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202. Linking Physical Activity to Breast Cancer Risk via Inflammation, Part 1: The Effect of Physical Activity on Inflammation

Author

Swain, Christopher T.V., primary, Drummond, Ann E., additional, Milne, Roger L., additional, English, Dallas R., additional, Brown, Kristy A., additional, Lou, Makayla W.C., additional, Boing, Leonessa, additional, Bageley, Amy, additional, Skinner, Tina L., additional, van Roekel, Eline H., additional, Moore, Melissa M., additional, Gaunt, Tom R., additional, Martin, Richard M., additional, Lewis, Sarah J., additional, and Lynch, Brigid M., additional

Published
2023
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203. Linking Physical Activity to Breast Cancer via Inflammation, Part 2: The Effect of Inflammation on Breast Cancer Risk

Author

Lou, Makayla W.C., primary, Drummond, Ann E., additional, Swain, Christopher T.V., additional, Milne, Roger L., additional, English, Dallas R., additional, Brown, Kristy A., additional, van Roekel, Eline H., additional, Skinner, Tina L., additional, Moore, Melissa M., additional, Gaunt, Tom R., additional, Martin, Richard M., additional, Lewis, Sarah J., additional, and Lynch, Brigid M., additional

Published
2023
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204. Patient-Reported Outcomes 12 Years after Localized Prostate Cancer Treatment

Author

Donovan, Jenny L., primary, Hamdy, Freddie C., additional, Lane, J. Athene, additional, Young, Grace J., additional, Metcalfe, Chris, additional, Walsh, Eleanor I., additional, Davis, Michael, additional, Steuart-Feilding, Thomas, additional, Blazeby, Jane M., additional, Avery, Kerry N. L., additional, Martin, Richard M., additional, Bollina, Prasad, additional, Doble, Andrew, additional, Doherty, Alan, additional, Gillatt, David, additional, Gnanapragasam, Vincent, additional, Hughes, Owen, additional, Kockelbergh, Roger, additional, Kynaston, Howard, additional, Paul, Alan, additional, Paez, Edgar, additional, Powell, Phillip, additional, Rosario, Derek J., additional, Rowe, Edward, additional, Mason, Malcolm, additional, Catto, James W. F., additional, Peters, Tim J., additional, Wade, Julia, additional, Turner, Emma L., additional, Williams, Naomi J., additional, Oxley, Jon, additional, Staffurth, John, additional, Bryant, Richard J., additional, and Neal, David E., additional

Published
2023
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205. Leisure time sedentary behaviour and risks of breast, colorectal, and prostate cancer: A Mendelian randomization analysis

Author

Papadimitriou, Nikos, primary, Kazmi, Nabila, additional, Dimou, Niki, additional, Tsilidis, Konstantinos K, additional, Martin, Richard M, additional, Lewis, Sarah J, additional, Lynch, Brigid M, additional, Hoffmeister, Michael, additional, Kweon, Sun-Seog, additional, Li, Li, additional, Milne, Roger L, additional, Sakoda, Lori C, additional, Schoen, Robert E, additional, Phipps, Amanda I, additional, Figueiredo, Jane C, additional, Peters, Ulrike, additional, Dixon-Suen, Suzanne C., additional, Gunter, Marc J, additional, and Murphy, Neil, additional

Published
2023
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207. Correction: IGF-1 and hyperglycaemia-induced FOXA1 and IGFBP-2 affect epithelial to mesenchymal transition in prostate epithelial cells

Author

Mansor, Rehanna, primary, Holly, Jeff, additional, Barker, Rachel, additional, Biernacka, Kalina, additional, Zielinska, Hanna, additional, Koupparis, Anthony, additional, Rowe, Edward, additional, Oxley, Jon, additional, Sewell, Alex, additional, Martin, Richard M., additional, Lane, Athene, additional, Hackshaw-McGeagh, Lucy, additional, and Perks, Claire, additional

Published
2023
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209. Spin-resolved electronic structure of ferromagnetic triple-layered ruthenate Sr$_4$Ru$_3$O$_{10}$

Author

Ngabonziza, Prosper, Denlinger, Jonathan D., Fedorov, Alexei V., Cao, Gang, Allen, J. W., Gebreyesus, G., and Martin, Richard M.

Subjects
Condensed Matter - Other Condensed Matter, Condensed Matter - Strongly Correlated Electrons, Strongly Correlated Electrons (cond-mat.str-el), cond-mat.other, FOS: Physical sciences, cond-mat.str-el, Other Condensed Matter (cond-mat.other)
Abstract

High-resolution angle- and spin-resolved photoemission spectroscopy reveals new features of the electronic structure of the ferromagnetic triple-layered ruthenate Sr$_4$Ru$_3$O$_{10}$. There are narrow spectral peaks $\sim$30 meV below the Fermi-level in two regions of the Brillouin zone: a hole-like band at the zone-center and a saddle-point van Hove singularity at the zone edge. Below T$_c$ each feature is almost completely spin-polarized, with opposite sign polarization and with strong Kondo-coherence-like temperature-dependent spectral weight variation suggestive of strong Hund's metal correlations. In addition, there are distinct Fermi surfaces for wide electron-like minority spin bands around the zone center and narrow hole-like majority spin Fermi surface contours around the zone corners. The origin of these features is in general agreement with density functional calculations, if they are shifted to reduce the exchange splitting, and scaled to take into account effects of correlation. Furthermore, the deduced narrow band origins from the tri-layer splitting of $d_{xz/yz}$ orbitals implies a layer-specific spin-polarization contribution from the narrow bands. Over a larger energy range, net spin-majority polarization of incoherent Ru $d$-bands is observed to extend down to the top of the oxygen bands, where additional narrow oxygen bands contribute to the magnetism with spin-minority polarization., Comment: 11 pages, 5 figures plus supplement 8 pages, 4 figures

Published
2023
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210. Physical activity, sedentary time and breast cancer risk: a Mendelian randomisation study

Author

Dixon-Suen, Suzanne C, Lewis, Sarah J, Martin, Richard M, English, Dallas R, Boyle, Terry, Giles, Graham G, Michailidou, Kyriaki, Bolla, Manjeet K, Wang, Qin, Dennis, Joe, Lush, Michael, Investigators, Abctb, Ahearn, Thomas U, Ambrosone, Christine B, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Augustinsson, Annelie, Auvinen, Päivi, Beane Freeman, Laura E, Becher, Heiko, Beckmann, Matthias W, Behrens, Sabine, Bermisheva, Marina, Blomqvist, Carl, Bogdanova, Natalia V, Bojesen, Stig E, Bonanni, Bernardo, Brenner, Hermann, Brüning, Thomas, Buys, Saundra S, Camp, Nicola J, Campa, Daniele, Canzian, Federico, Castelao, Jose E, Cessna, Melissa H, Chang-Claude, Jenny, Chanock, Stephen J, Clarke, Christine L, Conroy, Don M, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Daly, Mary B, Devilee, Peter, Dörk, Thilo, Dwek, Miriam, Eccles, Diana M, Eliassen, A Heather, Engel, Christoph, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Fletcher, Olivia, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, García-Closas, Montserrat, García-Sáenz, José A, Goldberg, Mark S, Guénel, Pascal, Gündert, Melanie, Hahnen, Eric, Haiman, Christopher A, Häberle, Lothar, Håkansson, Niclas, Hall, Per, Hamann, Ute, Hart, Steven N, Harvie, Michelle, Hillemanns, Peter, Hollestelle, Antoinette, Hooning, Maartje J, Hoppe, Reiner, Hopper, John, Howell, Anthony, Hunter, David J, Jakubowska, Anna, Janni, Wolfgang, John, Esther M, Jung, Audrey, Kaaks, Rudolf, Keeman, Renske, Kitahara, Cari M, Koutros, Stella, Kraft, Peter, Kristensen, Vessela N, Kubelka-Sabit, Katerina, Kurian, Allison W, Lacey, James V, Lambrechts, Diether, Le Marchand, Loic, Lindblom, Annika, Loibl, Sibylle, Lubiński, Jan, Mannermaa, Arto, Manoochehri, Mehdi, Margolin, Sara, Martinez, Maria Elena, Mavroudis, Dimitrios, Menon, Usha, Mulligan, Anna Marie, Murphy, Rachel A, Collaborators, Nbcs, Nevanlinna, Heli, Nevelsteen, Ines, Newman, William G, Offit, Kenneth, Olshan, Andrew F, Olsson, Håkan, Orr, Nick, Patel, Alpa, Peto, Julian, Plaseska-Karanfilska, Dijana, Presneau, Nadege, Rack, Brigitte, Radice, Paolo, Rees-Punia, Erika, Rennert, Gad, Rennert, Hedy S, Romero, Atocha, Saloustros, Emmanouil, Sandler, Dale P, Schmidt, Marjanka K, Schmutzler, Rita K, Schwentner, Lukas, Scott, Christopher, Shah, Mitul, Shu, Xiao-Ou, Simard, Jacques, Southey, Melissa C, Stone, Jennifer, Surowy, Harald, Swerdlow, Anthony J, Tamimi, Rulla M, Tapper, William J, Taylor, Jack A, Terry, Mary Beth, Tollenaar, Rob AEM, Troester, Melissa A, Truong, Thérèse, Untch, Michael, Vachon, Celine M, Joseph, Vijai, Wappenschmidt, Barbara, Weinberg, Clarice R, Wolk, Alicja, Yannoukakos, Drakoulis, Zheng, Wei, Ziogas, Argyrios, Dunning, Alison M, Pharoah, Paul DP, Easton, Douglas F, Milne, Roger L, Lynch, Brigid M, Breast Cancer Association Consortium, Law and Economics, Medical Oncology, Dixon-Suen, Suzanne C [0000-0003-3714-8386], Boyle, Terry [0000-0001-6741-330X], Romero, Atocha [0000-0002-1634-7397], Lynch, Brigid M [0000-0001-8060-547X], Apollo - University of Cambridge Repository, Dixon-Suen, Suzanne C, Lewis, Sarah J, Martin, Richard M, English, Dallas R, Boyle, Terry, Lynch, Brigid M, ABCTB Investigators, NBCS Collaborators, and Breast Canc Assoc Consortium

Subjects
Breast Neoplasms, Physical Therapy, Sports Therapy and Rehabilitation, Polymorphism, Single Nucleotide, Article, Basic medicine, breast cancer risk, SDG 3 - Good Health and Well-being, Risk Factors, sedentary behaviour, Genetics, Humans, Orthopedics and Sports Medicine, Breast, causal inference, Exercise, Manchester Cancer Research Centre, Physical activity, genetic variants, Breast Neoplasms/epidemiology, ResearchInstitutes_Networks_Beacons/mcrc, General Medicine, Mendelian Randomization Analysis, FOS: Biological sciences, Clinical medicine, instruments, physical inactivity, Sedentary Behaviour, Female, ICEP, Sedentary Behavior
Abstract

ObjectivesPhysical inactivity and sedentary behaviour are associated with higher breast cancer risk in observational studies, but ascribing causality is difficult. Mendelian randomisation (MR) assesses causality by simulating randomised trial groups using genotype. We assessed whether lifelong physical activity or sedentary time, assessed using genotype, may be causally associated with breast cancer risk overall, pre/post-menopause, and by case-groups defined by tumour characteristics.MethodsWe performed two-sample inverse-variance-weighted MR using individual-level Breast Cancer Association Consortium case-control data from 130 957 European-ancestry women (69 838 invasive cases), and published UK Biobank data (n=91 105–377 234). Genetic instruments were single nucleotide polymorphisms (SNPs) associated in UK Biobank with wrist-worn accelerometer-measured overall physical activity (nsnps=5) or sedentary time (nsnps=6), or accelerometer-measured (nsnps=1) or self-reported (nsnps=5) vigorous physical activity.ResultsGreater genetically-predicted overall activity was associated with lower breast cancer overall risk (OR=0.59; 95% confidence interval (CI) 0.42 to 0.83 per-standard deviation (SD;~8 milligravities acceleration)) and for most case-groups. Genetically-predicted vigorous activity was associated with lower risk of pre/perimenopausal breast cancer (OR=0.62; 95% CI 0.45 to 0.87,≥3 vs. 0 self-reported days/week), with consistent estimates for most case-groups. Greater genetically-predicted sedentary time was associated with higher hormone-receptor-negative tumour risk (OR=1.77; 95% CI 1.07 to 2.92 per-SD (~7% time spent sedentary)), with elevated estimates for most case-groups. Results were robust to sensitivity analyses examining pleiotropy (including weighted-median-MR, MR-Egger).ConclusionOur study provides strong evidence that greater overall physical activity, greater vigorous activity, and lower sedentary time are likely to reduce breast cancer risk. More widespread adoption of active lifestyles may reduce the burden from the most common cancer in women.

Published
2022

212. The effects of height and BMI on prostate cancer incidence and mortality: a Mendelian randomization study in 20,848 cases and 20,214 controls from the PRACTICAL consortium

Author

PRACTICAL consortium, Davies, Neil M., Gaunt, Tom R., Lewis, Sarah J., Holly, Jeff, Donovan, Jenny L., Hamdy, Freddie C., Kemp, John P., Eeles, Rosalind, Easton, Doug, Kote-Jarai, Zsofia, Olama, Ali Amin Al, Benlloch, Sara, Muir, Kenneth, Giles, Graham G., Wiklund, Fredrik, Gronberg, Henrik, Haiman, Christopher A., Schleutker, Johanna, Nordestgaard, Børge G., Travis, Ruth C., Neal, David, Pashayan, Nora, Khaw, Kay-Tee, Stanford, Janet L., Blot, William J., Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S., Cybulski, Cezary, Cannon-Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R., Pandha, Hardev, Lathrop, Mark, Smith, George Davey, and Martin, Richard M.

Published
2015

213. Publisher Correction: Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author

Conti, David V., Darst, Burcu F., Moss, Lilit C., Saunders, Edward J., Sheng, Xin, Chou, Alisha, Schumacher, Fredrick R., Olama, Ali Amin Al, Benlloch, Sara, Dadaev, Tokhir, Brook, Mark N., Sahimi, Ali, Hoffmann, Thomas J., Takahashi, Atushi, Matsuda, Koichi, Momozawa, Yukihide, Fujita, Masashi, Muir, Kenneth, Lophatananon, Artitaya, Wan, Peggy, Le Marchand, Loic, Wilkens, Lynne R., Stevens, Victoria L., Gapstur, Susan M., Carter, Brian D., Schleutker, Johanna, Tammela, Teuvo L. J., Sipeky, Csilla, Auvinen, Anssi, Giles, Graham G., Southey, Melissa C., MacInnis, Robert J., Cybulski, Cezary, Wokołorczyk, Dominika, Lubiński, Jan, Neal, David E., Donovan, Jenny L., Hamdy, Freddie C., Martin, Richard M., Nordestgaard, Børge G., Nielsen, Sune F., Weischer, Maren, Bojesen, Stig E., Røder, Martin Andreas, Iversen, Peter, Batra, Jyotsna, Chambers, Suzanne, Moya, Leire, Horvath, Lisa, Clements, Judith A., Tilley, Wayne, Risbridger, Gail P., Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordström, Tobias, Pashayan, Nora, Dunning, Alison M., Ghoussaini, Maya, Travis, Ruth C., Key, Tim J., Riboli, Elio, Park, Jong Y., Sellers, Thomas A., Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie J., Mucci, Lorelei A., Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David J., Penney, Kathryn L., Turman, Constance, Tangen, Catherine M., Goodman, Phyllis J., Thompson, Jr., Ian M., Hamilton, Robert J., Fleshner, Neil E., Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet L., Ostrander, Elaine A., Geybels, Milan S., Koutros, Stella, Freeman, Laura E. Beane, Stampfer, Meir, Wolk, Alicja, Håkansson, Niclas, Andriole, Gerald L., Hoover, Robert N., Machiela, Mitchell J., Sørensen, Karina Dalsgaard, Borre, Michael, Blot, William J., Zheng, Wei, Yeboah, Edward D., Mensah, James E., Lu, Yong-Jie, Zhang, Hong-Wei, Feng, Ninghan, Mao, Xueying, Wu, Yudong, Zhao, Shan-Chao, Sun, Zan, Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., West, Catharine M. L., Burnet, Neil, Barnett, Gill, Maier, Christiane, Schnoeller, Thomas, Luedeke, Manuel, Kibel, Adam S., Drake, Bettina F., Cussenot, Olivier, Cancel-Tassin, Géraldine, Menegaux, Florence, Truong, Thérèse, Koudou, Yves Akoli, John, Esther M., Grindedal, Eli Marie, Maehle, Lovise, Khaw, Kay-Tee, Ingles, Sue A., Stern, Mariana C., Vega, Ana, Gómez-Caamaño, Antonio, Fachal, Laura, Rosenstein, Barry S., Kerns, Sarah L., Ostrer, Harry, Teixeira, Manuel R., Paulo, Paula, Brandão, Andreia, Watya, Stephen, Lubwama, Alexander, Bensen, Jeannette T., Fontham, Elizabeth T. H., Mohler, James, Taylor, Jack A., Kogevinas, Manolis, Llorca, Javier, Castaño-Vinyals, Gemma, Cannon-Albright, Lisa, Teerlink, Craig C., Huff, Chad D., Strom, Sara S., Multigner, Luc, Blanchet, Pascal, Brureau, Laurent, Kaneva, Radka, Slavov, Chavdar, Mitev, Vanio, Leach, Robin J., Weaver, Brandi, Brenner, Hermann, Cuk, Katarina, Holleczek, Bernd, Saum, Kai-Uwe, Klein, Eric A., Hsing, Ann W., Kittles, Rick A., Murphy, Adam B., Logothetis, Christopher J., Kim, Jeri, Neuhausen, Susan L., Steele, Linda, Ding, Yuan Chun, Isaacs, William B., Nemesure, Barbara, Hennis, Anselm J. M., Carpten, John, Pandha, Hardev, Michael, Agnieszka, De Ruyck, Kim, De Meerleer, Gert, Ost, Piet, Xu, Jianfeng, Razack, Azad, Lim, Jasmine, Teo, Soo-Hwang, Newcomb, Lisa F., Lin, Daniel W., Fowke, Jay H., Neslund-Dudas, Christine, Rybicki, Benjamin A., Gamulin, Marija, Lessel, Davor, Kulis, Tomislav, Usmani, Nawaid, Singhal, Sandeep, Parliament, Matthew, Claessens, Frank, Joniau, Steven, Van den Broeck, Thomas, Gago-Dominguez, Manuela, Castelao, Jose Esteban, Martinez, Maria Elena, Larkin, Samantha, Townsend, Paul A., Aukim-Hastie, Claire, Bush, William S., Aldrich, Melinda C., Crawford, Dana C., Srivastava, Shiv, Cullen, Jennifer C., Petrovics, Gyorgy, Casey, Graham, Roobol, Monique J., Jenster, Guido, van Schaik, Ron H. N., Hu, Jennifer J., Sanderson, Maureen, Varma, Rohit, McKean-Cowdin, Roberta, Torres, Mina, Mancuso, Nicholas, Berndt, Sonja I., Van Den Eeden, Stephen K., Easton, Douglas F., Chanock, Stephen J., Cook, Michael B., Wiklund, Fredrik, Nakagawa, Hidewaki, Witte, John S., Eeles, Rosalind A., Kote-Jarai, Zsofia, and Haiman, Christopher A.

Published
2021
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214. Characterizing prostate cancer risk through multi-ancestry genome-wide discovery of 187 novel risk variants

Author

Wang, Anqi, Shen, Jiayi, Rodriguez, Alex A., Saunders, Edward J., Chen, Fei, Janivara, Rohini, Darst, Burcu F., Sheng, Xin, Xu, Yili, Chou, Alisha J., Benlloch, Sara, Dadaev, Tokhir, Brook, Mark N., Plym, Anna, Sahimi, Ali, Hoffman, Thomas J., 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 P., Schleutker, Johanna, Tammela, Teuvo L. J., Sipeky, Csilla, Auvinen, Anssi, Giles, Graham G., Southey, Melissa C., MacInnis, Robert J., Cybulski, Cezary, Wokolorczyk, Dominika, Lubinski, Jan, Rentsch, Christopher T., Cho, Kelly, Mcmahon, Benjamin H., Neal, David E., Donovan, Jenny L., Hamdy, Freddie C., Martin, Richard M., Nordestgaard, Borge G., Nielsen, Sune F., Weischer, Maren, Bojesen, Stig E., Røder, Andreas, Stroomberg, Hein V., Batra, Jyotsna, Chambers, Suzanne, Horvath, Lisa, Clements, Judith A., Tilly, Wayne, Risbridger, Gail P., Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordstrom, Tobias, Pashayan, Nora, Dunning, Alison M., Ghoussaini, Maya, Travis, Ruth C., Key, Tim J., Riboli, Elio, Park, Jong Y., Sellers, Thomas A., Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie, Cook, Michael B., Mucci, Lorelei A., Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David J., Penney, Kathryn L., Turman, Constance, Tangen, Catherine M., Goodman, Phyllis J., Thompson, Ian M., Hamilton, Robert J., Fleshner, Neil E., Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet L., Ostrander, Elaine A., Koutros, Stella, Beane Freeman, Laura E., Stampfer, Meir, Wolk, Alicja, Håkansson, Niclas, Andriole, Gerald L., Hoover, Robert N., Machiela, Mitchell J., Sørensen, Karina Dalsgaard, Borre, Michael, Blot, William J., Zheng, Wei, Yeboah, Edward D., Mensah, James E., Lu, Yong-Jie, Zhang, Hong-Wei, Feng, Ninghan, Mao, Xueying, Wu, Yudong, Zhao, Shan-Chao, Sun, Zan, Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., West, Catharine M. L., Barnett, Gill, Maier, Christiane, Schnoeller, Thomas, Luedeke, Manuel, Kibel, Adam S., Drake, Bettina F., Cussenot, Olivier, Cancel-Tassin, Geraldine, Menegaux, Florence, Truong, Thérèse, Koudou, Yves Akoli, John, Esther M., Grindedal, Eli Marie, Maehle, Lovise, Khaw, Kay-Tee, Ingles, Sue A., Stern, Mariana C., Vega, Ana, Gómez-Caamaño, Antonio, Fachal, Laura, Rosenstein, Barry S., Kerns, Sarah L., Ostrer, Harry, Teixeira, Manuel R., Paulo, Paula, Brandão, Andreia, Watya, Stephen, Lubwama, Alexander, Bensen, Jeannette T., Butler, Ebonee N., Mohler, James L., Taylor, Jack A., Kogevinas, Manolis, Dierssen-Sotos, Trinidad, Castaño-Vinyals, Gemma, Cannon-Albright, Lisa, Teerlink, Craig C., Huff, Chad D., Pilie, Patrick, Yu, Yao, Bohlender, Ryan J., Gu, Jian, Strom, Sara S., Multigner, Luc, Blanchet, Pascal, Brureau, Laurent, Kaneva, Radka, Slavov, Chavdar, Mitev, Vanio, Leach, Robin J., Brenner, Hermann, Chen, Xuechen, Holleczek, Bernd, Schöttker, Ben, Klein, Eric A., Hsing, Ann W., Kittles, Rick A., Murphy, Adam B., Logothetis, Christopher J., Kim, Jeri, Neuhausen, Susan L., Steele, Linda, Ding, Yuan Chun, Isaacs, William B., Nemesure, Barbara, Hennis, Anselm J. M., Carpten, John, Pandha, Hardev, Michael, Agnieszka, De Ruyck, Kim, De Meerleer, Gert, Ost, Piet, Xu, Jianfeng, Razack, Azad, Lim, Jasmine, Teo, Soo-Hwang, Newcomb, Lisa F., Lin, Daniel W., Fowke, Jay H., Neslund-Dudas, Christine M., Rybicki, Benjamin A., Gamulin, Marija, Lessel, Davor, Kulis, Tomislav, Usmani, Nawaid, Abraham, Aswin, Singhal, Sandeep, Parliament, Matthew, Claessens, Frank, Joniau, Steven, Van den Broeck, Thomas, Gago-Dominguez, Manuela, Castelao, Jose Esteban, Martinez, Maria Elena, Larkin, Samantha, Townsend, Paul A., Aukim-Hastie, Claire, Bush, William S., Aldrich, Melinda C., Crawford, Dana C., Srivastava, Shiv, Cullen, Jennifer, Petrovics, Gyorgy, Casey, Graham, Wang, Ying, Tettey, Yao, Lachance, Joseph, Tang, Wei, Biritwum, Richard B., Adjei, Andrew A., Tay, Evelyn, Truelove, Ann, Niwa, Shelley, Yamoah, Kosj, Govindasami, Koveela, Chokkalingam, Anand P., Keaton, Jacob M., Hellwege, Jacklyn N., Clark, Peter E., Jalloh, Mohamed, Gueye, Serigne M., Niang, Lamine, Ogunbiyi, Olufemi, Shittu, Olayiwola, Amodu, Olukemi, Adebiyi, Akindele O., Aisuodionoe-Shadrach, Oseremen I., Ajibola, Hafees O., Jamda, Mustapha A., Oluwole, Olabode P., Nwegbu, Maxwell, Adusei, Ben, Mante, Sunny, Darkwa-Abrahams, Afua, Diop, Halimatou, Gundell, Susan M., Roobol, Monique J., Jenster, Guido, van Schaik, Ron H. N., Hu, Jennifer J., Sanderson, Maureen, Kachuri, Linda, Varma, Rohit, McKean-Cowdin, Roberta, Torres, Mina, Preuss, Michael H., Loos, Ruth J. F., Zawistowski, Matthew, Zöllner, Sebastian, Lu, Zeyun, Van Den Eeden, Stephen K., Easton, Douglas F., Ambs, Stefan, Edwards, Todd L., Mägi, Reedik, Rebbeck, Timothy R., Fritsche, Lars, Chanock, Stephen J., Berndt, Sonja I., Wiklund, Fredrik, Nakagawa, Hidewaki, Witte, John S., Gaziano, J. Michael, Justice, Amy C., Mancuso, Nick, Terao, Chikashi, Eeles, Rosalind A., Kote-Jarai, Zsofia, Madduri, Ravi K., Conti, David V., and Haiman, Christopher A.

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
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216. Genetically proxied glucose-lowering drug target perturbation and risk of cancer: a Mendelian randomisation analysis.

Author

Yarmolinsky, James, Bouras, Emmanouil, Constantinescu, Andrei, Burrows, Kimberley, Bull, Caroline J., Vincent, Emma E., Martin, Richard M., Dimopoulou, Olympia, Lewis, Sarah J., Moreno, Victor, Vujkovic, Marijana, Chang, Kyong-Mi, Voight, Benjamin F., Tsao, Philip S., Gunter, Marc J., Hampe, Jochen, Pellatt, Andrew J., Pharoah, Paul D. P., Schoen, Robert E., and Gallinger, Steven

Abstract

Aims/hypothesis: Epidemiological studies have generated conflicting findings on the relationship between glucose-lowering medication use and cancer risk. Naturally occurring variation in genes encoding glucose-lowering drug targets can be used to investigate the effect of their pharmacological perturbation on cancer risk. Methods: We developed genetic instruments for three glucose-lowering drug targets (peroxisome proliferator activated receptor γ [PPARG]; sulfonylurea receptor 1 [ATP binding cassette subfamily C member 8 (ABCC8)]; glucagon-like peptide 1 receptor [GLP1R]) using summary genetic association data from a genome-wide association study of type 2 diabetes in 148,726 cases and 965,732 controls in the Million Veteran Program. Genetic instruments were constructed using cis-acting genome-wide significant (p<5×10−8) SNPs permitted to be in weak linkage disequilibrium (r2<0.20). Summary genetic association estimates for these SNPs were obtained from genome-wide association study (GWAS) consortia for the following cancers: breast (122,977 cases, 105,974 controls); colorectal (58,221 cases, 67,694 controls); prostate (79,148 cases, 61,106 controls); and overall (i.e. site-combined) cancer (27,483 cases, 372,016 controls). Inverse-variance weighted random-effects models adjusting for linkage disequilibrium were employed to estimate causal associations between genetically proxied drug target perturbation and cancer risk. Co-localisation analysis was employed to examine robustness of findings to violations of Mendelian randomisation (MR) assumptions. A Bonferroni correction was employed as a heuristic to define associations from MR analyses as 'strong' and 'weak' evidence. Results: In MR analysis, genetically proxied PPARG perturbation was weakly associated with higher risk of prostate cancer (for PPARG perturbation equivalent to a 1 unit decrease in inverse rank normal transformed HbA1c: OR 1.75 [95% CI 1.07, 2.85], p=0.02). In histological subtype-stratified analyses, genetically proxied PPARG perturbation was weakly associated with lower risk of oestrogen receptor-positive breast cancer (OR 0.57 [95% CI 0.38, 0.85], p=6.45×10−3). In co-localisation analysis, however, there was little evidence of shared causal variants for type 2 diabetes liability and cancer endpoints in the PPARG locus, although these analyses were likely underpowered. There was little evidence to support associations between genetically proxied PPARG perturbation and colorectal or overall cancer risk or between genetically proxied ABCC8 or GLP1R perturbation with risk across cancer endpoints. Conclusions/interpretation: Our drug target MR analyses did not find consistent evidence to support an association of genetically proxied PPARG, ABCC8 or GLP1R perturbation with breast, colorectal, prostate or overall cancer risk. Further evaluation of these drug targets using alternative molecular epidemiological approaches may help to further corroborate the findings presented in this analysis. Data availability: Summary genetic association data for select cancer endpoints were obtained from the public domain: breast cancer (https://bcac.ccge.medschl.cam.ac.uk/bcacdata/); and overall prostate cancer (http://practical.icr.ac.uk/blog/). Summary genetic association data for colorectal cancer can be accessed by contacting GECCO (kafdem at fredhutch.org). Summary genetic association data on advanced prostate cancer can be accessed by contacting PRACTICAL (practical at icr.ac.uk). Summary genetic association data on type 2 diabetes from Vujkovic et al (Nat Genet, 2020) can be accessed through dbGAP under accession number phs001672.v3.p1 (pha004945.1 refers to the European-specific summary statistics). UK Biobank data can be accessed by registering with UK Biobank and completing the registration form in the Access Management System (AMS) (https://www.ukbiobank.ac.uk/enable-your-research/apply-for-access). [ABSTRACT FROM AUTHOR]

Published
2023
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217. Mendelian randomization study of sleep traits and risk of colorectal cancer

Author

Dimopoulou, Olympia, primary, Fuller, Harriett, additional, Richmond, Rebecca C, additional, Bouras, Emmanouil, additional, Hayes, Bryony, additional, Dimou, Niki, additional, Murphy, Neil, additional, Brenner, Hermann, additional, Gsur, Andrea, additional, Marchand, Loic Le, additional, Moreno, Victor, additional, Pai, Rish K, additional, Phipps, Amanda I, additional, Um, Caroline Y, additional, Duijnhoven, Franzel JB, additional, Vodicka, Pavel, additional, Martin, Richard M, additional, Platz, Elizabeth A, additional, Gunter, Marc J, additional, Peters, Ulrike, additional, Lewis, Sarah J, additional, Cao, Yin, additional, and Tsilidis, Konstantinos K, additional

Published
2022
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218. Linking Physical Activity to Breast Cancer Risk via Insulin/Insulin-Like Growth Factor Signaling System, Part 1: The Effect of Physical Activity on the Insulin/Insulin-Like Growth Factor Signaling System

Author

Swain, Christopher T.V., primary, Drummond, Ann E., additional, Milne, Roger L., additional, English, Dallas R., additional, Brown, Kristy A., additional, Chong, Jamie E., additional, Skinner, Tina L., additional, van Roekel, Eline H., additional, Moore, Melissa M., additional, Gaunt, Tom R., additional, Martin, Richard M., additional, Lewis, Sarah J., additional, and Lynch, Brigid M., additional

Published
2022
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219. Linking Physical Activity to Breast Cancer Risk via the Insulin/Insulin-like Growth Factor Signaling System, Part 2: The Effect of Insulin/Insulin-like Growth Factor Signaling on Breast Cancer Risk

Author

Drummond, Ann E., primary, Swain, Christopher T.V., additional, Milne, Roger L., additional, English, Dallas R., additional, Brown, Kristy A., additional, Skinner, Tina L., additional, Lay, Jannelle, additional, van Roekel, Eline H., additional, Moore, Melissa M., additional, Gaunt, Tom R., additional, Martin, Richard M., additional, Lewis, Sarah J., additional, and Lynch, Brigid M., additional

Published
2022
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220. Cost-Effectiveness Analysis of Prostate Cancer Screening in the UK: A Decision Model Analysis Based on the CAP Trial

Author

Keeney, Edna, primary, Sanghera, Sabina, additional, Martin, Richard M., additional, Gulati, Roman, additional, Wiklund, Fredrik, additional, Walsh, Eleanor I., additional, Donovan, Jenny L., additional, Hamdy, Freddie, additional, Neal, David E., additional, Lane, J. Athene, additional, Turner, Emma L., additional, Thom, Howard, additional, and Clements, Mark S., additional

Published
2022
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226. The relationship between blood pressure and risk of renal cell carcinoma

Author

Alcala, Karine, Mariosa, Daniela, Smith-Byrne, Karl, Nasrollahzadeh Nesheli, Dariush, Carreras-Torres, Robert, Ardanaz Aicua, Eva, Bondonno, Nicola P, Bonet, Catalina, Brunström, Mattias, Bueno-De-Mesquita, Bas, Chirlaque, María-Dolores, Christakoudi, Sofia, Heath, Alicia K, Kaaks, Rudolf, Katzke, Verena, Krogh, Vittorio, Ljungberg, Börje, Martin, Richard M, May, Anne, Melander, Olle, Palli, Domenico, Rodriguez-Barranco, Miguel, Sacerdote, Carlotta, Stocks, Tanja, Tjønneland, Anne, Travis, Ruth C., Vermeulen, Roel, Chanock, Stephen, Purdue, Mark, Weiderpass, Elisabete, Muller, David, Brennan, Paul, Johansson, Mattias, and IRAS OH Epidemiology Chemical Agents

Subjects
systolic blood pressure, Mendelian randomization, diastolic blood pressure, kidney cancer, RCC
Abstract

Background: The relation between blood pressure and kidney cancer risk is well established but complex and different study designs have reported discrepant findings on the relative importance of diastolic blood pressure (DBP) and systolic blood pressure (SBP). In this study, we sought to describe the temporal relation between diastolic and SBP with renal cell carcinoma (RCC) risk in detail. Methods: Our study involved two prospective cohorts: the European Prospective Investigation into Cancer and Nutrition study and UK Biobank, including >700 000 participants and 1692 incident RCC cases. Risk analyses were conducted using flexible parametric survival models for DBP and SBP both separately as well as with mutuality adjustment and then adjustment for extended risk factors. We also carried out univariable and multivariable Mendelian randomization (MR) analyses (DBP: ninstruments = 251, SBP: ninstruments = 213) to complement the analyses of measured DBP and SBP. Results: In the univariable analysis, we observed clear positive associations with RCC risk for both diastolic and SBP when measured ≥5 years before diagnosis and suggestive evidence for a stronger risk association in the year leading up to diagnosis. In mutually adjusted analysis, the long-term risk association of DBP remained, with a hazard ratio (HR) per standard deviation increment 10 years before diagnosis (HR10y) of 1.20 (95% CI: 1.10-1.30), whereas the association of SBP was attenuated (HR10y: 1.00, 95% CI: 0.91-1.10). In the complementary multivariable MR analysis, we observed an odds ratio for a 1-SD increment (ORsd) of 1.34 (95% CI: 1.08-1.67) for genetically predicted DBP and 0.70 (95% CI: 0.56-0.88) for genetically predicted SBP. Conclusion: The results of this observational and MR study are consistent with an important role of DBP in RCC aetiology. The relation between SBP and RCC risk was less clear but does not appear to be independent of DBP. © 2022 World Health Organization,. All rights reserved. The World Health Organization has granted the Publisher permission for the reproduction of this article.

Published
2022

228. Prostate cancer–Exercise and Metformin Trial (Pre-EMpT): study protocol for a feasibility factorial randomized controlled trial in men with localised or locally advanced prostate cancer

Author

McGeagh, Lucy, primary, Robles, Luke A., additional, Persad, Raj, additional, Rowe, Edward, additional, Bahl, Amit, additional, Aning, Jonathan, additional, Koupparis, Anthony, additional, Abrams, Paul, additional, Perks, Claire, additional, Holly, Jeffrey, additional, Johnson, Lyndsey, additional, Shiridzinomwa, Constance, additional, Challapalli, Amarnath, additional, Shingler, Ellie, additional, Taylor, Hilary, additional, Oxley, Jon, additional, Sandu, Meda, additional, Martin, Richard M., additional, and Lane, J. Athene, additional

Published
2022
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229. Genetically-proxied impaired GIPR signalling and risk of 6 cancers

Author

Rogers, Miranda, primary, Gill, Dipender, additional, Ahlqvist, Emma, additional, Robinson, Tim, additional, Mariosa, Daniela, additional, Johansson, Mattias, additional, Penha, Ricardo Cortez Cardoso, additional, Dossus, Laure, additional, Gunter, Marc J, additional, Moreno, Victor, additional, Davey Smith, George, additional, Martin, Richard M, additional, and Yarmolinsky, James, additional

Published
2022
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231. Circulating Isovalerylcarnitine and Lung Cancer Risk: Evidence from Mendelian Randomization and Prediagnostic Blood Measurements

Author

Smith-Byrne, Karl, primary, Cerani, Agustin, additional, Guida, Florence, additional, Zhou, Sirui, additional, Agudo, Antonio, additional, Aleksandrova, Krasimira, additional, Barricarte, Aurelio, additional, Barranco, Miguel Rodríguez, additional, Bochers, Christoph H., additional, Gram, Inger Torhild, additional, Han, Jun, additional, Amos, Christopher I., additional, Hung, Rayjean J., additional, Grankvist, Kjell, additional, Nøst, Therese Haugdhal, additional, Imaz, Liher, additional, Chirlaque-López, María Dolores, additional, Johansson, Mikael, additional, Kaaks, Rudolf, additional, Kühn, Tilman, additional, Martin, Richard M., additional, McKay, James D., additional, Pala, Valeria, additional, Robbins, Hilary A., additional, Sandanger, Torkjel M., additional, Schibli, David, additional, Schulze, Matthias B., additional, Travis, Ruth C., additional, Vineis, Paolo, additional, Weiderpass, Elisabete, additional, Brennan, Paul, additional, Johansson, Mattias, additional, and Richards, J. Brent, additional

Published
2022
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232. Epigenetic markers of adverse lifestyle identified among night shift workers

Author

Hulls, Paige M., primary, McCartney, Daniel L., additional, Bao, Yanchun, additional, Walker, Rosie M., additional, de Vocht, Frank, additional, Martin, Richard M., additional, Relton, Caroline L., additional, Evans, Kathryn L., additional, Kumari, Meena, additional, Marioni, Riccardo E., additional, and Richmond, Rebecca C., additional

Published
2022
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237. Effect of a Low-Intensity PSA-Based Screening Intervention on Prostate Cancer Mortality: The CAP Randomized Clinical Trial

Author

Martin, Richard M., Donovan, Jenny L., Turner, Emma L., Metcalfe, Chris, Young, Grace J., Walsh, Eleanor I., Lane, J. Athene, Noble, Sian, Oliver, Steven E., Evans, Simon, Sterne, Jonathan A. C., Holding, Peter, Ben-Shlomo, Yoav, Brindle, Peter, Williams, Naomi J., Hill, Elizabeth M., Ng, Siaw Yein, Toole, Jessica, Tazewell, Marta K., Hughes, Laura J., Davies, Charlotte F., Thorn, Joanna C., Down, Elizabeth, Davey Smith, George, Neal, David E., and Hamdy, Freddie C.

Published
2018
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239. Circulating vitamin D concentration and risk of seven cancers: Mendelian randomisation study

Author

Dimitrakopoulou, Vasiliki I, Tsilidis, Konstantinos K, Haycock, Philip C, Dimou, Niki L, Al-Dabhani, Kawthar, Martin, Richard M, Lewis, Sarah J, Gunter, Marc J, Mondul, Alison, Shui, Irene M, Theodoratou, Evropi, Nimptsch, Katharina, Lindström, Sara, Albanes, Demetrius, Kühn, Tilman, Key, Timothy J, Travis, Ruth C, Vimaleswaran, Karani Santhanakrishnan, Kraft, Peter, Pierce, Brandon L, and Schildkraut, Joellen M

Published
2017
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245. Role of DNA methylation in the relationship between glioma risk factors and glioma incidence: a two-step Mendelian randomization study.

Author

Howell, Amy E., Relton, Caroline, Martin, Richard M., Zheng, Jie, and Kurian, Kathreena M.

Subjects
TELOMERES, GLIOMAS, DNA methylation, LDL cholesterol, GENOME-wide association studies, FALSE discovery rate
Abstract

Genetic evidence suggests glioma risk is altered by leukocyte telomere length, allergic disease (asthma, hay fever or eczema), alcohol consumption, childhood obesity, low-density lipoprotein cholesterol (LDLc) and triglyceride levels. DNA methylation (DNAm) variation influences many of these glioma-related traits and is an established feature of glioma. Yet the causal relationship between DNAm variation with both glioma incidence and glioma risk factors is unknown. We applied a two-step Mendelian randomization (MR) approach and several sensitivity analyses (including colocalization and Steiger filtering) to assess the association of DNAm with glioma risk factors and glioma incidence. We used data from a recently published catalogue of germline genetic variants robustly associated with DNAm variation in blood (32,851 participants) and data from a genome-wide association study of glioma risk (12,488 cases and 18,169 controls, sub-divided into 6191 glioblastoma cases and 6305 non-glioblastoma cases). MR evidence indicated that DNAm at 3 CpG sites (cg01561092, cg05926943, cg01584448) in one genomic region (HEATR3) had a putative association with glioma and glioblastoma risk (False discovery rate [FDR] < 0.05). Steiger filtering provided evidence against reverse causation. Colocalization presented evidence against genetic confounding and suggested that differential DNAm at the 3 CpG sites and glioma were driven by the same genetic variant. MR provided little evidence to suggest that DNAm acts as a mediator on the causal pathway between risk factors previously examined and glioma onset. To our knowledge, this is the first study to use MR to appraise the causal link of DNAm with glioma risk factors and glioma onset. Subsequent analyses are required to improve the robustness of our results and rule out horizontal pleiotropy. [ABSTRACT FROM AUTHOR]

Published
2023
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249. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer:a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author

Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, and consortium, The PRACTICAL

Subjects
Cancer och onkologi, prospective analysis, Epidemiology, General Medicine, prostate cancer, aggressive prostate cancer, Cancer and Oncology, Mendelian randomization, international consortia, Insulin-like growth factor-I, ICEP, Bristol Population Health Science Institute
Abstract

Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.

Published
2022

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