46 results on '"Giles, Graham G."'
Search Results
2. Dietary factors and DNA methylation-based markers of ageing in 5310 middle-aged and older Australian adults
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Cribb, Lachlan, Hodge, Allison M., Southey, Melissa C., Giles, Graham G., Milne, Roger L., and Dugué, Pierre-Antoine
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- 2024
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3. Genetic risk impacts the association of menopausal hormone therapy with colorectal cancer risk
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Tian, Yu, Lin, Yi, Qu, Conghui, Arndt, Volker, Baurley, James W., Berndt, Sonja I., Bien, Stephanie A., Bishop, D. Timothy, Brenner, Hermann, Buchanan, Daniel D., Budiarto, Arif, Campbell, Peter T., Carreras-Torres, Robert, Casey, Graham, Chan, Andrew T., Chen, Rui, Chen, Xuechen, Conti, David V., Díez-Obrero, Virginia, Dimou, Niki, Drew, David A., Figueiredo, Jane C., Gallinger, Steven, Giles, Graham G., Gruber, Stephen B., Gunter, Marc J., Harlid, Sophia, Harrison, Tabitha A., Hidaka, Akihisa, Hoffmeister, Michael, Huyghe, Jeroen R., Jenkins, Mark A., Jordahl, Kristina M., Joshi, Amit D., Keku, Temitope O., Kawaguchi, Eric, Kim, Andre E., Kundaje, Anshul, Larsson, Susanna C., Marchand, Loic Le, Lewinger, Juan Pablo, Li, Li, Moreno, Victor, Morrison, John, Murphy, Neil, Nan, Hongmei, Nassir, Rami, Newcomb, Polly A., Obón-Santacana, Mireia, Ogino, Shuji, Ose, Jennifer, Pardamean, Bens, Pellatt, Andrew J., Peoples, Anita R., Platz, Elizabeth A., Potter, John D., Prentice, Ross L., Rennert, Gad, Ruiz-Narvaez, Edward A., Sakoda, Lori C., Schoen, Robert E., Shcherbina, Anna, Stern, Mariana C., Su, Yu-Ru, Thibodeau, Stephen N., Thomas, Duncan C., Tsilidis, Konstantinos K., van Duijnhoven, Franzel J. B., Van Guelpen, Bethany, Visvanathan, Kala, White, Emily, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Peters, Ulrike, Gauderman, W. James, Hsu, Li, and Chang-Claude, Jenny
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- 2024
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4. Self-rated health, epigenetic ageing, and long-term mortality in older Australians
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Li, Danmeng Lily, Hodge, Allison M., Southey, Melissa C., Giles, Graham G., Milne, Roger L., and Dugué, Pierre-Antoine
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- 2024
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5. Epidemiology of prostate cancer
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Giles, Graham G., primary
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- 2024
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6. Integrative multi-omics analyses to identify the genetic and functional mechanisms underlying ovarian cancer risk regions
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Dareng, Eileen O., Coetzee, Simon G., Tyrer, Jonathan P., Peng, Pei-Chen, Rosenow, Will, Chen, Stephanie, Davis, Brian D., Dezem, Felipe Segato, Seo, Ji-Heui, Nameki, Robbin, Reyes, Alberto L., Aben, Katja K.H., Anton-Culver, Hoda, Antonenkova, Natalia N., Aravantinos, Gerasimos, Bandera, Elisa V., Beane Freeman, Laura E., Beckmann, Matthias W., Beeghly-Fadiel, Alicia, Benitez, Javier, Bernardini, Marcus Q., Bjorge, Line, Black, Amanda, Bogdanova, Natalia V., Bolton, Kelly L., Brenton, James D., Budzilowska, Agnieszka, Butzow, Ralf, Cai, Hui, Campbell, Ian, Cannioto, Rikki, Chang-Claude, Jenny, Chanock, Stephen J., Chen, Kexin, Chenevix-Trench, Georgia, Chiew, Yoke-Eng, Cook, Linda S., DeFazio, Anna, Dennis, Joe, Doherty, Jennifer A., Dörk, Thilo, du Bois, Andreas, Dürst, Matthias, Eccles, Diana M., Ene, Gabrielle, Fasching, Peter A., Flanagan, James M., Fortner, Renée T., Fostira, Florentia, Gentry-Maharaj, Aleksandra, Giles, Graham G., Goodman, Marc T., Gronwald, Jacek, Haiman, Christopher A., Håkansson, Niclas, Heitz, Florian, Hildebrandt, Michelle A.T., Høgdall, Estrid, Høgdall, Claus K., Huang, Ruea-Yea, Jensen, Allan, Jones, Michael E., Kang, Daehee, Karlan, Beth Y., Karnezis, Anthony N., Kelemen, Linda E., Kennedy, Catherine J., Khusnutdinova, Elza K., Kiemeney, Lambertus A., Kjaer, Susanne K., Kupryjanczyk, Jolanta, Labrie, Marilyne, Lambrechts, Diether, Larson, Melissa C., Le, Nhu D., Lester, Jenny, Li, Lian, Lubiński, Jan, Lush, Michael, Marks, Jeffrey R., Matsuo, Keitaro, May, Taymaa, McLaughlin, John R., McNeish, Iain A., Menon, Usha, Missmer, Stacey, Modugno, Francesmary, Moffitt, Melissa, Monteiro, Alvaro N., Moysich, Kirsten B., Narod, Steven A., Nguyen-Dumont, Tu, Odunsi, Kunle, Olsson, Håkan, Onland-Moret, N. Charlotte, Park, Sue K., Pejovic, Tanja, Permuth, Jennifer B., Piskorz, Anna, Prokofyeva, Darya, Riggan, Marjorie J., Risch, Harvey A., Rodríguez-Antona, Cristina, Rossing, Mary Anne, Sandler, Dale P., Setiawan, V. Wendy, Shan, Kang, Song, Honglin, Southey, Melissa C., Steed, Helen, Sutphen, Rebecca, Swerdlow, Anthony J., Teo, Soo Hwang, Terry, Kathryn L., Thompson, Pamela J., Vestrheim Thomsen, Liv Cecilie, Titus, Linda, Trabert, Britton, Travis, Ruth, Tworoger, Shelley S., Valen, Ellen, Van Nieuwenhuysen, Els, Edwards, Digna Velez, Vierkant, Robert A., Webb, Penelope M., Weinberg, Clarice R., Weise, Rayna Matsuno, Wentzensen, Nicolas, White, Emily, Winham, Stacey J., Wolk, Alicja, Woo, Yin-Ling, Wu, Anna H., Yan, Li, Yannoukakos, Drakoulis, Zeinomar, Nur, Zheng, Wei, Ziogas, Argyrios, Berchuck, Andrew, Goode, Ellen L., Huntsman, David G., Pearce, Celeste L., Ramus, Susan J., Sellers, Thomas A., Freedman, Matthew L., Lawrenson, Kate, Schildkraut, Joellen M., Hazelett, Dennis, Plummer, Jasmine T., Kar, Siddhartha, Jones, Michelle R., Pharoah, Paul D.P., and Gayther, Simon A.
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- 2024
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7. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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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.
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- 2024
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8. Dietary Fiber Intake and Risk of Advanced and Aggressive Forms of Prostate Cancer: A Pooled Analysis of 15 Prospective Cohort Studies
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Sidahmed, Elkhansa, Freedland, Stephen J., Wang, Molin, Wu, Kana, Albanes, Demetrius, Barnett, Matt, van den Brandt, Piet A., Cook, Michael B., Giles, Graham G., Giovannucci, Edward, Haiman, Christopher A., Larsson, Susanna C., Key, Timothy J., Loftfield, Erikka, Männistö, Satu, McCullough, Marjorie L., Milne, Roger L., Neuhouser, Marian L., Platz, Elizabeth A., Perez-Cornago, Aurora, Sawada, Norie, Schenk, Jeannette M., Sinha, Rashmi, Tsugane, Shoichiro, Visvanathan, Kala, Wang, Ying, White, Kami K., Willett, Walter C., Wolk, Alicja, Ziegler, Regina G., Genkinger, Jeanine M., and Smith-Warner, Stephanie A.
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- 2024
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9. Role of Polyunsaturated Fat in Modifying Cardiovascular Risk Associated With Family History of Cardiovascular Disease: Pooled De Novo Results From 15 Observational Studies
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Laguzzi, Federica, Åkesson, Agneta, Marklund, Matti, Qian, Frank, Gigante, Bruna, Bartz, Traci M., Bassett, Julie K., Birukov, Anna, Campos, Hannia, Hirakawa, Yoichiro, Imamura, Fumiaki, Jäger, Susanne, Lankinen, Maria, Murphy, Rachel A., Senn, Mackenzie, Tanaka, Toshiko, Tintle, Nathan, Virtanen, Jyrki K., Yamagishi, Kazumasa, Allison, Matthew, Brouwer, Ingeborg A., De Faire, Ulf, Eiriksdottir, Gudny., Ferrucci, Luigi, Forouhi, Nita G., Geleijnse, Johanna M., Hodge, Allison M, Kimura, Hitomi, Laakso, Markku, Risérus, Ulf, van Westing, Anniek C., Bandinelli, Stefania, Baylin, Ana, Giles, Graham G., Gudnason, Vilmundur, Iso, Hiroyasu, Lemaitre, Rozenn N., Ninomiya, Toshiharu, Post, Wendy S., Psaty, Bruce M., Salonen, Jukka T., Schulze, Matthias B., Tsai, Michael Y., Uusitupa, Matti, Wareham, Nicholas J., Oh, Seung-Won, Wood, Alexis C., Harris, William S., Siscovick, David, Mozaffarian, Dariush, and Leander, Karin
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- 2024
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10. Prevalence of Germline Pathogenic Variants in Renal Cancer Predisposition Genes in a Population-Based Study of Renal Cell Carcinoma.
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Bruinsma, Fiona, Harraka, Philip, Jordan, Susan, Park, Daniel J., Pope, Bernard, Steen, Jason, Milne, Roger L., Giles, Graham G., Winship, Ingrid, Tucker, Katherine M., Southey, Melissa C., and Nguyen-Dumont, Tu
- Subjects
RESEARCH funding ,FISHER exact test ,DESCRIPTIVE statistics ,GENETIC variation ,RENAL cell carcinoma ,DISEASE susceptibility ,DATA analysis software ,GENETIC mutation ,GENETIC testing - Abstract
Simple Summary: Studies of genetic predisposition to renal cell carcinoma (RCC) have been highly variable in design and have reported similarly highly variable rates of cases identified as carrying pathogenic variants in cancer susceptibility genes (4–26%). The aim of our study was to conduct a population-based study of genetic predisposition to RCC. We conducted a 21-gene panel sequencing study and identified that 18/1029 participants (1.7%) carried a pathogenic or likely pathogenic (PLP) variant. Genes with PLP variants included BAP1, FH, FLCN, MITF, MSH6, SDHB, TSC1, and VHL. This study provides further evidence that family history alone may not be sufficient for identifying all individuals who are at increased genetic risk of renal cell carcinoma, and further research is urgently needed to understand how to target genetic testing to identify those at high genetic risk of kidney cancer. Renal cell carcinoma (RCC) has been associated with germline pathogenic or likely pathogenic (PLP) variants in recognised cancer susceptibility genes. Studies of RCC using gene panel sequencing have been highly variable in terms of study design, genes included, and reported prevalence of PLP variant carriers (4–26%). Studies that restricted their analysis to established RCC predisposition genes identified variants in 1–6% of cases. This work assessed the prevalence of clinically actionable PLP variants in renal cancer predisposition genes in an Australian population-based sample of RCC cases. Germline DNA from 1029 individuals diagnosed with RCC who were recruited through the Victoria and Queensland cancer registries were screened using a custom amplicon-based panel of 21 genes. Mean age at cancer diagnosis was 60 ± 10 years, and two-thirds (690, 67%) of the participants were men. Eighteen participants (1.7%) were found to carry a PLP variant. Genes with PLP variants included BAP1, FH, FLCN, MITF, MSH6, SDHB, TSC1, and VHL. Most carriers of PLP variants did not report a family history of the disease. Further exploration of the clinical utility of gene panel susceptibility testing for all RCCs is warranted. [ABSTRACT FROM AUTHOR]
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- 2024
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11. Saliva-derived DNA is suitable for the detection of clonal haematopoiesis of indeterminate potential.
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O'Reilly, Robert L., Burke, Jared, Harraka, Philip, Yeh, Paul, Howlett, Kerryn, Behrouzfar, Kiarash, Rewse, Amanda, Tsimiklis, Helen, Giles, Graham G., Bubb, Kristen J., Nicholls, Stephen J., Milne, Roger L., and Southey, Melissa C.
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HEMATOPOIESIS ,DNA ,NUCLEOTIDE sequencing ,SOMATIC mutation ,SALIVA - Abstract
Clonal haematopoiesis of indeterminate potential (CHIP) has been associated with many adverse health outcomes. However, further research is required to understand the critical genes and pathways relevant to CHIP subtypes, evaluate how CHIP clones evolve with time, and further advance functional characterisation and therapeutic studies. Large epidemiological studies are well placed to address these questions but often collect saliva rather than blood from participants. Paired saliva- and blood-derived DNA samples from 94 study participants were sequenced using a targeted CHIP-gene panel. The ten genes most frequently identified to carry CHIP-associated variants were analysed. Fourteen unique variants associated with CHIP, ten in DNMT3A, two in TP53 and two in TET2, were identified with a variant allele fraction (VAF) between 0.02 and 0.2 and variant depth ≥ 5 reads. Eleven of these CHIP-associated variants were detected in both the blood- and saliva-derived DNA sample. Three variants were detected in blood with a VAF > 0.02 but fell below this threshold in the paired saliva sample (VAF 0.008—0.013). Saliva-derived DNA is suitable for detecting CHIP-associated variants. Saliva can offer a cost-effective biospecimen that could both advance CHIP research and facilitate clinical translation into settings such as risk prediction, precision prevention, and treatment monitoring. [ABSTRACT FROM AUTHOR]
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- 2024
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12. Detection of differentially methylated CpGs between tumour and adjacent benign cells in diagnostic prostate cancer samples.
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FitzGerald, Liesel M., Jung, Chol-hee, Wong, Ee Ming, Joo, JiHoon E., Bassett, Julie K., Dowty, James G., Wang, Xiaoyu, Dai, James Y., Stanford, Janet L., O'Callaghan, Neil, Nottle, Tim, Pedersen, John, Giles, Graham G., and Southey, Melissa C.
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TRANSURETHRAL prostatectomy ,PROSTATE cancer prognosis ,RADICAL prostatectomy ,BENIGN tumors ,NEEDLE biopsy ,PROSTATE - Abstract
Differentially methylated CpG sites (dmCpGs) that distinguish prostate tumour from adjacent benign tissue could aid in the diagnosis and prognosis of prostate cancer. Previously, the identification of such dmCpGs has only been undertaken in radical prostatectomy (RP) samples and not primary diagnostic tumour samples (needle biopsy or transurethral resection of the prostate). We interrogated an Australian dataset comprising 125 tumour and 43 adjacent histologically benign diagnostic tissue samples, including 41 paired samples, using the Infinium Human Methylation450 BeadChip. Regression analyses of paired tumour and adjacent benign samples identified 2,386 significant dmCpGs (Bonferroni p < 0.01; delta-β ≥ 40%), with LASSO regression selecting 16 dmCpGs that distinguished tumour samples in the full Australian diagnostic dataset (AUC = 0.99). Results were validated in independent North American (n
paired = 19; AUC = 0.87) and The Cancer Genome Atlas (TCGA; npaired = 50; AUC = 0.94) RP datasets. Two of the 16 dmCpGs were in genes that were significantly down-regulated in Australian tumour samples (Bonferroni p < 0.01; GSTM2 and PRKCB). Ten additional dmCpGs distinguished low (n = 34) and high Gleason (n = 88) score tumours in the diagnostic Australian dataset (AUC = 0.95), but these performed poorly when applied to the RP datasets (North American: AUC = 0.66; TCGA: AUC = 0.62). The DNA methylation marks identified here could augment and improve current diagnostic tests and/or form the basis of future prognostic tests. [ABSTRACT FROM AUTHOR]- Published
- 2024
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13. Fine-mapping analysis including over 254,000 East Asian and European descendants identifies 136 putative colorectal cancer susceptibility genes
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Chen, Zhishan, primary, Guo, Xingyi, additional, Tao, Ran, additional, Huyghe, Jeroen R., additional, Law, Philip J., additional, Fernandez-Rozadilla, Ceres, additional, Ping, Jie, additional, Jia, Guochong, additional, Long, Jirong, additional, Li, Chao, additional, Shen, Quanhu, additional, Xie, Yuhan, additional, Timofeeva, Maria N., additional, Thomas, Minta, additional, Schmit, Stephanie L., additional, Díez-Obrero, Virginia, additional, Devall, Matthew, additional, Moratalla-Navarro, Ferran, additional, Fernandez-Tajes, Juan, additional, Palles, Claire, additional, Sherwood, Kitty, additional, Briggs, Sarah E. W., additional, Svinti, Victoria, additional, Donnelly, Kevin, additional, Farrington, Susan M., additional, Blackmur, James, additional, Vaughan-Shaw, Peter G., additional, Shu, Xiao-Ou, additional, Lu, Yingchang, additional, Broderick, Peter, additional, Studd, James, additional, Harrison, Tabitha A., additional, Conti, David V., additional, Schumacher, Fredrick R., additional, Melas, Marilena, additional, Rennert, Gad, additional, Obón-Santacana, Mireia, additional, Martín-Sánchez, Vicente, additional, Oh, Jae Hwan, additional, Kim, Jeongseon, additional, Jee, Sun Ha, additional, Jung, Keum Ji, additional, Kweon, Sun-Seog, additional, Shin, Min-Ho, additional, Shin, Aesun, additional, Ahn, Yoon-Ok, additional, Kim, Dong-Hyun, additional, Oze, Isao, additional, Wen, Wanqing, additional, Matsuo, Keitaro, additional, Matsuda, Koichi, additional, Tanikawa, Chizu, additional, Ren, Zefang, additional, Gao, Yu-Tang, additional, Jia, Wei-Hua, additional, Hopper, John L., additional, Jenkins, Mark A., additional, Win, Aung Ko, additional, Pai, Rish K., additional, Figueiredo, Jane C., additional, Haile, Robert W., additional, Gallinger, Steven, additional, Woods, Michael O., additional, Newcomb, Polly A., additional, Duggan, David, additional, Cheadle, Jeremy P., additional, Kaplan, Richard, additional, Kerr, Rachel, additional, Kerr, David, additional, Kirac, Iva, additional, Böhm, Jan, additional, Mecklin, Jukka-Pekka, additional, Jousilahti, Pekka, additional, Knekt, Paul, additional, Aaltonen, Lauri A., additional, Rissanen, Harri, additional, Pukkala, Eero, additional, Eriksson, Johan G., additional, Cajuso, Tatiana, additional, Hänninen, Ulrika, additional, Kondelin, Johanna, additional, Palin, Kimmo, additional, Tanskanen, Tomas, additional, Renkonen-Sinisalo, Laura, additional, Männistö, Satu, additional, Albanes, Demetrius, additional, Weinstein, Stephanie J., additional, Ruiz-Narvaez, Edward, additional, Palmer, Julie R., additional, Buchanan, Daniel D., additional, Platz, Elizabeth A., additional, Visvanathan, Kala, additional, Ulrich, Cornelia M., additional, Siegel, Erin, additional, Brezina, Stefanie, additional, Gsur, Andrea, additional, Campbell, Peter T., additional, Chang-Claude, Jenny, additional, Hoffmeister, Michael, additional, Brenner, Hermann, additional, Slattery, Martha L., additional, Potter, John D., additional, Tsilidis, Kostas K., additional, Schulze, Matthias B., additional, Gunter, Marc J., additional, Murphy, Neil, additional, Castells, Antoni, additional, Castellví-Bel, Sergi, additional, Moreira, Leticia, additional, Arndt, Volker, additional, Shcherbina, Anna, additional, Bishop, D. Timothy, additional, Giles, Graham G., additional, Southey, Melissa C., additional, Idos, Gregory E., additional, McDonnell, Kevin J., additional, Abu-Ful, Zomoroda, additional, Greenson, Joel K., additional, Shulman, Katerina, additional, Lejbkowicz, Flavio, additional, Offit, Kenneth, additional, Su, Yu-Ru, additional, Steinfelder, Robert, additional, Keku, Temitope O., additional, van Guelpen, Bethany, additional, Hudson, Thomas J., additional, Hampel, Heather, additional, Pearlman, Rachel, additional, Berndt, Sonja I., additional, Hayes, Richard B., additional, Martinez, Marie Elena, additional, Thomas, Sushma S., additional, Pharoah, Paul D. P., additional, Larsson, Susanna C., additional, Yen, Yun, additional, Lenz, Heinz-Josef, additional, White, Emily, additional, Li, Li, additional, Doheny, Kimberly F., additional, Pugh, Elizabeth, additional, Shelford, Tameka, additional, Chan, Andrew T., additional, Cruz-Correa, Marcia, additional, Lindblom, Annika, additional, Hunter, David J., additional, Joshi, Amit D., additional, Schafmayer, Clemens, additional, Scacheri, Peter C., additional, Kundaje, Anshul, additional, Schoen, Robert E., additional, Hampe, Jochen, additional, Stadler, Zsofia K., additional, Vodicka, Pavel, additional, Vodickova, Ludmila, additional, Vymetalkova, Veronika, additional, Edlund, Christopher K., additional, Gauderman, W. James, additional, Shibata, David, additional, Toland, Amanda, additional, Markowitz, Sanford, additional, Kim, Andre, additional, Chanock, Stephen J., additional, van Duijnhoven, Franzel, additional, Feskens, Edith J. M., additional, Sakoda, Lori C., additional, Gago-Dominguez, Manuela, additional, Wolk, Alicja, additional, Pardini, Barbara, additional, FitzGerald, Liesel M., additional, Lee, Soo Chin, additional, Ogino, Shuji, additional, Bien, Stephanie A., additional, Kooperberg, Charles, additional, Li, Christopher I., additional, Lin, Yi, additional, Prentice, Ross, additional, Qu, Conghui, additional, Bézieau, Stéphane, additional, Yamaji, Taiki, additional, Sawada, Norie, additional, Iwasaki, Motoki, additional, Le Marchand, Loic, additional, Wu, Anna H., additional, Qu, Chenxu, additional, McNeil, Caroline E., additional, Coetzee, Gerhard, additional, Hayward, Caroline, additional, Deary, Ian J., additional, Harris, Sarah E., additional, Theodoratou, Evropi, additional, Reid, Stuart, additional, Walker, Marion, additional, Ooi, Li Yin, additional, Lau, Ken S., additional, Zhao, Hongyu, additional, Hsu, Li, additional, Cai, Qiuyin, additional, Dunlop, Malcolm G., additional, Gruber, Stephen B., additional, Houlston, Richard S., additional, Moreno, Victor, additional, Casey, Graham, additional, Peters, Ulrike, additional, Tomlinson, Ian, additional, and Zheng, Wei, additional
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- 2024
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14. Breast and bowel cancers diagnosed in people ‘too young to have cancer’: A blueprint for research using family and twin studies
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Hopper, John L., primary, Li, Shuai, additional, MacInnis, Robert J., additional, Dowty, James G., additional, Nguyen, Tuong L., additional, Bui, Minh, additional, Dite, Gillian S., additional, Esser, Vivienne F. C., additional, Ye, Zhoufeng, additional, Makalic, Enes, additional, Schmidt, Daniel F., additional, Goudey, Benjamin, additional, Alpen, Karen, additional, Kapuscinski, Miroslaw, additional, Win, Aung Ko, additional, Dugué, Pierre‐Antoine, additional, Milne, Roger L., additional, Jayasekara, Harindra, additional, Brooks, Jennifer D., additional, Malta, Sue, additional, Calais‐Ferreira, Lucas, additional, Campbell, Alexander C., additional, Young, Jesse T., additional, Nguyen‐Dumont, Tu, additional, Sung, Joohon, additional, Giles, Graham G., additional, Buchanan, Daniel, additional, Winship, Ingrid, additional, Terry, Mary Beth, additional, Southey, Melissa C., additional, and Jenkins, Mark A., additional
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- 2024
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15. Causation and familial confounding as explanations for the associations of polygenic risk scores with breast cancer: Evidence from innovative ICE FALCON and ICE CRISTAL analyses
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Li, Shuai, primary, Dite, Gillian S., additional, MacInnis, Robert J., additional, Bui, Minh, additional, Nguyen, Tuong L., additional, Esser, Vivienne F. C., additional, Ye, Zhoufeng, additional, Dowty, James G., additional, Makalic, Enes, additional, Sung, Joohon, additional, Giles, Graham G., additional, Southey, Melissa C., additional, and Hopper, John L., additional
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- 2024
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16. Data from Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures
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Ye, Zhoufeng, primary, Dite, Gillian S., primary, Nguyen, Tuong L., primary, MacInnis, Robert J., primary, Schmidt, Daniel F., primary, Makalic, Enes, primary, Al-Qershi, Osamah M., primary, Nguyen-Dumont, Tu, primary, Goudey, Benjamin, primary, Stone, Jennifer, primary, Dowty, James G., primary, Giles, Graham G., primary, Southey, Melissa C., primary, Hopper, John L., primary, and Li, Shuai, primary
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- 2024
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17. Supplementary Methods S1 from Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures
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Ye, Zhoufeng, primary, Dite, Gillian S., primary, Nguyen, Tuong L., primary, MacInnis, Robert J., primary, Schmidt, Daniel F., primary, Makalic, Enes, primary, Al-Qershi, Osamah M., primary, Nguyen-Dumont, Tu, primary, Goudey, Benjamin, primary, Stone, Jennifer, primary, Dowty, James G., primary, Giles, Graham G., primary, Southey, Melissa C., primary, Hopper, John L., primary, and Li, Shuai, primary
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- 2024
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18. Supplementary Figure S1 from Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures
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Ye, Zhoufeng, primary, Dite, Gillian S., primary, Nguyen, Tuong L., primary, MacInnis, Robert J., primary, Schmidt, Daniel F., primary, Makalic, Enes, primary, Al-Qershi, Osamah M., primary, Nguyen-Dumont, Tu, primary, Goudey, Benjamin, primary, Stone, Jennifer, primary, Dowty, James G., primary, Giles, Graham G., primary, Southey, Melissa C., primary, Hopper, John L., primary, and Li, Shuai, primary
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- 2024
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19. Supplementary Table S1 from Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures
- Author
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Ye, Zhoufeng, primary, Dite, Gillian S., primary, Nguyen, Tuong L., primary, MacInnis, Robert J., primary, Schmidt, Daniel F., primary, Makalic, Enes, primary, Al-Qershi, Osamah M., primary, Nguyen-Dumont, Tu, primary, Goudey, Benjamin, primary, Stone, Jennifer, primary, Dowty, James G., primary, Giles, Graham G., primary, Southey, Melissa C., primary, Hopper, John L., primary, and Li, Shuai, primary
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- 2024
- Full Text
- View/download PDF
20. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Yarmolinsky, James, primary, Robinson, Jamie W., additional, Mariosa, Daniela, additional, Karhunen, Ville, additional, Huang, Jian, additional, Dimou, Niki, additional, Murphy, Neil, additional, Burrows, Kimberley, additional, Bouras, Emmanouil, additional, Smith-Byrne, Karl, additional, Lewis, Sarah J., additional, Galesloot, Tessel E., additional, Kiemeney, Lambertus A., additional, Vermeulen, Sita, additional, Martin, Paul, additional, Albanes, Demetrius, additional, Hou, Lifang, additional, Newcomb, Polly A., additional, White, Emily, additional, Wolk, Alicja, additional, Wu, Anna H., additional, Le Marchand, Loïc, additional, Phipps, Amanda I., additional, Buchanan, Daniel D., additional, Zhao, Sizheng Steven, additional, Gill, Dipender, additional, Chanock, Stephen J., additional, Purdue, Mark P., additional, Davey Smith, George, additional, Brennan, Paul, additional, Herzig, Karl-Heinz, additional, Järvelin, Marjo-Riitta, additional, Amos, Chris I., additional, Hung, Rayjean J., additional, Dehghan, Abbas, additional, Johansson, Mattias, additional, Gunter, Marc J., additional, Tsilidis, Kostas K., additional, Martin, Richard M., additional, Landi, Maria Teresa, additional, Stevens, Victoria, additional, Wang, Ying, additional, Albanes, Demetrios, additional, Caporaso, Neil, additional, Amos, Christopher I., additional, Shete, Sanjay, additional, Bickeböller, Heike, additional, Risch, Angela, additional, Houlston, Richard, additional, Lam, Stephen, additional, Tardon, Adonina, additional, Chen, Chu, additional, Bojesen, Stig E., additional, Wichmann, H-Erich, additional, Christiani, David, additional, Rennert, Gadi, additional, Arnold, Susanne, additional, Field, John K., additional, Le Marchand, Loic, additional, Melander, Olle, additional, Brunnström, Hans, additional, Liu, Geoffrey, additional, Andrew, Angeline, additional, Shen, Hongbing, additional, Zienolddiny, Shan, additional, Grankvist, Kjell, additional, Johansson, Mikael, additional, Teare, M. Dawn, additional, Hong, Yun-Chul, additional, Yuan, Jian-Min, additional, Lazarus, Philip, additional, Schabath, Matthew B., additional, Aldrich, Melinda C., additional, Eeles, Rosalind A., additional, Haiman, Christopher A., additional, Kote-Jarai, Zsofia, additional, Schumacher, Fredrick R., additional, Benlloch, Sara, additional, Al Olama, Ali Amin, additional, Muir, Kenneth R., additional, Berndt, Sonja I., additional, Conti, David V., additional, Wiklund, Fredrik, additional, Chanock, Stephen, additional, Tangen, Catherine M., additional, Batra, Jyotsna, additional, Clements, Judith A., additional, Grönberg, Henrik, additional, Pashayan, Nora, additional, Schleutker, Johanna, additional, Weinstein, Stephanie J., additional, West, Catharine M.L., additional, Mucci, Lorelei A., additional, Cancel-Tassin, Géraldine, additional, Koutros, Stella, additional, Sørensen, Karina Dalsgaard, additional, Grindedal, Eli Marie, additional, Neal, David E., additional, Hamdy, Freddie C., additional, Donovan, Jenny L., additional, Travis, Ruth C., additional, Hamilton, Robert J., additional, Ingles, Sue Ann, additional, Rosenstein, Barry S., additional, Lu, Yong-Jie, additional, Giles, Graham G., additional, MacInnis, Robert J., additional, Kibel, Adam S., additional, Vega, Ana, additional, Kogevinas, Manolis, additional, Penney, Kathryn L., additional, Park, Jong Y., additional, Stanfrod, Janet L., additional, Cybulski, Cezary, additional, Nordestgaard, Børge G., additional, Nielsen, Sune F., additional, Brenner, Hermann, additional, Maier, Christiane, additional, Logothetis, Christopher J., additional, John, Esther M., additional, Teixeira, Manuel R., additional, Neuhausen, Susan L., additional, De Ruyck, Kim, additional, Razack, Azad, additional, Newcomb, Lisa F., additional, Lessel, Davor, additional, Kaneva, Radka, additional, Usmani, Nawaid, additional, Claessens, Frank, additional, Townsend, Paul A., additional, Castelao, Jose Esteban, additional, Roobol, Monique J., additional, Menegaux, Florence, additional, Khaw, Kay-Tee, additional, Cannon-Albright, Lisa, additional, Pandha, Hardev, additional, Thibodeau, Stephen N., additional, Hunter, David J., additional, Kraft, Peter, additional, Blot, William J., additional, and Riboli, Elio, additional
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- 2024
- Full Text
- View/download PDF
21. Observational and genetic associations between cardiorespiratory fitness and cancer : a UK Biobank and international consortia study
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Watts, Eleanor L., Gonzales, Tomas I., Strain, Tessa, Saint-Maurice, Pedro F., Bishop, D. Timothy, Chanock, Stephen J., Johansson, Mattias, Keku, Temitope O., Le Marchand, Loic, Moreno, Victor, Newcomb, Polly A., Newton, Christina C., Pai, Rish K., Purdue, Mark P., Ulrich, Cornelia M., Smith-Byrne, Karl, van Guelpen, Bethany, Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Olama, Ali Amin Al, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Wang, Ying, 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., Stanford, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Kim, Jeri, 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, Day, Felix R., Wijndaele, Katrien, Wareham, Nicholas J., Matthews, Charles E., Moore, Steven C., Brage, Soren, Watts, Eleanor L., Gonzales, Tomas I., Strain, Tessa, Saint-Maurice, Pedro F., Bishop, D. Timothy, Chanock, Stephen J., Johansson, Mattias, Keku, Temitope O., Le Marchand, Loic, Moreno, Victor, Newcomb, Polly A., Newton, Christina C., Pai, Rish K., Purdue, Mark P., Ulrich, Cornelia M., Smith-Byrne, Karl, van Guelpen, Bethany, Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Olama, Ali Amin Al, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Wang, Ying, 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., Stanford, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Kim, Jeri, 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, Day, Felix R., Wijndaele, Katrien, Wareham, Nicholas J., Matthews, Charles E., Moore, Steven C., and Brage, Soren
- Abstract
Background: The association of fitness with cancer risk is not clear. Methods: We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of lung, colorectal, endometrial, breast, and prostate cancer in a subset of UK Biobank participants who completed a submaximal fitness test in 2009-12 (N = 72,572). We also investigated relationships using two-sample Mendelian randomisation (MR), odds ratios (ORs) were estimated using the inverse-variance weighted method. Results: After a median of 11 years of follow-up, 4290 cancers of interest were diagnosed. A 3.5 ml O2⋅min−1⋅kg−1 total-body mass increase in fitness (equivalent to 1 metabolic equivalent of task (MET), approximately 0.5 standard deviation (SD)) was associated with lower risks of endometrial (HR = 0.81, 95% CI: 0.73–0.89), colorectal (0.94, 0.90–0.99), and breast cancer (0.96, 0.92–0.99). In MR analyses, a 0.5 SD increase in genetically predicted O2⋅min−1⋅kg−1 fat-free mass was associated with a lower risk of breast cancer (OR = 0.92, 95% CI: 0.86–0.98). After adjusting for adiposity, both the observational and genetic associations were attenuated. Discussion: Higher fitness levels may reduce risks of endometrial, colorectal, and breast cancer, though relationships with adiposity are complex and may mediate these relationships. Increasing fitness, including via changes in body composition, may be an effective strategy for cancer prevention.
- Published
- 2024
- Full Text
- View/download PDF
22. Observational and genetic associations between cardiorespiratory fitness and cancer:a UK Biobank and international consortia study
- Author
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Watts, Eleanor L., Gonzales, Tomas I., Strain, Tessa, Saint-Maurice, Pedro F., Bishop, D. Timothy, Chanock, Stephen J., Johansson, Mattias, Keku, Temitope O., Le Marchand, Loic, Moreno, Victor, Newcomb, Polly A., Newton, Christina C., Pai, Rish K., Purdue, Mark P., Ulrich, Cornelia M., Smith-Byrne, Karl, Van Guelpen, Bethany, Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Olama, Ali Amin Al, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Wang, Ying, 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., Stanford, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Kim, Jeri, 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, Day, Felix R., Wijndaele, Katrien, Wareham, Nicholas J., Matthews, Charles E., Moore, Steven C., Brage, Soren, Watts, Eleanor L., Gonzales, Tomas I., Strain, Tessa, Saint-Maurice, Pedro F., Bishop, D. Timothy, Chanock, Stephen J., Johansson, Mattias, Keku, Temitope O., Le Marchand, Loic, Moreno, Victor, Newcomb, Polly A., Newton, Christina C., Pai, Rish K., Purdue, Mark P., Ulrich, Cornelia M., Smith-Byrne, Karl, Van Guelpen, Bethany, Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Olama, Ali Amin Al, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Wang, Ying, 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., Stanford, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Kim, Jeri, 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, Day, Felix R., Wijndaele, Katrien, Wareham, Nicholas J., Matthews, Charles E., Moore, Steven C., and Brage, Soren
- Abstract
Background: The association of fitness with cancer risk is not clear. Methods: We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of lung, colorectal, endometrial, breast, and prostate cancer in a subset of UK Biobank participants who completed a submaximal fitness test in 2009-12 (N = 72,572). We also investigated relationships using two-sample Mendelian randomisation (MR), odds ratios (ORs) were estimated using the inverse-variance weighted method.Results: After a median of 11 years of follow-up, 4290 cancers of interest were diagnosed. A 3.5 ml O2⋅min−1⋅kg−1 total-body mass increase in fitness (equivalent to 1 metabolic equivalent of task (MET), approximately 0.5 standard deviation (SD)) was associated with lower risks of endometrial (HR = 0.81, 95% CI: 0.73–0.89), colorectal (0.94, 0.90–0.99), and breast cancer (0.96, 0.92–0.99). In MR analyses, a 0.5 SD increase in genetically predicted O2⋅min−1⋅kg−1 fat-free mass was associated with a lower risk of breast cancer (OR = 0.92, 95% CI: 0.86–0.98). After adjusting for adiposity, both the observational and genetic associations were attenuated. Discussion: Higher fitness levels may reduce risks of endometrial, colorectal, and breast cancer, though relationships with adiposity are complex and may mediate these relationships. Increasing fitness, including via changes in body composition, may be an effective strategy for cancer prevention.
- Published
- 2024
23. Fine-mapping analysis including over 254 000 East Asian and European descendants identifies 136 putative colorectal cancer susceptibility genes
- Author
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Chen, Zhishan, Guo, Xingyi, Tao, Ran, Huyghe, Jeroen R., Law, Philip J., Fernandez-Rozadilla, Ceres, Ping, Jie, Jia, Guochong, Long, Jirong, Li, Chao, Shen, Quanhu, Xie, Yuhan, Timofeeva, Maria N., Thomas, Minta, Schmit, Stephanie L., Díez-Obrero, Virginia, Devall, Matthew, Moratalla-Navarro, Ferran, Fernandez-Tajes, Juan, Palles, Claire, Sherwood, Kitty, Briggs, Sarah E. W., Svinti, Victoria, Donnelly, Kevin, Farrington, Susan M., Blackmur, James, Vaughan-Shaw, Peter G., Shu, Xiao-Ou, Lu, Yingchang, Broderick, Peter, Studd, James, Harrison, Tabitha A., Conti, David V., Schumacher, Fredrick R., Melas, Marilena, Rennert, Gad, Obón-Santacana, Mireia, Martín-Sánchez, Vicente, Oh, Jae Hwan, Kim, Jeongseon, Jee, Sun Ha, Jung, Keum Ji, Kweon, Sun-Seog, Shin, Min-Ho, Shin, Aesun, Ahn, Yoon-Ok, Kim, Dong-Hyun, Oze, Isao, Wen, Wanqing, Matsuo, Keitaro, Matsuda, Koichi, Tanikawa, Chizu, Ren, Zefang, Gao, Yu-Tang, Jia, Wei-Hua, Hopper, John L., Jenkins, Mark A., Win, Aung Ko, Pai, Rish K., Figueiredo, Jane C., Haile, Robert W., Gallinger, Steven, Woods, Michael O., Newcomb, Polly A., Duggan, David, Cheadle, Jeremy P., Kaplan, Richard, Kerr, Rachel, Kerr, David, Kirac, Iva, Böhm, Jan, Mecklin, Jukka-Pekka, Jousilahti, Pekka, Knekt, Paul, Aaltonen, Lauri A., Rissanen, Harri, Pukkala, Eero, Eriksson, Johan G., Cajuso, Tatiana, Hänninen, Ulrika, Kondelin, Johanna, Palin, Kimmo, Tanskanen, Tomas, Renkonen-Sinisalo, Laura, Männistö, Satu, Albanes, Demetrius, Weinstein, Stephanie J., Ruiz-Narvaez, Edward, Palmer, Julie R., Buchanan, Daniel D., Platz, Elizabeth A., Visvanathan, Kala, Ulrich, Cornelia M., Siegel, Erin, Brezina, Stefanie, Gsur, Andrea, Campbell, Peter T., Chang-Claude, Jenny, Hoffmeister, Michael, Brenner, Hermann, Slattery, Martha L., Potter, John D., Tsilidis, Kostas K., Schulze, Matthias B., Gunter, Marc J., Murphy, Neil, Castells, Antoni, Castellví-Bel, Sergi, Moreira, Leticia, Arndt, Volker, Shcherbina, Anna, Bishop, D. Timothy, Giles, Graham G., Southey, Melissa C., Idos, Gregory E., McDonnell, Kevin J., Abu-Ful, Zomoroda, Greenson, Joel K., Shulman, Katerina, Lejbkowicz, Flavio, Offit, Kenneth, Su, Yu-Ru, Steinfelder, Robert, Keku, Temitope O., van Guelpen, Bethany, Hudson, Thomas J., Hampel, Heather, Pearlman, Rachel, Berndt, Sonja I., Hayes, Richard B., Martinez, Marie Elena, Thomas, Sushma S., Pharoah, Paul D. P., Larsson, Susanna C., Yen, Yun, Lenz, Heinz-Josef, White, Emily, Li, Li, Doheny, Kimberly F., Pugh, Elizabeth, Shelford, Tameka, Chan, Andrew T., Cruz-Correa, Marcia, Lindblom, Annika, Hunter, David J., Joshi, Amit D., Schafmayer, Clemens, Scacheri, Peter C., Kundaje, Anshul, Schoen, Robert E., Hampe, Jochen, Stadler, Zsofia K., Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Edlund, Christopher K., Gauderman, W. James, Shibata, David, Toland, Amanda, Markowitz, Sanford, Kim, Andre, Chanock, Stephen J., van Duijnhoven, Franzel, Feskens, Edith J. M., Sakoda, Lori C., Gago-Dominguez, Manuela, Wolk, Alicja, Pardini, Barbara, FitzGerald, Liesel M., Lee, Soo Chin, Ogino, Shuji, Bien, Stephanie A., Kooperberg, Charles, Li, Christopher I., Lin, Yi, Prentice, Ross, Qu, Conghui, Bézieau, Stéphane, Yamaji, Taiki, Sawada, Norie, Iwasaki, Motoki, Le Marchand, Loic, Wu, Anna H., Qu, Chenxu, McNeil, Caroline E., Coetzee, Gerhard, Hayward, Caroline, Deary, Ian J., Harris, Sarah E., Theodoratou, Evropi, Reid, Stuart, Walker, Marion, Ooi, Li Yin, Lau, Ken S., Zhao, Hongyu, Hsu, Li, Cai, Qiuyin, Dunlop, Malcolm G., Gruber, Stephen B., Houlston, Richard S., Moreno, Victor, Casey, Graham, Peters, Ulrike, Tomlinson, Ian, Zheng, Wei, Chen, Zhishan, Guo, Xingyi, Tao, Ran, Huyghe, Jeroen R., Law, Philip J., Fernandez-Rozadilla, Ceres, Ping, Jie, Jia, Guochong, Long, Jirong, Li, Chao, Shen, Quanhu, Xie, Yuhan, Timofeeva, Maria N., Thomas, Minta, Schmit, Stephanie L., Díez-Obrero, Virginia, Devall, Matthew, Moratalla-Navarro, Ferran, Fernandez-Tajes, Juan, Palles, Claire, Sherwood, Kitty, Briggs, Sarah E. W., Svinti, Victoria, Donnelly, Kevin, Farrington, Susan M., Blackmur, James, Vaughan-Shaw, Peter G., Shu, Xiao-Ou, Lu, Yingchang, Broderick, Peter, Studd, James, Harrison, Tabitha A., Conti, David V., Schumacher, Fredrick R., Melas, Marilena, Rennert, Gad, Obón-Santacana, Mireia, Martín-Sánchez, Vicente, Oh, Jae Hwan, Kim, Jeongseon, Jee, Sun Ha, Jung, Keum Ji, Kweon, Sun-Seog, Shin, Min-Ho, Shin, Aesun, Ahn, Yoon-Ok, Kim, Dong-Hyun, Oze, Isao, Wen, Wanqing, Matsuo, Keitaro, Matsuda, Koichi, Tanikawa, Chizu, Ren, Zefang, Gao, Yu-Tang, Jia, Wei-Hua, Hopper, John L., Jenkins, Mark A., Win, Aung Ko, Pai, Rish K., Figueiredo, Jane C., Haile, Robert W., Gallinger, Steven, Woods, Michael O., Newcomb, Polly A., Duggan, David, Cheadle, Jeremy P., Kaplan, Richard, Kerr, Rachel, Kerr, David, Kirac, Iva, Böhm, Jan, Mecklin, Jukka-Pekka, Jousilahti, Pekka, Knekt, Paul, Aaltonen, Lauri A., Rissanen, Harri, Pukkala, Eero, Eriksson, Johan G., Cajuso, Tatiana, Hänninen, Ulrika, Kondelin, Johanna, Palin, Kimmo, Tanskanen, Tomas, Renkonen-Sinisalo, Laura, Männistö, Satu, Albanes, Demetrius, Weinstein, Stephanie J., Ruiz-Narvaez, Edward, Palmer, Julie R., Buchanan, Daniel D., Platz, Elizabeth A., Visvanathan, Kala, Ulrich, Cornelia M., Siegel, Erin, Brezina, Stefanie, Gsur, Andrea, Campbell, Peter T., Chang-Claude, Jenny, Hoffmeister, Michael, Brenner, Hermann, Slattery, Martha L., Potter, John D., Tsilidis, Kostas K., Schulze, Matthias B., Gunter, Marc J., Murphy, Neil, Castells, Antoni, Castellví-Bel, Sergi, Moreira, Leticia, Arndt, Volker, Shcherbina, Anna, Bishop, D. Timothy, Giles, Graham G., Southey, Melissa C., Idos, Gregory E., McDonnell, Kevin J., Abu-Ful, Zomoroda, Greenson, Joel K., Shulman, Katerina, Lejbkowicz, Flavio, Offit, Kenneth, Su, Yu-Ru, Steinfelder, Robert, Keku, Temitope O., van Guelpen, Bethany, Hudson, Thomas J., Hampel, Heather, Pearlman, Rachel, Berndt, Sonja I., Hayes, Richard B., Martinez, Marie Elena, Thomas, Sushma S., Pharoah, Paul D. P., Larsson, Susanna C., Yen, Yun, Lenz, Heinz-Josef, White, Emily, Li, Li, Doheny, Kimberly F., Pugh, Elizabeth, Shelford, Tameka, Chan, Andrew T., Cruz-Correa, Marcia, Lindblom, Annika, Hunter, David J., Joshi, Amit D., Schafmayer, Clemens, Scacheri, Peter C., Kundaje, Anshul, Schoen, Robert E., Hampe, Jochen, Stadler, Zsofia K., Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Edlund, Christopher K., Gauderman, W. James, Shibata, David, Toland, Amanda, Markowitz, Sanford, Kim, Andre, Chanock, Stephen J., van Duijnhoven, Franzel, Feskens, Edith J. M., Sakoda, Lori C., Gago-Dominguez, Manuela, Wolk, Alicja, Pardini, Barbara, FitzGerald, Liesel M., Lee, Soo Chin, Ogino, Shuji, Bien, Stephanie A., Kooperberg, Charles, Li, Christopher I., Lin, Yi, Prentice, Ross, Qu, Conghui, Bézieau, Stéphane, Yamaji, Taiki, Sawada, Norie, Iwasaki, Motoki, Le Marchand, Loic, Wu, Anna H., Qu, Chenxu, McNeil, Caroline E., Coetzee, Gerhard, Hayward, Caroline, Deary, Ian J., Harris, Sarah E., Theodoratou, Evropi, Reid, Stuart, Walker, Marion, Ooi, Li Yin, Lau, Ken S., Zhao, Hongyu, Hsu, Li, Cai, Qiuyin, Dunlop, Malcolm G., Gruber, Stephen B., Houlston, Richard S., Moreno, Victor, Casey, Graham, Peters, Ulrike, Tomlinson, Ian, and Zheng, Wei
- Abstract
Genome-wide association studies (GWAS) have identified more than 200 common genetic variants independently associated with colorectal cancer (CRC) risk, but the causal variants and target genes are mostly unknown. We sought to fine-map all known CRC risk loci using GWAS data from 100,204 cases and 154,587 controls of East Asian and European ancestry. Our stepwise conditional analyses revealed 238 independent association signals of CRC risk, each with a set of credible causal variants (CCVs), of which 28 signals had a single CCV. Our cis-eQTL/mQTL and colocalization analyses using colorectal tissue-specific transcriptome and methylome data separately from 1299 and 321 individuals, along with functional genomic investigation, uncovered 136 putative CRC susceptibility genes, including 56 genes not previously reported. Analyses of single-cell RNA-seq data from colorectal tissues revealed 17 putative CRC susceptibility genes with distinct expression patterns in specific cell types. Analyses of whole exome sequencing data provided additional support for several target genes identified in this study as CRC susceptibility genes. Enrichment analyses of the 136 genes uncover pathways not previously linked to CRC risk. Our study substantially expanded association signals for CRC and provided additional insight into the biological mechanisms underlying CRC development.
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- 2024
- Full Text
- View/download PDF
24. Association of tea and coffee consumption and biliary tract cancer risk: The Biliary Tract Cancers Pooling Project.
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Yu-Han Huang, Loftfield, Erikka, Argirion, Ilona, Adami, Hans-Olov, Albanes, Demetrius, Chan, Andrew T., Fedirko, Veronika, Fraser, Gary E., Freedman, Neal D., Giles, Graham G., Hartge, Patricia, Katzke, Verena, Knutsen, Synnove F., Lacey Jr, James, Liao, Linda M., Juhua Luo, Milne, Roger L., O'Brien, Katie M., Peters, Ulrike, and Poynter, Jenny N.
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- 2024
- Full Text
- View/download PDF
25. Body size, diet quality, and epigenetic ageing: cross-sectional and longitudinal analyses
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Li, Danmeng Lily, primary, Hodge, Allison M, additional, Cribb, Lachlan, additional, Southey, Melissa C, additional, Giles, Graham G, additional, Milne, Roger L, additional, and Dugué, Pierre-Antoine, additional
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- 2024
- Full Text
- View/download PDF
26. Table S2. from Adherence to 2018 WCRF/AICR Cancer Prevention Recommendations and Risk of Cancer: The Melbourne Collaborative Cohort Study
- Author
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Peng, Yang, primary, Bassett, Julie K., primary, Hodge, Allison M., primary, Melaku, Yohannes Adama, primary, Afshar, Nina, primary, Hopper, John L., primary, MacInnis, Robert J., primary, Lynch, Brigid M., primary, Smith-Warner, Stephanie A., primary, Giles, Graham G., primary, Milne, Roger L., primary, and Jayasekara, Harindra, primary
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- 2024
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27. Supplementary Tables 1a-3d from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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28. Supplementary Figure 4 from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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29. Supplementary Figure 2 from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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30. Figure S1. from Adherence to 2018 WCRF/AICR Cancer Prevention Recommendations and Risk of Cancer: The Melbourne Collaborative Cohort Study
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Peng, Yang, primary, Bassett, Julie K., primary, Hodge, Allison M., primary, Melaku, Yohannes Adama, primary, Afshar, Nina, primary, Hopper, John L., primary, MacInnis, Robert J., primary, Lynch, Brigid M., primary, Smith-Warner, Stephanie A., primary, Giles, Graham G., primary, Milne, Roger L., primary, and Jayasekara, Harindra, primary
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- 2024
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31. Data from Adherence to 2018 WCRF/AICR Cancer Prevention Recommendations and Risk of Cancer: The Melbourne Collaborative Cohort Study
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Peng, Yang, primary, Bassett, Julie K., primary, Hodge, Allison M., primary, Melaku, Yohannes Adama, primary, Afshar, Nina, primary, Hopper, John L., primary, MacInnis, Robert J., primary, Lynch, Brigid M., primary, Smith-Warner, Stephanie A., primary, Giles, Graham G., primary, Milne, Roger L., primary, and Jayasekara, Harindra, primary
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- 2024
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32. Supplementary Figure 5 from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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33. Supplementary Figure 3 from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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34. Supplementary Figure 1 from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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35. Data from A Population-Based Family Case–Control Study of Sun Exposure and Follicular Lymphoma Risk
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Odutola, Michael K., primary, van Leeuwen, Marina T., primary, Bruinsma, Fiona, primary, Turner, Jennifer, primary, Hertzberg, Mark, primary, Seymour, John F., primary, Prince, H. Miles, primary, Trotman, Judith, primary, Verner, Emma, primary, Roncolato, Fernando, primary, Opat, Stephen, primary, Lindeman, Robert, primary, Tiley, Campbell, primary, Milliken, Samuel T., primary, Underhill, Craig R., primary, Benke, Geza, primary, Giles, Graham G., primary, and Vajdic, Claire M., primary
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- 2024
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36. Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures.
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Zhoufeng Ye, Dite, Gillian S., Nguyen, Tuong L., MacInnis, Robert J., Schmidt, Daniel F., Makalic, Enes, Al-Qershi, Osamah M., Tu Nguyen-Dumont, Goudey, Benjamin, Stone, Jennifer, Dowty, James G., Giles, Graham G., Southey, Melissa C., Hopper, John L., and Shuai Li
- Abstract
Background: Cirrus is an automated risk predictor for breast cancer that comprises texture-based mammographic features and is mostly independent of mammographic density. We investigated genetic and environmental variance of variation in Cirrus. Methods: We measured Cirrus for 3,195 breast cancer-free participants, including 527 pairs of monozygotic (MZ) twins, 271 pairs of dizygotic (DZ) twins, and 1,599 siblings of twins. Multivariate normal models were used to estimate the variance and familial correlations of age-adjusted Cirrus as a function of age. The classic twin model was expanded to allow the shared environment effects to differ by zygosity. The SNP-based heritability was estimated for a subset of 2,356 participants. Results: There was no evidence that the variance or familial correlations depended on age. The familial correlations were 0.52 (SE, 0.03) for MZ pairs and 0.16(SE, 0.03) for DZ and non-twin sister pairs combined. Shared environmental factors specific to MZ pairs accounted for 20% of the variance. Additive genetic factors accounted for 32% (SE = 5%) of the variance, consistent with the SNP-based heritability of 36% (SE = 16%). Conclusion: Cirrus is substantially familial due to genetic factors and an influence of shared environmental factors that was evident for MZ twin pairs only. The latter could be due to nongenetic factors operating in utero or in early life that are shared by MZ twins. [ABSTRACT FROM AUTHOR]
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- 2024
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37. Association of hormonal and reproductive factors with differentiated thyroid cancer risk in women: a pooled prospective cohort analysis.
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O'Grady, Thomas J, Rinaldi, Sabina, Michels, Kara A, Adami, Hans-Olov, Buring, Julie E, Chen, Yu, Clendenen, Tess V, D'Aloisio, Aimee, DeHart, Jessica Clague, Franceschi, Silvia, Freedman, Neal D, Gierach, Gretchen L, Giles, Graham G, Lacey, James V, Lee, I-Min, Liao, Linda M, Linet, Martha S, McCullough, Marjorie L, Patel, Alpa V, and Prizment, Anna
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MENARCHE ,ORAL contraceptives ,CONTRACEPTION ,THYROID cancer ,DISEASE risk factors ,SEX hormones ,COHORT analysis ,PROPORTIONAL hazards models - Abstract
Background The incidence of differentiated thyroid cancer (DTC) is higher in women than in men but whether sex steroid hormones contribute to this difference remains unclear. Studies of reproductive and hormonal factors and thyroid cancer risk have provided inconsistent results. Methods Original data from 1 252 907 women in 16 cohorts in North America, Europe, Australia and Asia were combined to evaluate associations of DTC risk with reproductive and hormonal factors. Multivariable-adjusted Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% CIs. Results During follow-up, 2142 women were diagnosed with DTC. Factors associated with higher risk of DTC included younger age at menarche (<10 vs 10–11 years; HR, 1.28; 95% CI, 1.00–1.64), younger (<40; HR, 1.31; 95% CI, 1.05–1.62) and older (≥55; HR, 1.33; 95% CI, 1.05–1.68) ages at menopause (vs 40–44 years), ever use of menopausal hormone therapy (HR, 1.16; 95% CI, 1.02–1.33) and previous hysterectomy (HR, 1.25; 95% CI, 1.13–1.39) or bilateral oophorectomy (HR, 1.14; 95% CI, 1.00–1.29). Factors associated with lower risk included longer-term use (≥5 vs <5 years) of oral contraceptives (HR, 0.86; 95% CI, 0.76–0.96) among those who ever used oral contraception and baseline post-menopausal status (HR, 0.82; 95% CI, 0.70–0.96). No associations were observed for parity, duration of menopausal hormone therapy use or lifetime number of reproductive years or ovulatory cycles. Conclusions Our study provides some evidence linking reproductive and hormonal factors with risk of DTC. Results should be interpreted cautiously considering the modest strength of the associations and potential for exposure misclassification and detection bias. Prospective studies of pre-diagnostic circulating sex steroid hormone measurements and DTC risk may provide additional insight. [ABSTRACT FROM AUTHOR]
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- 2024
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38. A Population-Based Family Case-Control Study of Sun Exposure and Follicular Lymphoma Risk.
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Odutola, Michael K., van Leeuwen, Marina T., Bruinsma, Fiona, Turner, Jennifer, Hertzberg, Mark, Seymour, John F., Prince, H. Miles, Trotman, Judith, Verner, Emma, Roncolato, Fernando, Opat, Stephen, Lindeman, Robert, Tiley, Campbell, Milliken, Samuel T., Underhill, Craig R., Benke, Geza, Giles, Graham G., and Vajdic, Claire M.
- Abstract
Background: Epidemiologic evidence suggests an inverse association between sun exposure and follicular lymphoma risk. Methods: We conducted an Australian population-based family case-control study based on 666 cases and 459 controls (288 related, 171 unrelated). Participants completed a lifetime residence and work calendar and recalled outdoor hours on weekdays, weekends, and holidays in the warmer and cooler months at ages 10, 20, 30, and 40 years, and clothing types worn in the warmer months. We used a group-based trajectory modeling approach to identify outdoor hour trajectories over time and examined associations with follicular lymphoma risk using logistic regression. Results: We observed an inverse association between follicular lymphoma risk and several measures of high lifetime sun exposure, particularly intermittent exposure (weekends, holidays). Associations included reduced risk with increasing time outdoors on holidays in the warmer months [highest category OR = 0.56; 95% confidence interval (CI), 0.42-0.76; P
trend < 0.01], high outdoor hours on weekends in the warmer months (highest category OR = 0.71; 95% CI, 0.52-0.96), and increasing time outdoors in the warmer and cooler months combined (highest category OR = 0.66; 95% CI, 0.50-0.91; Ptrend 0.01). Risk was reduced for high outdoor hour maintainers in the warmer months across the decade years (OR = 0.71; 95% CI, 0.53-0.96). Conclusions: High total and intermittent sun exposure, particularly in the warmer months, may be protective against the development of follicular lymphoma. [ABSTRACT FROM AUTHOR]- Published
- 2024
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39. Adherence to 2018 WCRF/AICR Cancer Prevention Recommendations and Risk of Cancer: The Melbourne Collaborative Cohort Study.
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Yang Peng, Bassett, Julie K., Hodge, Allison M., Melaku, Yohannes Adama, Afshar, Nina, Hopper, John L., MacInnis, Robert J., Lynch, Brigid M., Smith-Warner, Stephanie A., Giles, Graham G., Milne, Roger L., and Jayasekara, Harindra
- Abstract
Background: We examined associations between adherence to adaptations of the 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) cancer prevention recommendations and total, exposure-related and site-specific cancer risk. Methods: A total of 20,001 participants ages 40 to 69 years at enrollment into the Melbourne Collaborative Cohort Study in 1990 to 1994, who had diet, body size, and lifestyle reassessed in 2003 to 2007 ("baseline"), were followed-up through June 2021. We constructed diet and standardized lifestyle scores based on core WCRF/AICR recommendations on diet, alcohol intake, body size and physical activity, and additional scores incorporating weight change, sedentary behavior, and smoking. Associations with cancer risk were estimated using Cox regression, adjusting for confounders. Results: During follow-up (mean = 16 years), 4,710 incident cancers were diagnosed. For highest quintile ("most adherent") of the standardized lifestyle score, compared with lowest ("least adherent"), a HR of 0.82 [95% confidence interval (CI): 0.74-0.92] was observed for total cancer. This association was stronger with smoking included in the score (HR = 0.74; 95% CI: 0.67-0.81). A higher score was associated with lower breast and prostate cancer risk for the standardized score, and with lung, stomach, rectal, and pancreatic cancer risk when the score included smoking. Our analyses identified alcohol use, waist circumference and smoking as key drivers of associations with total cancer risk. Conclusions: Adherence to WCRF/AICR cancer prevention recommendations is associated with lower cancer risk. [ABSTRACT FROM AUTHOR]
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- 2024
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40. Is renal cell carcinoma associated with MITF c.952G>A (p.E318K)?
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Harraka P, Bruinsma F, Nguyen-Dumont T, Jordan S, Giles GG, Winship IM, Tucker K, and Southey MC
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- Humans, Genetic Predisposition to Disease, Male, Carcinoma, Renal Cell genetics, Carcinoma, Renal Cell pathology, Microphthalmia-Associated Transcription Factor genetics, Microphthalmia-Associated Transcription Factor metabolism, Kidney Neoplasms genetics, Kidney Neoplasms pathology
- Abstract
Competing Interests: Competing interests: None declared.
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- 2024
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41. Genome-Wide Analysis to Assess if Heavy Alcohol Consumption Modifies the Association between SNPs and Pancreatic Cancer Risk.
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Ni Z, Kundu P, McKean DF, Wheeler W, Albanes D, Andreotti G, Antwi SO, Arslan AA, Bamlet WR, Beane-Freeman LE, Berndt SI, Bracci PM, Brennan P, Buring JE, Chanock SJ, Gallinger S, Gaziano JM, Giles GG, Giovannucci EL, Goggins MG, Goodman PJ, Haiman CA, Hassan MM, Holly EA, Hung RJ, Katzke V, Kooperberg C, Kraft P, LeMarchand L, Li D, McCullough ML, Milne RL, Moore SC, Neale RE, Oberg AL, Patel AV, Peters U, Rabe KG, Risch HA, Shu XO, Smith-Byrne K, Visvanathan K, Wactawski-Wende J, White E, Wolpin BM, Yu H, Zeleniuch-Jacquotte A, Zheng W, Zhong J, Amundadottir LT, Stolzenberg-Solomon RZ, and Klein AP
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- Humans, Case-Control Studies, Risk Factors, Genetic Predisposition to Disease, Male, Female, Middle Aged, Pancreatic Neoplasms genetics, Pancreatic Neoplasms epidemiology, Pancreatic Neoplasms etiology, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Alcohol Drinking adverse effects, Alcohol Drinking genetics, Alcohol Drinking epidemiology
- Abstract
Background: Pancreatic cancer is a leading cause of cancer-related death globally. Risk factors for pancreatic cancer include common genetic variants and potentially heavy alcohol consumption. We assessed if genetic variants modify the association between heavy alcohol consumption and pancreatic cancer risk., Methods: We conducted a genome-wide interaction analysis of single-nucleotide polymorphisms (SNP) by heavy alcohol consumption (more than three drinks per day) for pancreatic cancer in European ancestry populations from genome-wide association studies. Our analysis included 3,707 cases and 4,167 controls from case-control studies and 1,098 cases and 1,162 controls from cohort studies. Fixed-effect meta-analyses were conducted., Results: A potential novel region of association on 10p11.22, lead SNP rs7898449 (interaction P value (Pinteraction) = 5.1 × 10-8 in the meta-analysis; Pinteraction = 2.1 × 10-9 in the case-control studies; Pinteraction = 0.91 in the cohort studies), was identified. An SNP correlated with this lead SNP is an expression quantitative trait locus for the neuropilin 1 gene. Of the 17 genomic regions with genome-wide significant evidence of association with pancreatic cancer in prior studies, we observed suggestive evidence that heavy alcohol consumption modified the association for one SNP near LINC00673, rs11655237 on 17q25.1 (Pinteraction = 0.004)., Conclusions: We identified a novel genomic region that may be associated with pancreatic cancer risk in conjunction with heavy alcohol consumption located near an expression quantitative trait locus for neuropilin 1, a protein that plays an important role in the development and progression of pancreatic cancer., Impact: This work can provide insights into the etiology of pancreatic cancer, particularly in heavy drinkers., (©2024 American Association for Cancer Research.)
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- 2024
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42. Large-Scale Alternative Polyadenylation-Wide Association Studies to Identify Putative Cancer Susceptibility Genes.
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Guo X, Ping J, Yang Y, Su X, Shu XO, Wen W, Chen Z, Zhang Y, Tao R, Jia G, He J, Cai Q, Zhang Q, Giles GG, Pearlman R, Rennert G, Vodicka P, Phipps A, Gruber SB, Casey G, Peters U, Long J, Lin W, and Zheng W
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- Humans, Quantitative Trait Loci, Polymorphism, Single Nucleotide, Female, Male, Gene Expression Regulation, Neoplastic, RNA, Messenger genetics, RNA, Messenger metabolism, Cell Line, Tumor, Genetic Predisposition to Disease, Polyadenylation, Genome-Wide Association Study, Neoplasms genetics, 3' Untranslated Regions genetics
- Abstract
Alternative polyadenylation (APA) modulates mRNA processing in the 3'-untranslated regions (3' UTR), affecting mRNA stability and translation efficiency. Research into genetically regulated APA has the potential to provide insights into cancer risk. In this study, we conducted large APA-wide association studies to investigate associations between APA levels and cancer risk. Genetic models were built to predict APA levels in multiple tissues using genotype and RNA sequencing data from 1,337 samples from the Genotype-Tissue Expression project. Associations of genetically predicted APA levels with cancer risk were assessed by applying the prediction models to data from large genome-wide association studies of six common cancers among European ancestry populations: breast, ovarian, prostate, colorectal, lung, and pancreatic cancers. A total of 58 risk genes (corresponding to 76 APA sites) were associated with at least one type of cancer, including 25 genes previously not linked to cancer susceptibility. Of the identified risk APAs, 97.4% and 26.3% were supported by 3'-UTR APA quantitative trait loci and colocalization analyses, respectively. Luciferase reporter assays for four selected putative regulatory 3'-UTR variants demonstrated that the risk alleles of 3'-UTR variants, rs324015 (STAT6), rs2280503 (DIP2B), rs1128450 (FBXO38), and rs145220637 (LDHA), significantly increased the posttranscriptional activities of their target genes compared with reference alleles. Furthermore, knockdown of the target genes confirmed their ability to promote proliferation and migration. Overall, this study provides insights into the role of APA in the genetic susceptibility to common cancers. Significance: Systematic evaluation of associations of alternative polyadenylation with cancer risk reveals 58 putative susceptibility genes, highlighting the contribution of genetically regulated alternative polyadenylation of 3'UTRs to genetic susceptibility to cancer., (©2024 American Association for Cancer Research.)
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- 2024
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43. Association of tea and coffee consumption and biliary tract cancer risk: The Biliary Tract Cancers Pooling Project.
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Huang YH, Loftfield E, Argirion I, Adami HO, Albanes D, Chan AT, Fedirko V, Fraser GE, Freedman ND, Giles GG, Hartge P, Katzke V, Knutsen SF, Lacey J Jr, Liao LM, Luo J, Milne RL, O'Brien KM, Peters U, Poynter JN, Purdue MP, Robien K, Sandin S, Sandler DP, Setiawan VW, Kang JH, Simon TG, Sinha R, VoPham T, Weinstein SJ, White E, Zhang X, Zhu B, McGlynn KA, Campbell PT, Lee MH, and Koshiol J
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- Humans, Male, Female, Middle Aged, Aged, Incidence, Gallbladder Neoplasms epidemiology, Gallbladder Neoplasms etiology, Gallbladder Neoplasms prevention & control, Risk Factors, Adult, Bile Duct Neoplasms epidemiology, Bile Duct Neoplasms etiology, Coffee, Tea, Biliary Tract Neoplasms epidemiology, Biliary Tract Neoplasms etiology
- Abstract
Background and Aims: Tea and coffee are widely consumed beverages worldwide. We evaluated their association with biliary tract cancer (BTC) incidence., Approach and Results: We pooled data from 15 studies in the Biliary Tract Cancers Pooling Project to evaluate associations between tea and coffee consumption and biliary tract cancer development. We categorized participants as nondrinkers (0 cup/day), moderate drinkers (>0 and <3 cups/day), and heavy drinkers (≥3 cups/day). We estimated multivariable HRs and 95% CIs using Cox models. During 29,911,744 person-years of follow-up, 851 gallbladder, 588 intrahepatic bile duct, 753 extrahepatic bile duct, and 458 ampulla of Vater cancer cases were diagnosed. Individuals who drank tea showed a statistically significantly lower incidence rate of gallbladder cancer (GBC) relative to tea nondrinkers (HR=0.77; 95% CI, 0.64-0.91), and intrahepatic bile duct cancer (IHBDC) had an inverse association (HR=0.81; 95% CI, 0.66-1.00). However, no associations were observed for extrahepatic bile duct cancer (EHBDC) or ampulla of Vater cancer (AVC). In contrast, coffee consumption was positively associated with GBC, with a higher incidence rate for individuals consuming more coffee (HR<3 cups/day =1.29; 95% CI, 1.01-1.66; HR≥3 cups/day =1.49; 95% CI, 1.11-1.99, Ptrend=0.01) relative to coffee nondrinkers. However, there was no association between coffee consumption and GBC when restricted to coffee drinkers. There was little evidence of associations between coffee consumption and other biliary tract cancers., Conclusions: Tea consumption was associated with a lower incidence of GBC and possibly IHBDC. Further research is warranted to replicate the observed positive association between coffee and GBC., (Copyright © 2023 American Association for the Study of Liver Diseases.)
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- 2024
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44. Genetic and Environmental Causes of Variation in an Automated Breast Cancer Risk Factor Based on Mammographic Textures.
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Ye Z, Dite GS, Nguyen TL, MacInnis RJ, Schmidt DF, Makalic E, Al-Qershi OM, Nguyen-Dumont T, Goudey B, Stone J, Dowty JG, Giles GG, Southey MC, Hopper JL, and Li S
- Subjects
- Female, Humans, Breast, Mammography, Risk Factors, Twins, Dizygotic genetics, Twins, Monozygotic genetics, Breast Neoplasms diagnostic imaging, Breast Neoplasms genetics
- Abstract
Background: Cirrus is an automated risk predictor for breast cancer that comprises texture-based mammographic features and is mostly independent of mammographic density. We investigated genetic and environmental variance of variation in Cirrus., Methods: We measured Cirrus for 3,195 breast cancer-free participants, including 527 pairs of monozygotic (MZ) twins, 271 pairs of dizygotic (DZ) twins, and 1,599 siblings of twins. Multivariate normal models were used to estimate the variance and familial correlations of age-adjusted Cirrus as a function of age. The classic twin model was expanded to allow the shared environment effects to differ by zygosity. The SNP-based heritability was estimated for a subset of 2,356 participants., Results: There was no evidence that the variance or familial correlations depended on age. The familial correlations were 0.52 (SE, 0.03) for MZ pairs and 0.16(SE, 0.03) for DZ and non-twin sister pairs combined. Shared environmental factors specific to MZ pairs accounted for 20% of the variance. Additive genetic factors accounted for 32% (SE = 5%) of the variance, consistent with the SNP-based heritability of 36% (SE = 16%)., Conclusion: Cirrus is substantially familial due to genetic factors and an influence of shared environmental factors that was evident for MZ twin pairs only. The latter could be due to nongenetic factors operating in utero or in early life that are shared by MZ twins., Impact: Early-life factors, shared more by MZ pairs than DZ/non-twin sister pairs, could play a role in the variation in Cirrus, consistent with early life being recognized as a critical window of vulnerability to breast carcinogens., (©2023 American Association for Cancer Research.)
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- 2024
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45. Genotoxic colibactin mutational signature in colorectal cancer is associated with clinicopathological features, specific genomic alterations and better survival.
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Georgeson P, Steinfelder RS, Harrison TA, Pope BJ, Zaidi SH, Qu C, Lin Y, Joo JE, Mahmood K, Clendenning M, Walker R, Aglago EK, Berndt SI, Brenner H, Campbell PT, Cao Y, Chan AT, Chang-Claude J, Dimou N, Doheny KF, Drew DA, Figueiredo JC, French AJ, Gallinger S, Giannakis M, Giles GG, Goode EL, Gruber SB, Gsur A, Gunter MJ, Harlid S, Hoffmeister M, Hsu L, Huang WY, Huyghe JR, Manson JE, Moreno V, Murphy N, Nassir R, Newton CC, Nowak JA, Obón-Santacana M, Ogino S, Pai RK, Papadimitrou N, Potter JD, Schoen RE, Song M, Sun W, Toland AE, Trinh QM, Tsilidis K, Ugai T, Um CY, Macrae FA, Rosty C, Hudson TJ, Winship IM, Phipps AI, Jenkins MA, Peters U, and Buchanan DD
- Abstract
Background and Aims: The microbiome has long been suspected of a role in colorectal cancer (CRC) tumorigenesis. The mutational signature SBS88 mechanistically links CRC development with the strain of Escherichia coli harboring the pks island that produces the genotoxin colibactin, but the genomic, pathological and survival characteristics associated with SBS88-positive tumors are unknown., Methods: SBS88-positive CRCs were identified from targeted sequencing data from 5,292 CRCs from 17 studies and tested for their association with clinico-pathological features, oncogenic pathways, genomic characteristics and survival., Results: In total, 7.5% (398/5,292) of the CRCs were SBS88-positive, of which 98.7% (392/398) were microsatellite stable/microsatellite instability low (MSS/MSI-L), compared with 80% (3916/4894) of SBS88 negative tumors (p=1.5x10
-28 ). Analysis of MSS/MSI-L CRCs demonstrated that SBS88 positive CRCs were associated with the distal colon (OR=1.84, 95% CI=1.40-2.42, p=1x10-5 ) and rectum (OR=1.90, 95% CI=1.44-2.51, p=6x10-6 ) tumor sites compared with the proximal colon. The top seven recurrent somatic mutations associated with SBS88-positive CRCs demonstrated mutational contexts associated with colibactin-induced DNA damage, the strongest of which was the APC :c.835-8A>G mutation (OR=65.5, 95%CI=39.0-110.0, p=3x10-80 ). Large copy number alterations (CNAs) including CNA loss on 14q and gains on 13q, 16q and 20p were significantly enriched in SBS88-positive CRCs. SBS88-positive CRCs were associated with better CRC-specific survival (p=0.007; hazard ratio of 0.69, 95% CI=0.52-0.90) when stratified by age, sex, study, and by stage., Conclusion: SBS88-positivity, a biomarker of colibactin-induced DNA damage, can identify a novel subtype of CRC characterized by recurrent somatic mutations, copy number alterations and better survival. These findings provide new insights for treatment and prevention strategies for this subtype of CRC., Competing Interests: Competing Interests Dr. Marios Giannakis received research funding from Servier and Janssen, unrelated to this study. Dr. Stephen B Gruber co-founded Brogent International LLC, unrelated to this study. Dr. Jonathan A. Nowak received research support from Akoya Biosciences, Illumina, and NanoString, unrelated to this study. Dr. Rish K. Pai received consultant income from Alimentiv Inc., Allergan, Eli Lilly, and AbbVie, unrelated to this study. Dr. Robert E. Schoen received research support from Freenome, Immunovia, and Exact Sciences, unrelated to this study. All other authors declare no competing interests.- Published
- 2024
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46. Adherence to 2018 WCRF/AICR Cancer Prevention Recommendations and Risk of Cancer: The Melbourne Collaborative Cohort Study.
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Peng Y, Bassett JK, Hodge AM, Melaku YA, Afshar N, Hopper JL, MacInnis RJ, Lynch BM, Smith-Warner SA, Giles GG, Milne RL, and Jayasekara H
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- Male, Humans, United States, Cohort Studies, Risk Factors, Diet, Pancreatic Neoplasms, Financial Management
- Abstract
Background: We examined associations between adherence to adaptations of the 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) cancer prevention recommendations and total, exposure-related and site-specific cancer risk., Methods: A total of 20,001 participants ages 40 to 69 years at enrollment into the Melbourne Collaborative Cohort Study in 1990 to 1994, who had diet, body size, and lifestyle reassessed in 2003 to 2007 ("baseline"), were followed-up through June 2021. We constructed diet and standardized lifestyle scores based on core WCRF/AICR recommendations on diet, alcohol intake, body size and physical activity, and additional scores incorporating weight change, sedentary behavior, and smoking. Associations with cancer risk were estimated using Cox regression, adjusting for confounders., Results: During follow-up (mean = 16 years), 4,710 incident cancers were diagnosed. For highest quintile ("most adherent") of the standardized lifestyle score, compared with lowest ("least adherent"), a HR of 0.82 [95% confidence interval (CI): 0.74-0.92] was observed for total cancer. This association was stronger with smoking included in the score (HR = 0.74; 95% CI: 0.67-0.81). A higher score was associated with lower breast and prostate cancer risk for the standardized score, and with lung, stomach, rectal, and pancreatic cancer risk when the score included smoking. Our analyses identified alcohol use, waist circumference and smoking as key drivers of associations with total cancer risk., Conclusions: Adherence to WCRF/AICR cancer prevention recommendations is associated with lower cancer risk., Impact: With <0.2% of our sample fully adherent to the recommendations, the study emphasizes the vast potential for preventing cancer through modulation of lifestyle habits., (©2023 American Association for Cancer Research.)
- Published
- 2024
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