyotsna, APCB BioResource (Australian Prostate Cancer BioResource), Grönberg, Henrik, Walsh, Eleanor I, Turner, Emma L, Lane, Athene, Martin, Richard M, Neal, David E, Donovan, Jenny L, Hamdy, Freddie C, Nordestgaard, Børge G, Tangen, Catherine M, MacInnis, Robert J, Wolk, Alicja, Albanes, Demetrius, Haiman, Christopher A, Travis, Ruth C, Stanford, Janet L, Mucci, Lorelei A, West, Catharine ML, Nielsen, Sune F, Kibel, Adam S, Wiklund, Fredrik, Cussenot, Olivier, Berndt, Sonja I, Koutros, Stella, Sørensen, Karina Dalsgaard, Cybulski, Cezary, Grindedal, Eli Marie, Park, Jong Y, Ingles, Sue A, Maier, Christiane, Hamilton, Robert J, Rosenstein, Barry S, Vega, Ana, IMPACT Study Steering Committee and Collaborators, Kogevinas, Manolis, Penney, Kathryn L, Teixeira, Manuel R, Brenner, Hermann, John, Esther M, Kaneva, Radka, Logothetis, Christopher J, Neuhausen, Susan L, Razack, Azad, Newcomb, Lisa F, Canary PASS Investigators, Gamulin, Marija, Usmani, Nawaid, Claessens, Frank, Gago-Dominguez, Manuela, Townsend, Paul A, Roobol, Monique J, Zheng, Wei, Profile Study Steering Committee, Mills, Ian G, Andreassen, Ole A, Dale, Anders M, Seibert, Tyler M, and PRACTICAL Consortium

Subjects
UKGPCS collaborators, APCB BioResource, IMPACT Study Steering Committee and Collaborators, Canary PASS Investigators, Profile Study Steering Committee, PRACTICAL Consortium, Prevention, Urologic Diseases, Cancer, Prostate Cancer, Aging, Urology & Nephrology, Oncology and Carcinogenesis
Abstract

BackgroundPolygenic hazard scores (PHS) can identify individuals with increased risk of prostate cancer. We estimated the benefit of additional SNPs on performance of a previously validated PHS (PHS46).Materials and method180 SNPs, shown to be previously associated with prostate cancer, were used to develop a PHS model in men with European ancestry. A machine-learning approach, LASSO-regularized Cox regression, was used to select SNPs and to estimate their coefficients in the training set (75,596 men). Performance of the resulting model was evaluated in the testing/validation set (6,411 men) with two metrics: (1) hazard ratios (HRs) and (2) positive predictive value (PPV) of prostate-specific antigen (PSA) testing. HRs were estimated between individuals with PHS in the top 5% to those in the middle 40% (HR95/50), top 20% to bottom 20% (HR80/20), and bottom 20% to middle 40% (HR20/50). PPV was calculated for the top 20% (PPV80) and top 5% (PPV95) of PHS as the fraction of individuals with elevated PSA that were diagnosed with clinically significant prostate cancer on biopsy.Results166 SNPs had non-zero coefficients in the Cox model (PHS166). All HR metrics showed significant improvements for PHS166 compared to PHS46: HR95/50 increased from 3.72 to 5.09, HR80/20 increased from 6.12 to 9.45, and HR20/50 decreased from 0.41 to 0.34. By contrast, no significant differences were observed in PPV of PSA testing for clinically significant prostate cancer.ConclusionsIncorporating 120 additional SNPs (PHS166 vs PHS46) significantly improved HRs for prostate cancer, while PPV of PSA testing remained the same.

Published
2021

22. Polygenic hazard score is associated with prostate cancer in multi-ethnic populations.

Author

Huynh-Le, Minh-Phuong, Fan, Chun Chieh, Karunamuni, Roshan, Thompson, Wesley K, Martinez, Maria Elena, Eeles, Rosalind A, Kote-Jarai, Zsofia, Muir, Kenneth, Schleutker, Johanna, Pashayan, Nora, Batra, Jyotsna, Grönberg, Henrik, Neal, David E, Donovan, Jenny L, Hamdy, Freddie C, Martin, Richard M, Nielsen, Sune F, Nordestgaard, Børge G, Wiklund, Fredrik, Tangen, Catherine M, Giles, Graham G, Wolk, Alicja, Albanes, Demetrius, Travis, Ruth C, Blot, William J, Zheng, Wei, Sanderson, Maureen, Stanford, Janet L, Mucci, Lorelei A, West, Catharine ML, Kibel, Adam S, Cussenot, Olivier, Berndt, Sonja I, Koutros, Stella, Sørensen, Karina Dalsgaard, Cybulski, Cezary, Grindedal, Eli Marie, Menegaux, Florence, Khaw, Kay-Tee, Park, Jong Y, Ingles, Sue A, Maier, Christiane, Hamilton, Robert J, Thibodeau, Stephen N, Rosenstein, Barry S, Lu, Yong-Jie, Watya, Stephen, Vega, Ana, Kogevinas, Manolis, Penney, Kathryn L, Huff, Chad, Teixeira, Manuel R, Multigner, Luc, Leach, Robin J, Cannon-Albright, Lisa, Brenner, Hermann, John, Esther M, Kaneva, Radka, Logothetis, Christopher J, Neuhausen, Susan L, De Ruyck, Kim, Pandha, Hardev, Razack, Azad, Newcomb, Lisa F, Fowke, Jay H, Gamulin, Marija, Usmani, Nawaid, Claessens, Frank, Gago-Dominguez, Manuela, Townsend, Paul A, Bush, William S, Roobol, Monique J, Parent, Marie-Élise, Hu, Jennifer J, Mills, Ian G, Andreassen, Ole A, Dale, Anders M, Seibert, Tyler M, UKGPCS collaborators, APCB (Australian Prostate Cancer BioResource), NC-LA PCaP Investigators, IMPACT Study Steering Committee and Collaborators, Canary PASS Investigators, Profile Study Steering Committee, and PRACTICAL Consortium

Subjects
UKGPCS collaborators, APCB, NC-LA PCaP Investigators, IMPACT Study Steering Committee and Collaborators, Canary PASS Investigators, Profile Study Steering Committee, PRACTICAL Consortium, Humans, Prostatic Neoplasms, Neoplasm Invasiveness, Multivariate Analysis, Multifactorial Inheritance, Aged, Middle Aged, Ethnic Groups, Male, Self Report, Aging, Urologic Diseases, Cancer, Prostate Cancer
Abstract

Genetic models for cancer have been evaluated using almost exclusively European data, which could exacerbate health disparities. A polygenic hazard score (PHS1) is associated with age at prostate cancer diagnosis and improves screening accuracy in Europeans. Here, we evaluate performance of PHS2 (PHS1, adapted for OncoArray) in a multi-ethnic dataset of 80,491 men (49,916 cases, 30,575 controls). PHS2 is associated with age at diagnosis of any and aggressive (Gleason score ≥ 7, stage T3-T4, PSA ≥ 10 ng/mL, or nodal/distant metastasis) cancer and prostate-cancer-specific death. Associations with cancer are significant within European (n = 71,856), Asian (n = 2,382), and African (n = 6,253) genetic ancestries (p

Published
2021

24. Integrating genetics and metabolomics from multi-ethnic and multi-fluid data reveals putative mechanisms for age-related macular degeneration

Author

Han, Xikun, Lains, Ines, Li, Jun, Li, Jinglun, Chen, Yiheng, Yu, Bing, Qi, Qibin, Boerwinkle, Eric, Kaplan, Robert, Thyagarajan, Bharat, Daviglus, Martha, Joslin, Charlotte E., Cai, Jianwen, Guasch-Ferré, Marta, Tobias, Deirdre K., Rimm, Eric, Ascherio, Alberto, Costenbader, Karen, Karlson, Elizabeth, Mucci, Lorelei, Eliassen, A. Heather, Zeleznik, Oana, Miller, John, Vavvas, Demetrios G., Kim, Ivana K., Silva, Rufino, Miller, Joan, Hu, Frank, Willett, Walter, Lasky-Su, Jessica, Kraft, Peter, Richards, J. Brent, MacGregor, Stuart, Husain, Deeba, and Liang, Liming

Published
2023
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26. A saturated map of common genetic variants associated with human height

Author

Yengo, Loïc, Vedantam, Sailaja, Marouli, Eirini, Sidorenko, Julia, Bartell, Eric, Sakaue, Saori, Graff, Marielisa, Eliasen, Anders U., Jiang, Yunxuan, Raghavan, Sridharan, Miao, Jenkai, Arias, Joshua D., Graham, Sarah E., Mukamel, Ronen E., Spracklen, Cassandra N., Yin, Xianyong, Chen, Shyh-Huei, Ferreira, Teresa, Highland, Heather H., Ji, Yingjie, Karaderi, Tugce, Lin, Kuang, Lüll, Kreete, Malden, Deborah E., Medina-Gomez, Carolina, Machado, Moara, Moore, Amy, Rüeger, Sina, Sim, Xueling, Vrieze, Scott, Ahluwalia, Tarunveer S., Akiyama, Masato, Allison, Matthew A., Alvarez, Marcus, Andersen, Mette K., Ani, Alireza, Appadurai, Vivek, Arbeeva, Liubov, Bhaskar, Seema, Bielak, Lawrence F., Bollepalli, Sailalitha, Bonnycastle, Lori L., Bork-Jensen, Jette, Bradfield, Jonathan P., Bradford, Yuki, Braund, Peter S., Brody, Jennifer A., Burgdorf, Kristoffer S., Cade, Brian E., Cai, Hui, Cai, Qiuyin, Campbell, Archie, Cañadas-Garre, Marisa, Catamo, Eulalia, Chai, Jin-Fang, Chai, Xiaoran, Chang, Li-Ching, Chang, Yi-Cheng, Chen, Chien-Hsiun, Chesi, Alessandra, Choi, Seung Hoan, Chung, Ren-Hua, Cocca, Massimiliano, Concas, Maria Pina, Couture, Christian, Cuellar-Partida, Gabriel, Danning, Rebecca, Daw, E. Warwick, Degenhard, Frauke, Delgado, Graciela E., Delitala, Alessandro, Demirkan, Ayse, Deng, Xuan, Devineni, Poornima, Dietl, Alexander, Dimitriou, Maria, Dimitrov, Latchezar, Dorajoo, Rajkumar, Ekici, Arif B., Engmann, Jorgen E., Fairhurst-Hunter, Zammy, Farmaki, Aliki-Eleni, Faul, Jessica D., Fernandez-Lopez, Juan-Carlos, Forer, Lukas, Francescatto, Margherita, Freitag-Wolf, Sandra, Fuchsberger, Christian, Galesloot, Tessel E., Gao, Yan, Gao, Zishan, Geller, Frank, Giannakopoulou, Olga, Giulianini, Franco, Gjesing, Anette P., Goel, Anuj, Gordon, Scott D., Gorski, Mathias, Grove, Jakob, Guo, Xiuqing, Gustafsson, Stefan, Haessler, Jeffrey, Hansen, Thomas F., Havulinna, Aki S., Haworth, Simon J., He, Jing, Heard-Costa, Nancy, Hebbar, Prashantha, Hindy, George, Ho, Yuk-Lam A., Hofer, Edith, Holliday, Elizabeth, Horn, Katrin, Hornsby, Whitney E., Hottenga, Jouke-Jan, Huang, Hongyan, Huang, Jie, Huerta-Chagoya, Alicia, Huffman, Jennifer E., Hung, Yi-Jen, Huo, Shaofeng, Hwang, Mi Yeong, Iha, Hiroyuki, Ikeda, Daisuke D., Isono, Masato, Jackson, Anne U., Jäger, Susanne, Jansen, Iris E., Johansson, Ingegerd, Jonas, Jost B., Jonsson, Anna, Jørgensen, Torben, Kalafati, Ioanna-Panagiota, Kanai, Masahiro, Kanoni, Stavroula, Kårhus, Line L., Kasturiratne, Anuradhani, Katsuya, Tomohiro, Kawaguchi, Takahisa, Kember, Rachel L., Kentistou, Katherine A., Kim, Han-Na, Kim, Young Jin, Kleber, Marcus E., Knol, Maria J., Kurbasic, Azra, Lauzon, Marie, Le, Phuong, Lea, Rodney, Lee, Jong-Young, Leonard, Hampton L., Li, Shengchao A., Li, Xiaohui, Li, Xiaoyin, Liang, Jingjing, Lin, Honghuang, Lin, Shih-Yi, Liu, Jun, Liu, Xueping, Lo, Ken Sin, Long, Jirong, Lores-Motta, Laura, Luan, Jian’an, Lyssenko, Valeriya, Lyytikäinen, Leo-Pekka, Mahajan, Anubha, Mamakou, Vasiliki, Mangino, Massimo, Manichaikul, Ani, Marten, Jonathan, Mattheisen, Manuel, Mavarani, Laven, McDaid, Aaron F., Meidtner, Karina, Melendez, Tori L., Mercader, Josep M., Milaneschi, Yuri, Miller, Jason E., Millwood, Iona Y., Mishra, Pashupati P., Mitchell, Ruth E., Møllehave, Line T., Morgan, Anna, Mucha, Soeren, Munz, Matthias, Nakatochi, Masahiro, Nelson, Christopher P., Nethander, Maria, Nho, Chu Won, Nielsen, Aneta A., Nolte, Ilja M., Nongmaithem, Suraj S., Noordam, Raymond, Ntalla, Ioanna, Nutile, Teresa, Pandit, Anita, Christofidou, Paraskevi, Pärna, Katri, Pauper, Marc, Petersen, Eva R. B., Petersen, Liselotte V., Pitkänen, Niina, Polašek, Ozren, Poveda, Alaitz, Preuss, Michael H., Pyarajan, Saiju, Raffield, Laura M., Rakugi, Hiromi, Ramirez, Julia, Rasheed, Asif, Raven, Dennis, Rayner, Nigel W., Riveros, Carlos, Rohde, Rebecca, Ruggiero, Daniela, Ruotsalainen, Sanni E., Ryan, Kathleen A., Sabater-Lleal, Maria, Saxena, Richa, Scholz, Markus, Sendamarai, Anoop, Shen, Botong, Shi, Jingchunzi, Shin, Jae Hun, Sidore, Carlo, Sitlani, Colleen M., Slieker, Roderick C., Smit, Roelof A. J., Smith, Albert V., Smith, Jennifer A., Smyth, Laura J., Southam, Lorraine, Steinthorsdottir, Valgerdur, Sun, Liang, Takeuchi, Fumihiko, Tallapragada, Divya Sri Priyanka, Taylor, Kent D., Tayo, Bamidele O., Tcheandjieu, Catherine, Terzikhan, Natalie, Tesolin, Paola, Teumer, Alexander, Theusch, Elizabeth, Thompson, Deborah J., Thorleifsson, Gudmar, Timmers, Paul R. H. J., Trompet, Stella, Turman, Constance, Vaccargiu, Simona, van der Laan, Sander W., van der Most, Peter J., van Klinken, Jan B., van Setten, Jessica, Verma, Shefali S., Verweij, Niek, Veturi, Yogasudha, Wang, Carol A., Wang, Chaolong, Wang, Lihua, Wang, Zhe, Warren, Helen R., Bin Wei, Wen, Wickremasinghe, Ananda R., Wielscher, Matthias, Wiggins, Kerri L., Winsvold, Bendik S., Wong, Andrew, Wu, Yang, Wuttke, Matthias, Xia, Rui, Xie, Tian, Yamamoto, Ken, Yang, Jingyun, Yao, Jie, Young, Hannah, Yousri, Noha A., Yu, Lei, Zeng, Lingyao, Zhang, Weihua, Zhang, Xinyuan, Zhao, Jing-Hua, Zhao, Wei, Zhou, Wei, Zimmermann, Martina E., Zoledziewska, Magdalena, Adair, Linda S., Adams, Hieab H. H., Aguilar-Salinas, Carlos A., Al-Mulla, Fahd, Arnett, Donna K., Asselbergs, Folkert W., Åsvold, Bjørn Olav, Attia, John, Banas, Bernhard, Bandinelli, Stefania, Bennett, David A., Bergler, Tobias, Bharadwaj, Dwaipayan, Biino, Ginevra, Bisgaard, Hans, Boerwinkle, Eric, Böger, Carsten A., Bønnelykke, Klaus, Boomsma, Dorret I., Børglum, Anders D., Borja, Judith B., Bouchard, Claude, Bowden, Donald W., Brandslund, Ivan, Brumpton, Ben, Buring, Julie E., Caulfield, Mark J., Chambers, John C., Chandak, Giriraj R., Chanock, Stephen J., Chaturvedi, Nish, Chen, Yii-Der Ida, Chen, Zhengming, Cheng, Ching-Yu, Christophersen, Ingrid E., Ciullo, Marina, Cole, John W., Collins, Francis S., Cooper, Richard S., Cruz, Miguel, Cucca, Francesco, Cupples, L. Adrienne, Cutler, Michael J., Damrauer, Scott M., Dantoft, Thomas M., de Borst, Gert J., de Groot, Lisette C. P. G. M., De Jager, Philip L., de Kleijn, Dominique P. V., Janaka de Silva, H., Dedoussis, George V., den Hollander, Anneke I., Du, Shufa, Easton, Douglas F., Elders, Petra J. M., Eliassen, A. Heather, Ellinor, Patrick T., Elmståhl, Sölve, Erdmann, Jeanette, Evans, Michele K., Fatkin, Diane, Feenstra, Bjarke, Feitosa, Mary F., Ferrucci, Luigi, Ford, Ian, Fornage, Myriam, Franke, Andre, Franks, Paul W., Freedman, Barry I., Gasparini, Paolo, Gieger, Christian, Girotto, Giorgia, Goddard, Michael E., Golightly, Yvonne M., Gonzalez-Villalpando, Clicerio, Gordon-Larsen, Penny, Grallert, Harald, Grant, Struan F. A., Grarup, Niels, Griffiths, Lyn, Gudnason, Vilmundur, Haiman, Christopher, Hakonarson, Hakon, Hansen, Torben, Hartman, Catharina A., Hattersley, Andrew T., Hayward, Caroline, Heckbert, Susan R., Heng, Chew-Kiat, Hengstenberg, Christian, Hewitt, Alex W., Hishigaki, Haretsugu, Hoyng, Carel B., Huang, Paul L., Huang, Wei, Hunt, Steven C., Hveem, Kristian, Hyppönen, Elina, Iacono, William G., Ichihara, Sahoko, Ikram, M. Arfan, Isasi, Carmen R., Jackson, Rebecca D., Jarvelin, Marjo-Riitta, Jin, Zi-Bing, Jöckel, Karl-Heinz, Joshi, Peter K., Jousilahti, Pekka, Jukema, J. Wouter, Kähönen, Mika, Kamatani, Yoichiro, Kang, Kui Dong, Kaprio, Jaakko, Kardia, Sharon L. R., Karpe, Fredrik, Kato, Norihiro, Kee, Frank, Kessler, Thorsten, Khera, Amit V., Khor, Chiea Chuen, Kiemeney, Lambertus A. L. M., Kim, Bong-Jo, Kim, Eung Kweon, Kim, Hyung-Lae, Kirchhof, Paulus, Kivimaki, Mika, Koh, Woon-Puay, Koistinen, Heikki A., Kolovou, Genovefa D., Kooner, Jaspal S., Kooperberg, Charles, Köttgen, Anna, Kovacs, Peter, Kraaijeveld, Adriaan, Kraft, Peter, Krauss, Ronald M., Kumari, Meena, Kutalik, Zoltan, Laakso, Markku, Lange, Leslie A., Langenberg, Claudia, Launer, Lenore J., Le Marchand, Loic, Lee, Hyejin, Lee, Nanette R., Lehtimäki, Terho, Li, Huaixing, Li, Liming, Lieb, Wolfgang, Lin, Xu, Lind, Lars, Linneberg, Allan, Liu, Ching-Ti, Liu, Jianjun, Loeffler, Markus, London, Barry, Lubitz, Steven A., Lye, Stephen J., Mackey, David A., Mägi, Reedik, Magnusson, Patrik K. E., Marcus, Gregory M., Vidal, Pedro Marques, Martin, Nicholas G., März, Winfried, Matsuda, Fumihiko, McGarrah, Robert W., McGue, Matt, McKnight, Amy Jayne, Medland, Sarah E., Mellström, Dan, Metspalu, Andres, Mitchell, Braxton D., Mitchell, Paul, Mook-Kanamori, Dennis O., Morris, Andrew D., Mucci, Lorelei A., Munroe, Patricia B., Nalls, Mike A., Nazarian, Saman, Nelson, Amanda E., Neville, Matt J., Newton-Cheh, Christopher, Nielsen, Christopher S., Nöthen, Markus M., Ohlsson, Claes, Oldehinkel, Albertine J., Orozco, Lorena, Pahkala, Katja, Pajukanta, Päivi, Palmer, Colin N. A., Parra, Esteban J., Pattaro, Cristian, Pedersen, Oluf, Pennell, Craig E., Penninx, Brenda W. J. H., Perusse, Louis, Peters, Annette, Peyser, Patricia A., Porteous, David J., Posthuma, Danielle, Power, Chris, Pramstaller, Peter P., Province, Michael A., Qi, Qibin, Qu, Jia, Rader, Daniel J., Raitakari, Olli T., Ralhan, Sarju, Rallidis, Loukianos S., Rao, Dabeeru C., Redline, Susan, Reilly, Dermot F., Reiner, Alexander P., Rhee, Sang Youl, Ridker, Paul M., Rienstra, Michiel, Ripatti, Samuli, Ritchie, Marylyn D., Roden, Dan M., Rosendaal, Frits R., Rotter, Jerome I., Rudan, Igor, Rutters, Femke, Sabanayagam, Charumathi, Saleheen, Danish, Salomaa, Veikko, Samani, Nilesh J., Sanghera, Dharambir K., Sattar, Naveed, Schmidt, Börge, Schmidt, Helena, Schmidt, Reinhold, Schulze, Matthias B., Schunkert, Heribert, Scott, Laura J., Scott, Rodney J., Sever, Peter, Shiroma, Eric J., Shoemaker, M. Benjamin, Shu, Xiao-Ou, Simonsick, Eleanor M., Sims, Mario, Singh, Jai Rup, Singleton, Andrew B., Sinner, Moritz F., Smith, J. Gustav, Snieder, Harold, Spector, Tim D., Stampfer, Meir J., Stark, Klaus J., Strachan, David P., ‘t Hart, Leen M., Tabara, Yasuharu, Tang, Hua, Tardif, Jean-Claude, Thanaraj, Thangavel A., Timpson, Nicholas J., Tönjes, Anke, Tremblay, Angelo, Tuomi, Tiinamaija, Tuomilehto, Jaakko, Tusié-Luna, Maria-Teresa, Uitterlinden, Andre G., van Dam, Rob M., van der Harst, Pim, Van der Velde, Nathalie, van Duijn, Cornelia M., van Schoor, Natasja M., Vitart, Veronique, Völker, Uwe, Vollenweider, Peter, Völzke, Henry, Wacher-Rodarte, Niels H., Walker, Mark, Wang, Ya Xing, Wareham, Nicholas J., Watanabe, Richard M., Watkins, Hugh, Weir, David R., Werge, Thomas M., Widen, Elisabeth, Wilkens, Lynne R., Willemsen, Gonneke, Willett, Walter C., Wilson, James F., Wong, Tien-Yin, Woo, Jeong-Taek, Wright, Alan F., Wu, Jer-Yuarn, Xu, Huichun, Yajnik, Chittaranjan S., Yokota, Mitsuhiro, Yuan, Jian-Min, Zeggini, Eleftheria, Zemel, Babette S., Zheng, Wei, Zhu, Xiaofeng, Zmuda, Joseph M., Zonderman, Alan B., Zwart, John-Anker, Chasman, Daniel I., Cho, Yoon Shin, Heid, Iris M., McCarthy, Mark I., Ng, Maggie C. Y., O’Donnell, Christopher J., Rivadeneira, Fernando, Thorsteinsdottir, Unnur, Sun, Yan V., Tai, E. Shyong, Boehnke, Michael, Deloukas, Panos, Justice, Anne E., Lindgren, Cecilia M., Loos, Ruth J. F., Mohlke, Karen L., North, Kari E., Stefansson, Kari, Walters, Robin G., Winkler, Thomas W., Young, Kristin L., Loh, Po-Ru, Yang, Jian, Esko, Tõnu, Assimes, Themistocles L., Auton, Adam, Abecasis, Goncalo R., Willer, Cristen J., Locke, Adam E., Berndt, Sonja I., Lettre, Guillaume, Frayling, Timothy M., Okada, Yukinori, Wood, Andrew R., Visscher, Peter M., and Hirschhorn, Joel N.

Published
2022
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28. ExPeCT: a randomised trial examining the impact of exercise on quality of life in men with metastatic prostate cancer

Author

Sheill, Gráinne, Brady, Lauren, Hayes, Brian, Baird, Anne-Marie, Guinan, Emer, Vishwakarma, Rishabh, Brophy, Caroline, Vlajnic, Tatjana, Casey, Orla, Murphy, Verena, Greene, John, Allott, Emma, Hussey, Juliette, Cahill, Fidelma, Van Hemelrijck, Mieke, Peat, Nicola, Mucci, Lorelei, Cunningham, Moya, Grogan, Liam, Lynch, Thomas, Manecksha, Rustom P., McCaffrey, John, O’Donnell, Dearbhaile, Sheils, Orla, O’Leary, John, Rudman, Sarah, McDermott, Ray, and Finn, Stephen

Published
2023
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29. Implementation of Germline Testing for Prostate Cancer: Philadelphia Prostate Cancer Consensus Conference 2019.

Author

Giri, Veda N, Knudsen, Karen E, Kelly, William K, Cheng, Heather H, Cooney, Kathleen A, Cookson, Michael S, Dahut, William, Weissman, Scott, Soule, Howard R, Petrylak, Daniel P, Dicker, Adam P, AlDubayan, Saud H, Toland, Amanda E, Pritchard, Colin C, Pettaway, Curtis A, Daly, Mary B, Mohler, James L, Parsons, J Kellogg, Carroll, Peter R, Pilarski, Robert, Blanco, Amie, Woodson, Ashley, Rahm, Alanna, Taplin, Mary-Ellen, Polascik, Thomas J, Helfand, Brian T, Hyatt, Colette, Morgans, Alicia K, Feng, Felix, Mullane, Michael, Powers, Jacqueline, Concepcion, Raoul, Lin, Daniel W, Wender, Richard, Mark, James Ryan, Costello, Anthony, Burnett, Arthur L, Sartor, Oliver, Isaacs, William B, Xu, Jianfeng, Weitzel, Jeffrey, Andriole, Gerald L, Beltran, Himisha, Briganti, Alberto, Byrne, Lindsey, Calvaresi, Anne, Chandrasekar, Thenappan, Chen, David YT, Den, Robert B, Dobi, Albert, Crawford, E David, Eastham, James, Eggener, Scott, Freedman, Matthew L, Garnick, Marc, Gomella, Patrick T, Handley, Nathan, Hurwitz, Mark D, Izes, Joseph, Karnes, R Jeffrey, Lallas, Costas, Languino, Lucia, Loeb, Stacy, Lopez, Ana Maria, Loughlin, Kevin R, Lu-Yao, Grace, Malkowicz, S Bruce, Mann, Mark, Mille, Patrick, Miner, Martin M, Morgan, Todd, Moreno, Jose, Mucci, Lorelei, Myers, Ronald E, Nielsen, Sarah M, O'Neil, Brock, Pinover, Wayne, Pinto, Peter, Poage, Wendy, Raj, Ganesh V, Rebbeck, Timothy R, Ryan, Charles, Sandler, Howard, Schiewer, Matthew, Scott, E Michael D, Szymaniak, Brittany, Tester, William, Trabulsi, Edouard J, Vapiwala, Neha, Yu, Evan Y, Zeigler-Johnson, Charnita, and Gomella, Leonard G

Subjects
Biotechnology, Aging, Genetics, Prevention, Clinical Research, Cancer, Prostate Cancer, Genetic Testing, Urologic Diseases, Health Services, Good Health and Well Being, Germ-Line Mutation, History, 20th Century, Humans, Male, Prostatic Neoplasms, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeGermline testing (GT) is a central feature of prostate cancer (PCA) treatment, management, and hereditary cancer assessment. Critical needs include optimized multigene testing strategies that incorporate evolving genetic data, consistency in GT indications and management, and alternate genetic evaluation models that address the rising demand for genetic services.MethodsA multidisciplinary consensus conference that included experts, stakeholders, and national organization leaders was convened in response to current practice challenges and to develop a genetic implementation framework. Evidence review informed questions using the modified Delphi model. The final framework included criteria with strong (> 75%) agreement (Recommend) or moderate (50% to 74%) agreement (Consider).ResultsLarge germline panels and somatic testing were recommended for metastatic PCA. Reflex testing-initial testing of priority genes followed by expanded testing-was suggested for multiple scenarios. Metastatic disease or family history suggestive of hereditary PCA was recommended for GT. Additional family history and pathologic criteria garnered moderate consensus. Priority genes to test for metastatic disease treatment included BRCA2, BRCA1, and mismatch repair genes, with broader testing, such as ATM, for clinical trial eligibility. BRCA2 was recommended for active surveillance discussions. Screening starting at age 40 years or 10 years before the youngest PCA diagnosis in a family was recommended for BRCA2 carriers, with consideration in HOXB13, BRCA1, ATM, and mismatch repair carriers. Collaborative (point-of-care) evaluation models between health care and genetic providers was endorsed to address the genetic counseling shortage. The genetic evaluation framework included optimal pretest informed consent, post-test discussion, cascade testing, and technology-based approaches.ConclusionThis multidisciplinary, consensus-driven PCA genetic implementation framework provides novel guidance to clinicians and patients tailored to the precision era. Multiple research, education, and policy needs remain of importance.

Published
2020

30. The COronavirus Pandemic Epidemiology (COPE) Consortium: A Call to Action

Author

Chan, Andrew T, Drew, David A, Nguyen, Long H, Joshi, Amit D, Ma, Wenjie, Guo, Chuan-Guo, Lo, Chun-Han, Mehta, Raaj S, Kwon, Sohee, Sikavi, Daniel R, Magicheva-Gupta, Marina V, Fatehi, Zahra S, Flynn, Jacqueline J, Leonardo, Brianna M, Albert, Christine M, Andreotti, Gabriella, Beane-Freeman, Laura E, Balasubramanian, Bijal A, Brownstein, John S, Bruinsma, Fiona, Cowan, Annie N, Deka, Anusila, Ernst, Michael E, Figueiredo, Jane C, Franks, Paul W, Gardner, Christopher D, Ghobrial, Irene M, Haiman, Christopher A, Hall, Janet E, Deming-Halverson, Sandra L, Kirpach, Brenda, Lacey, James V, Le Marchand, Loïc, Marinac, Catherine R, Martinez, Maria Elena, Milne, Roger L, Murray, Anne M, Nash, Denis, Palmer, Julie R, Patel, Alpa V, Rosenberg, Lynn, Sandler, Dale P, Sharma, Shreela V, Schurman, Shepherd H, Wilkens, Lynne R, Chavarro, Jorge E, Eliassen, A Heather, Hart, Jaime E, Kang, Jae Hee, Koenen, Karestan C, Kubzansky, Laura D, Mucci, Lorelei A, Ourselin, Sebastien, Rich-Edwards, Janet W, Song, Mingyang, Stampfer, Meir J, Steves, Claire J, Willett, Walter C, Wolf, Jonathan, and Spector, Tim

Subjects
Pneumonia & Influenza, Nutrition, Clinical Research, Cancer, Infectious Diseases, Prevention, 2.4 Surveillance and distribution, Aetiology, Good Health and Well Being, Betacoronavirus, COVID-19, Coronavirus Infections, Data Collection, Humans, Models, Biological, Pandemics, Pneumonia, Viral, Public Health, SARS-CoV-2, Smartphone, Software, United Kingdom, United States, COPE Consortium, Medical and Health Sciences, Epidemiology
Abstract

The rapid pace of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; COVID-19) pandemic presents challenges to the real-time collection of population-scale data to inform near-term public health needs as well as future investigations. We established the COronavirus Pandemic Epidemiology (COPE) consortium to address this unprecedented crisis on behalf of the epidemiology research community. As a central component of this initiative, we have developed a COVID Symptom Study (previously known as the COVID Symptom Tracker) mobile application as a common data collection tool for epidemiologic cohort studies with active study participants. This mobile application collects information on risk factors, daily symptoms, and outcomes through a user-friendly interface that minimizes participant burden. Combined with our efforts within the general population, data collected from nearly 3 million participants in the United States and United Kingdom are being used to address critical needs in the emergency response, including identifying potential hot spots of disease and clinically actionable risk factors. The linkage of symptom data collected in the app with information and biospecimens already collected in epidemiology cohorts will position us to address key questions related to diet, lifestyle, environmental, and socioeconomic factors on susceptibility to COVID-19, clinical outcomes related to infection, and long-term physical, mental health, and financial sequalae. We call upon additional epidemiology cohorts to join this collective effort to strengthen our impact on the current health crisis and generate a new model for a collaborative and nimble research infrastructure that will lead to more rapid translation of our work for the betterment of public health.

Published
2020

31. Baldness and Risk of Prostate Cancer in the Health Professionals Follow-up Study

Author

Khan, Saud, Caldwell, Joshua, Wilson, Kathryn M, Gonzalez-Feliciano, Amparo G, Peisch, Samuel, Pernar, Claire H, Graff, Rebecca E, Giovannucci, Edward L, Mucci, Lorelei A, Gerke, Travis A, and Markt, Sarah C

Subjects
Biomedical and Clinical Sciences, Health Services and Systems, Health Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Prevention, Clinical Research, Urologic Diseases, Prostate Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, Alopecia, Follow-Up Studies, Humans, Male, Middle Aged, Prospective Studies, Prostatic Neoplasms, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundThe association between male pattern baldness and prostate cancer has been inconsistent. We prospectively investigated the association between baldness at age 45 and prostate cancer risk in the Health Professionals Follow-up Study (HPFS), focusing on clinical and molecular markers.MethodsBaldness was self-reported on the 1992 questionnaire using the modified Norwood-Hamilton scale prior to diagnosis. We estimated HRs between baldness and prostate cancer risk among 36,760 men, with follow-up through 2014. We also investigated whether baldness was associated with prostate cancer defined by tumor protein expression of androgen receptor and the presence of the TMPRSS2:ERG fusion.ResultsDuring 22 years, 5,157 prostate cancer cases were identified. Fifty-six percent of the men had either frontal or vertex baldness. No significant associations were found between baldness and prostate cancer risk. Among men younger than 60 years, there was a statistically significant association between frontal and severe vertex baldness and overall prostate cancer (HR: 1.74; 95% confidence interval: 1.23-2.48). Baldness was not significantly associated with expression of molecular subtypes defined by AR and TMPRSS2:ERG IHC of prostate tumors.ConclusionsThis study showed no association between baldness at age 45 and prostate cancer risk, overall or for clinical or molecular markers. The association between baldness and overall prostate cancer among younger men is intriguing, but caution is warranted when interpreting this finding.ImpactThe null findings from this large cohort study, together with previous literature's inconclusive findings across baldness patterns, suggest that baldness is not a consistent biomarker for prostate cancer risk or progression.

Published
2020

32. Family history of prostate cancer and the incidence of ERG- and phosphatase and tensin homolog-defined prostate cancer.

Author

Hashim, Dana, Gonzalez-Feliciano, Amparo, Ahearn, Thomas, Pettersson, Andreas, Barber, Lauren, Pernar, Claire, Ebot, Ericka, Finn, Stephen, Giovannucci, Edward, Lis, Rosina, Loda, Massimo, Parmigiani, Giovanni, Lotan, Tamara, Kantoff, Philip, Mucci, Lorelei, Graff, Rebecca, and Isikbay, Masis

Subjects
PTEN, TMPRSS2:ERG, family history, molecular subtypes, prostate cancer, Adult, Aged, Biomarkers, Tumor, Cohort Studies, Genetic Predisposition to Disease, Humans, Incidence, Male, Middle Aged, PTEN Phosphohydrolase, Prostatic Neoplasms, Risk Factors, Transcriptional Regulator ERG
Abstract

Family history is among the strongest known risk factors for prostate cancer (PCa). Emerging data suggest molecular subtypes of PCa, including two somatic genetic aberrations: fusions of androgen-regulated promoters with ERG and, separately, phosphatase and tensin homolog (PTEN) loss. We examined associations between family history and incidence of these subtypes in 44,126 men from the prospective Health Professionals Follow-up Study. ERG and PTEN status were assessed by immunohistochemistry. Multivariable competing risks models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between self-reported family history of PCa and molecular subtypes of disease. Thirteen percent of men had a positive family history of PCa at baseline. During a median follow-up of 18.5 years, 5,511 PCa cases were diagnosed. Among them, 888 were assayed for ERG status (47% ERG-positive) and 715 were assayed for PTEN loss (14% PTEN null). Family history was more strongly associated with risk of ERG-negative (HR: 2.15; 95% CI: 1.71-2.70) than ERG-positive (HR: 1.49; 95% CI: 1.13-1.95) disease (pheterogeneity : 0.04). The strongest difference was among men with an affected father (HRERG-negative : 2.09; 95% CI: 1.64-2.66; HRERG-positive : 1.30; 95% CI: 0.96-1.76; pheterogeneity : 0.01). Family history of PCa was positively associated with both PTEN null (HR: 2.10; 95% CI: 1.26-3.49) and PTEN intact (HR: 1.72; 95% CI: 1.39-2.13) PCa (pheterogeneity : 0.47). Our results indicate that PCa family history may be positively associated with PCa in all ERG and PTEN subtypes, suggesting a role of genetic susceptibility in their development. It is possible that ERG-negative disease could be especially associated with positive family history.

Published
2020

33. The association between neighborhood greenness and incidence of lethal prostate cancer: A prospective cohort study.

Author

Iyer, Hari, James, Peter, Valeri, Linda, Hart, Jaime, Pernar, Claire, Mucci, Lorelei, Holmes, Michelle, Laden, Francine, and Rebbeck, Timothy

Subjects
Built environment, Causal mediation, Cohort studies, Green space, Physical activity, Prostate cancer
Abstract

BACKGROUND: Growing evidence suggests that neighborhood contextual environment could influence risk factors and, therefore, incidence of lethal prostate cancer. We studied the association between neighborhood greenness and lethal prostate cancer incidence and assessed mediation by vigorous physical activity. METHODS: A total of 47,958 participants were followed in the Health Professionals Follow-up Study from 1986 to 2014. Neighborhood greenness exposure was estimated using normalized difference vegetation index (NDVI) with 1 km resolution, assigned to home or work addresses at start of follow-up. Adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) were estimated using sequentially adjusted Cox models with individual and contextual prostate cancer risk factors as covariates. Analyses were compared among those whose addresses were constant over follow-up and stratified by population density and address type. RESULTS: We observed 898 cases over 1,054,743 person-years. An interquartile range increase in NDVI was associated with 5% lower rate of lethal prostate cancer (aHR = 0.95, 95% CI = 0.88, 1.03), with stronger associations in nonmovers (aHR = 0.92, 95% CI = 0.85, 1.01). Inverse associations were observed among men in high (aHR = 0.90, 95% CI = 0.82, 0.99) but not low (aHR = 1.11, 95% CI = 0.95, 1.29, P het = 0.086) population density areas, and those reporting from work (aHR = 0.87, 95% CI = 0.75, 1.01) but not home (aHR = 1.04, 95% CI = 0.91, 1.17, P het = 0.10) addresses. There was no evidence of mediation by vigorous physical activity. CONCLUSION: We report inverse associations between neighborhood greenness and lethal prostate cancer when restricting to nonmovers and in high population density areas. Replication could confirm findings and clarify mechanisms.

Published
2020

34. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF‐I, IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 in a pooled analysis of 16,024 men from 22 studies

Author

Watts, Eleanor L, Perez‐Cornago, Aurora, Appleby, Paul N, Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno‐de‐Mesquita, H Bas, Chan, June M, Chen, Chu, Chubb, SA Paul, Cook, Michael B, Deschasaux, Mélanie, Donovan, Jenny L, English, Dallas R, Flicker, Leon, Freedman, Neal D, Galan, Pilar, Giles, Graham G, Giovannucci, Edward L, Gunter, Marc J, Habel, Laurel A, Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C, Hercberg, Serge, Holly, Jeff M, Huang, Jiaqi, Huang, Wen‐Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J Athene, Layne, Tracy M, Le Marchand, Loic, Martin, Richard M, Metter, E Jeffrey, Mikami, Kazuya, Milne, Roger L, Morris, Howard A, Mucci, Lorelei A, Neal, David E, Neuhouser, Marian L, Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H, Pollak, Michael, Rowlands, Mari‐Anne, Schaefer, Catherine A, Schenk, Jeannette M, Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K, Van Den Eeden, Stephen K, Weinstein, Stephanie J, Wilkens, Lynne, Yeap, Bu B, Key, Timothy J, Allen, Naomi E, and Travis, Ruth C

Subjects
Cancer, Aging, Urologic Diseases, Adult, Aged, Aged, 80 and over, Anthropometry, Biomarkers, Tumor, Cross-Sectional Studies, Humans, Insulin-Like Growth Factor Binding Proteins, Insulin-Like Growth Factor I, Insulin-Like Growth Factor II, Male, Middle Aged, Neoplasms, Prospective Studies, Young Adult, IGFs, IGFBPs, pooled analysis, correlates, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Insulin-like growth factors (IGFs) and insulin-like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross-sectional associations of these exposures with circulating concentrations of IGFs (IGF-I and IGF-II) and IGFBPs (IGFBP-1, IGFBP-2 and IGFBP-3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22-89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGF-I, IGF-II and IGFBP-3. Higher body mass index was associated with lower concentrations of IGFBP-1 and IGFBP-2. Taller height was associated with higher concentrations of IGF-I and IGFBP-3 and lower concentrations of IGFBP-1. Smokers had higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGFBP-3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF-II and lower concentrations of IGF-I and IGFBP-2. African Americans had lower concentrations of IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 and Hispanics had lower IGF-I, IGF-II and IGFBP-3 than non-Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.

Published
2019

37. Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer

Author

Boufaied, Nadia, primary, Chetta, Paolo, additional, Hallal, Tarek, additional, Cacciatore, Stefano, additional, Lalli, Daniela, additional, Luthold, Carole, additional, Homsy, Kevin, additional, Imada, Eddie L., additional, Syamala, Sudeepa, additional, Photopoulos, Cornelia, additional, Di Matteo, Anna, additional, de Polo, Anna, additional, Storaci, Alessandra Maria, additional, Huang, Ying, additional, Giunchi, Francesca, additional, Sheridan, Patricia A., additional, Michelotti, Gregory, additional, Nguyen, Quang-De, additional, Zhao, Xin, additional, Liu, Yang, additional, Davicioni, Elai, additional, Spratt, Daniel E., additional, Sabbioneda, Simone, additional, Maga, Giovanni, additional, Mucci, Lorelei A., additional, Ghigna, Claudia, additional, Marchionni, Luigi, additional, Butler, Lisa M., additional, Ellis, Leigh, additional, Bordeleau, François, additional, Loda, Massimo, additional, Vaira, Valentina, additional, Labbé, David P., additional, and Zadra, Giorgia, additional

Published
2024
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38. Supplementary Figure S1 from Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer

Author

Boufaied, Nadia, primary, Chetta, Paolo, primary, Hallal, Tarek, primary, Cacciatore, Stefano, primary, Lalli, Daniela, primary, Luthold, Carole, primary, Homsy, Kevin, primary, Imada, Eddie L., primary, Syamala, Sudeepa, primary, Photopoulos, Cornelia, primary, Di Matteo, Anna, primary, de Polo, Anna, primary, Storaci, Alessandra Maria, primary, Huang, Ying, primary, Giunchi, Francesca, primary, Sheridan, Patricia A., primary, Michelotti, Gregory, primary, Nguyen, Quang-De, primary, Zhao, Xin, primary, Liu, Yang, primary, Davicioni, Elai, primary, Spratt, Daniel E., primary, Sabbioneda, Simone, primary, Maga, Giovanni, primary, Mucci, Lorelei A., primary, Ghigna, Claudia, primary, Marchionni, Luigi, primary, Butler, Lisa M., primary, Ellis, Leigh, primary, Bordeleau, François, primary, Loda, Massimo, primary, Vaira, Valentina, primary, Labbé, David P., primary, and Zadra, Giorgia, primary

Published
2024
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39. Data from Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer

Author

Boufaied, Nadia, primary, Chetta, Paolo, primary, Hallal, Tarek, primary, Cacciatore, Stefano, primary, Lalli, Daniela, primary, Luthold, Carole, primary, Homsy, Kevin, primary, Imada, Eddie L., primary, Syamala, Sudeepa, primary, Photopoulos, Cornelia, primary, Di Matteo, Anna, primary, de Polo, Anna, primary, Storaci, Alessandra Maria, primary, Huang, Ying, primary, Giunchi, Francesca, primary, Sheridan, Patricia A., primary, Michelotti, Gregory, primary, Nguyen, Quang-De, primary, Zhao, Xin, primary, Liu, Yang, primary, Davicioni, Elai, primary, Spratt, Daniel E., primary, Sabbioneda, Simone, primary, Maga, Giovanni, primary, Mucci, Lorelei A., primary, Ghigna, Claudia, primary, Marchionni, Luigi, primary, Butler, Lisa M., primary, Ellis, Leigh, primary, Bordeleau, François, primary, Loda, Massimo, primary, Vaira, Valentina, primary, Labbé, David P., primary, and Zadra, Giorgia, primary

Published
2024
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40. Supplementary Tables S1-S19 from Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer

Author

Boufaied, Nadia, primary, Chetta, Paolo, primary, Hallal, Tarek, primary, Cacciatore, Stefano, primary, Lalli, Daniela, primary, Luthold, Carole, primary, Homsy, Kevin, primary, Imada, Eddie L., primary, Syamala, Sudeepa, primary, Photopoulos, Cornelia, primary, Di Matteo, Anna, primary, de Polo, Anna, primary, Storaci, Alessandra Maria, primary, Huang, Ying, primary, Giunchi, Francesca, primary, Sheridan, Patricia A., primary, Michelotti, Gregory, primary, Nguyen, Quang-De, primary, Zhao, Xin, primary, Liu, Yang, primary, Davicioni, Elai, primary, Spratt, Daniel E., primary, Sabbioneda, Simone, primary, Maga, Giovanni, primary, Mucci, Lorelei A., primary, Ghigna, Claudia, primary, Marchionni, Luigi, primary, Butler, Lisa M., primary, Ellis, Leigh, primary, Bordeleau, François, primary, Loda, Massimo, primary, Vaira, Valentina, primary, Labbé, David P., primary, and Zadra, Giorgia, primary

Published
2024
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41. Supplementary Information from Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer

Author

Boufaied, Nadia, primary, Chetta, Paolo, primary, Hallal, Tarek, primary, Cacciatore, Stefano, primary, Lalli, Daniela, primary, Luthold, Carole, primary, Homsy, Kevin, primary, Imada, Eddie L., primary, Syamala, Sudeepa, primary, Photopoulos, Cornelia, primary, Di Matteo, Anna, primary, de Polo, Anna, primary, Storaci, Alessandra Maria, primary, Huang, Ying, primary, Giunchi, Francesca, primary, Sheridan, Patricia A., primary, Michelotti, Gregory, primary, Nguyen, Quang-De, primary, Zhao, Xin, primary, Liu, Yang, primary, Davicioni, Elai, primary, Spratt, Daniel E., primary, Sabbioneda, Simone, primary, Maga, Giovanni, primary, Mucci, Lorelei A., primary, Ghigna, Claudia, primary, Marchionni, Luigi, primary, Butler, Lisa M., primary, Ellis, Leigh, primary, Bordeleau, François, primary, Loda, Massimo, primary, Vaira, Valentina, primary, Labbé, David P., primary, and Zadra, Giorgia, primary

Published
2024
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42. Characterising the contribution of rare protein-coding germline variants to prostate cancer risk and severity in 37,184 cases

Author

Mitchell, Jonathan, primary, Camacho, Niedzica, additional, Shea, Patrick, additional, Stopsack, Konrad, additional, Joseph, Vijai, additional, Burren, Oliver Simon, additional, Dhindsa, Ryan, additional, Nag, Abhishek, additional, Berchuck, Jacob, additional, O'Neill, Amanda, additional, Abbasi, Ali, additional, Zoghbi, Anthony, additional, Alegre-Diaz, Jesus, additional, Kuri-Morales, Pablo, additional, Berumen, Jaime, additional, Tapia-Conyer, Roberto, additional, Emberson, Jonathan, additional, Torres, Jason, additional, Collins, Rory, additional, Wang, Quanli, additional, Goldstein, David, additional, Matakidou, Athena, additional, Haefliger, Carolina, additional, Anderson-Dring, Lauren, additional, March, Ruth, additional, Jobanputra, Vaidehi, additional, Dougherty, Brian, additional, Carss, Keren, additional, Petrovski, Slave, additional, Kantoff, Philip, additional, Offit, Kenneth, additional, Mucci, Lorelei, additional, Pomerantz, Mark, additional, and Fabre, Margarete, additional

Published
2024
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43. PD50-10 FREE PSA AND RISK OF GLEASON GRADE GROUP ≥2 AND FATAL PROSTATE CANCER IN BLACK MEN: IMPLICATIONS FOR RISK-STRATIFIED SCREENING

Author

Yim, Kendrick, primary, Magnani, Chris, additional, Carlsson, Sigrid, additional, Shrubsole, Martha, additional, Penney, Kathryn, additional, Lilja, Hans, additional, Vickers, Andrew, additional, Trinh, Quoc, additional, Eggener, Scott, additional, Mucci, Lorelei, additional, and Preston, Mark A., additional

Published
2024
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45. Alcohol Intake and Risk of Lethal Prostate Cancer in the Health Professionals Follow-Up Study.

Author

Downer, Mary K, Kenfield, Stacey A, Stampfer, Meir J, Wilson, Kathryn M, Dickerman, Barbra A, Giovannucci, Edward L, Rimm, Eric B, Wang, Molin, Mucci, Lorelei A, Willett, Walter C, Chan, June M, and Van Blarigan, Erin L

Subjects
Humans, Prostatic Neoplasms, Neoplasm Staging, Proportional Hazards Models, Risk, Cohort Studies, Follow-Up Studies, Prospective Studies, Alcohol Drinking, Health Occupations, Adult, Aged, Middle Aged, United States, Male, Prevention, Alcoholism, Alcohol Use and Health, Clinical Research, Substance Misuse, Cancer, Aging, Urologic Diseases, Prostate Cancer, Good Health and Well Being, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeIt is unknown whether alcohol intake is associated with the risk of lethal (metastatic or fatal) prostate cancer. We examine (1) whether alcohol intake among men at risk of prostate cancer is associated with diagnosis of lethal prostate cancer and (2) whether intake among men with nonmetastatic prostate cancer is associated with metastasis or death.MethodsThis prospective cohort study uses the Health Professionals Follow-Up Study (1986 to 2012). Our analysis of alcohol intake among men at risk of prostate cancer included 47,568 cancer-free men. Our analysis of alcohol intake among men with prostate cancer was restricted to 5,182 men diagnosed with nonmetastatic prostate cancer during follow-up. We examine the association of total alcohol, red and white wine, beer, and liquor with lethal prostate cancer and death. Multivariate Cox proportional hazards regression estimated hazard ratios (HRs) and 95% CIs.ResultsAlcohol drinkers had a lower risk of lethal prostate cancer (any v none: HR, 0.84 [95% CI, 0.71 to 0.99]) without a dose-response relationship. Total alcohol intake among patients with prostate cancer was not associated with progression to lethal prostate cancer (any v none: HR, 0.99 [95% CI, 0.57 to 1.72]), whereas moderate red wine intake was associated with a lower risk (any v none: HR, 0.50 [95% CI, 0.29 to 0.86]; P trend = .05). Compared with none, 15 to 30 g/d of total alcohol after prostate cancer diagnosis was associated with a lower risk of death (HR, 0.71 [95% CI, 0.50 to 1.00]), as was red wine (any v none: HR, 0.74 [95% CI, 0.57 to 0.97]; P trend = .007).ConclusionCancer-free men who consumed alcohol had a slightly lower risk of lethal prostate cancer compared with abstainers. Among men with prostate cancer, red wine was associated with a lower risk of progression to lethal disease. These observed associations merit additional study but provide assurance that moderate alcohol consumption is safe for patients with prostate cancer.

Published
2019

46. Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry.

Author

Matejcic, Marco, Saunders, Edward J, Dadaev, Tokhir, Brook, Mark N, Wang, Kan, Sheng, Xin, Olama, Ali Amin Al, Schumacher, Fredrick R, Ingles, Sue A, Govindasami, Koveela, Benlloch, Sara, Berndt, Sonja I, Albanes, Demetrius, Koutros, Stella, Muir, Kenneth, Stevens, Victoria L, Gapstur, Susan M, Tangen, Catherine M, Batra, Jyotsna, Clements, Judith, Gronberg, Henrik, Pashayan, Nora, Schleutker, Johanna, Wolk, Alicja, West, Catharine, Mucci, Lorelei, Kraft, Peter, Cancel-Tassin, Géraldine, Sorensen, Karina D, Maehle, Lovise, Grindedal, Eli M, Strom, Sara S, Neal, David E, Hamdy, Freddie C, Donovan, Jenny L, Travis, Ruth C, Hamilton, Robert J, Rosenstein, Barry, Lu, Yong-Jie, Giles, Graham G, Kibel, Adam S, Vega, Ana, Bensen, Jeanette T, Kogevinas, Manolis, Penney, Kathryn L, Park, Jong Y, Stanford, Janet L, Cybulski, Cezary, Nordestgaard, Børge G, Brenner, Hermann, Maier, Christiane, Kim, Jeri, Teixeira, Manuel R, Neuhausen, Susan L, De Ruyck, Kim, Razack, Azad, Newcomb, Lisa F, Lessel, Davor, Kaneva, Radka, Usmani, Nawaid, Claessens, Frank, Townsend, Paul A, Gago-Dominguez, Manuela, Roobol, Monique J, Menegaux, Florence, Khaw, Kay-Tee, Cannon-Albright, Lisa A, Pandha, Hardev, Thibodeau, Stephen N, Schaid, Daniel J, PRACTICAL Consortium, Wiklund, Fredrik, Chanock, Stephen J, Easton, Douglas F, Eeles, Rosalind A, Kote-Jarai, Zsofia, Conti, David V, and Haiman, Christopher A

Subjects
PRACTICAL Consortium
Abstract

The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.

Published
2019

47. Expression of IGF/insulin receptor in prostate cancer tissue and progression to lethal disease

Author

Ahearn, Thomas U, Peisch, Sam, Pettersson, Andreas, Ebot, Ericka M, Zhou, Cindy Ke, Graff, Rebecca E, Sinnott, Jennifer A, Fazli, Ladan, Judson, Gregory L, Bismar, Tarek A, Rider, Jennifer R, Gerke, Travis, Chan, June M, Fiorentino, Michelangelo, Flavin, Richard, Sesso, Howard D, Finn, Stephen, Giovannucci, Edward L, Gleave, Martin, Loda, Massimo, Li, Zhe, Pollak, Michael, and Mucci, Lorelei A

Subjects
Clinical Research, Aging, Prostate Cancer, Diabetes, Urologic Diseases, Cancer, 2.1 Biological and endogenous factors, Aetiology, Aged, Apoptosis, Biomarkers, Tumor, Cell Proliferation, Disease Progression, Gene Expression Regulation, Neoplastic, Humans, Insulin, Insulin-Like Growth Factor I, Male, Oncogene Proteins, Fusion, Prostatic Neoplasms, Receptor, IGF Type 1, Receptor, Insulin, Receptors, Somatomedin, Signal Transduction, Transcriptional Regulator ERG, Transdisciplinary Prostate Cancer Partnership, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Circulating insulin-like growth factor-1 (IGF-1) is consistently associated with prostate cancer risk. IGF-1 binds to IGF-1 receptor (IGF1R) and insulin receptor (IR), activating cancer hallmark pathways. Experimental evidence suggests that TMPRSS2:ERG may interact with IGF/insulin signaling to influence progression. We investigated IGF1R and IR expression and its association with lethal prostate cancer among 769 men. Protein expression of IGF1R, IR and ERG (i.e. a surrogate of ERG fusion genes) were assayed by immunohistochemistry. Cox models estimated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for clinical characteristics. Among patients, 29% had strong tumor IGF1R expression and 10% had strong IR expression. During a mean follow-up of 13.2 years through 2012, 80 men (11%) developed lethal disease. Tumors with strong IGF1R or IR expression showed increased cell proliferation, decreased apoptosis and a higher prevalence of ERG. In multivariable models, strong IGF1R was associated with a borderline increased risk of lethal prostate cancer (HR 1.7; 95% CI 0.9-3.1). The association appeared greater in ERG-positive tumors (HR 2.8; 95% CI 0.9-8.4) than in ERG-negative tumors (HR 1.3; 95% CI 0.6-3.0, p-heterogeneity 0.08). There was no association between IR and lethal prostate cancer (HR 0.8; 95% CI 0.4-1.9). These results suggest that tumor IGF1R expression may play a role in prostate cancer progression to a lethal phenotype and that ERG-positive tumors may be more sensitive to IGF signaling. These data may improve our understanding of IGF signaling in prostate cancer and suggest therapeutic options for disease subtypes.

Published
2018

48. A prospective study of aspirin use and prostate cancer risk by TMPRSS2:ERG status

Author

Stopsack, Konrad H, Gonzalez-Feliciano, Amparo G, Peisch, Samuel F, Downer, Mary K, Gage, Riley A, Finn, Stephen, Lis, Rosina T, Graff, Rebecca E, Pettersson, Andreas, Pernar, Claire H, Loda, Massimo, Kantoff, Philip W, Ahearn, Thomas U, and Mucci, Lorelei A

Subjects
Biomedical and Clinical Sciences, Health Sciences, Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Prevention, Prostate Cancer, Genetics, Urologic Diseases, Cancer, Aging, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Aged, Anti-Inflammatory Agents, Non-Steroidal, Aspirin, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Oncogene Proteins, Fusion, Prognosis, Prospective Studies, Prostatic Neoplasms, United States, Transdisciplinary Prostate Cancer Partnership, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

Background: In a case-control study, aspirin use was associated with a lower risk of a common prostate cancer molecular subtype, the TMPRSS2:ERG gene fusion. We sought to validate this finding in a prospective cohort.Methods: In the Health Professionals Follow-up Study, 49,395 men reported on aspirin use on biennial questionnaires and were followed for prostate cancer incidence over 23 years. TMPRSS2:ERG status was assessed by IHC for presence of ERG on archival tumor specimens for 912 patients with prostate cancer, of whom 48% were ERG-positive.Results: In multivariable models, we found no association between regular use of aspirin and risk of ERG-positive prostate cancer (HR, 1.02; 95% confidence interval, 0.85-1.23), nor any association with duration or frequency of aspirin use. In restricting to cases with either high Gleason grade or advanced stage disease, there remained no association with aspirin use.Conclusions: Data from this prospective study with repeated assessments of aspirin use do not support the hypothesis that aspirin use is associated with a lower risk of ERG-positive prostate cancer.Impact: Aspirin use is unlikely to lower the risk of this common molecular subtype of prostate cancer. However, there is emerging data supporting the role of other lifestyle and genetic factors underlying the development of the TMPRSS2:ERG fusion. Cancer Epidemiol Biomarkers Prev; 27(10); 1231-3. ©2018 AACR.

Published
2018

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