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35 results on '"Ogino, Shuji"'

1. Genetic risk impacts the association of menopausal hormone therapy with colorectal cancer risk

Author

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

Published
2024
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2. Allometric versus traditional body-shape indices and risk of colorectal cancer: a Mendelian randomization analysis

Author

Rontogianni, Marina O., Bouras, Emmanouil, Aglago, Elom Kouassivi, Freisling, Heinz, Murphy, Neil, Cotterchio, Michelle, Hampe, Jochen, Lindblom, Annika, Pai, Rish K., Pharoah, Paul D. P., Phipps, Amanda I., van Duijnhoven, Franzel J. B., Visvanathan, Kala, van Guelpen, Bethany, Li, Christopher I., Brenner, Hermann, Pellatt, Andrew J., Ogino, Shuji, Gunter, Marc J., Peters, Ulrike, Christakoudi, Sofia, and Tsilidis, Konstantinos K.

Published
2024
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8. Analytical challenges in omics research on asthma and allergy: A National Institute of Allergy and Infectious Diseases workshop

Author

Bunyavanich, Supinda, Becker, Patrice M., Altman, Matthew C., Lasky-Su, Jessica, Ober, Carole, Zengler, Karsten, Berdyshev, Evgeny, Bonneau, Richard, Chatila, Talal, Chatterjee, Nilanjan, Chung, Kian Fan, Cutcliffe, Colleen, Davidson, Wendy, Dong, Gang, Fang, Gang, Fulkerson, Patricia, Himes, Blanca E., Liang, Liming, Mathias, Rasika A., Ogino, Shuji, Petrosino, Joseph, Price, Nathan D., Schadt, Eric, Schofield, James, Seibold, Max A., Steen, Hanno, Wheatley, Lisa, Zhang, Hongmei, Togias, Alkis, and Hasegawa, Kohei

Published
2024
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9. Body size and risk of colorectal cancer molecular defined subtypes and pathways: Mendelian randomization analyses

Author

Papadimitriou, Nikos, Qu, Conghui, Harrison, Tabitha A., Bever, Alaina M., Martin, Richard M., Tsilidis, Konstantinos K., Newcomb, Polly A., Thibodeau, Stephen N., Newton, Christina C., Um, Caroline Y., Obón-Santacana, Mireia, Moreno, Victor, Brenner, Hermann, Mandic, Marko, Chang-Claude, Jenny, Hoffmeister, Michael, Pellatt, Andrew J., Schoen, Robert E., Harlid, Sophia, Ogino, Shuji, Ugai, Tomotaka, Buchanan, Daniel D., Lynch, Brigid M., Gruber, Stephen B., Cao, Yin, Hsu, Li, Huyghe, Jeroen R., Lin, Yi, Steinfelder, Robert S., Sun, Wei, Van Guelpen, Bethany, Zaidi, Syed H., Toland, Amanda E., Berndt, Sonja I., Huang, Wen-Yi, Aglago, Elom K., Drew, David A., French, Amy J., Georgeson, Peter, Giannakis, Marios, Hullar, Meredith, Nowak, Johnathan A., Thomas, Claire E., Le Marchand, Loic, Cheng, Iona, Gallinger, Steven, Jenkins, Mark A., Gunter, Marc J., Campbell, Peter T., Peters, Ulrike, Song, Mingyang, Phipps, Amanda I., and Murphy, Neil

Published
2024
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10. Correction: The SIRT1 Deacetylase Suppresses Intestinal Tumorigenesis and Colon Cancer Growth

Author

Firestein, Ron, primary, Blander, Gil, additional, Michan, Shaday, additional, Oberdoerffer, Philipp, additional, Ogino, Shuji, additional, Campbell, Jennifer, additional, Bhimavarapu, Anupama, additional, Luikenhuis, Sandra, additional, de Cabo, Rafael, additional, Fuchs, Charles, additional, Hahn, William C., additional, Guarente, Leonard P., additional, and Sinclair, David A., additional

Published
2024
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11. Two genome-wide interaction loci modify the association of nonsteroidal anti-inflammatory drugs with colorectal cancer

Author

Drew, David A., primary, Kim, Andre E., additional, Lin, Yi, additional, Qu, Conghui, additional, Morrison, John, additional, Lewinger, Juan Pablo, additional, Kawaguchi, Eric, additional, Wang, Jun, additional, Fu, Yubo, additional, Zemlianskaia, Natalia, additional, Díez-Obrero, Virginia, additional, Bien, Stephanie A., additional, Dimou, Niki, additional, Albanes, Demetrius, additional, Baurley, James W., additional, Wu, Anna H., additional, Buchanan, Daniel D., additional, Potter, John D., additional, Prentice, Ross L., additional, Harlid, Sophia, additional, Arndt, Volker, additional, Barry, Elizabeth L., additional, Berndt, Sonja I., additional, Bouras, Emmanouil, additional, Brenner, Hermann, additional, Budiarto, Arif, additional, Burnett-Hartman, Andrea, additional, Campbell, Peter T., additional, Carreras-Torres, Robert, additional, Casey, Graham, additional, Chang-Claude, Jenny, additional, Conti, David V., additional, Devall, Matthew A.M., additional, Figueiredo, Jane C., additional, Gruber, Stephen B., additional, Gsur, Andrea, additional, Gunter, Marc J., additional, Harrison, Tabitha A., additional, Hidaka, Akihisa, additional, Hoffmeister, Michael, additional, Huyghe, Jeroen R., additional, Jenkins, Mark A., additional, Jordahl, Kristina M., additional, Kundaje, Anshul, additional, Le Marchand, Loic, additional, Li, Li, additional, Lynch, Brigid M., additional, Murphy, Neil, additional, Nassir, Rami, additional, Newcomb, Polly A., additional, Newton, Christina C., additional, Obón-Santacana, Mireia, additional, Ogino, Shuji, additional, Ose, Jennifer, additional, Pai, Rish K., additional, Palmer, Julie R., additional, Papadimitriou, Nikos, additional, Pardamean, Bens, additional, Pellatt, Andrew J., additional, Peoples, Anita R., additional, Platz, Elizabeth A., additional, Rennert, Gad, additional, Ruiz-Narvaez, Edward, additional, Sakoda, Lori C., additional, Scacheri, Peter C., additional, Schmit, Stephanie L., additional, Schoen, Robert E., additional, Stern, Mariana C., additional, Su, Yu-Ru, additional, Thomas, Duncan C., additional, Tian, Yu, additional, Tsilidis, Konstantinos K., additional, Ulrich, Cornelia M., additional, Um, Caroline Y., additional, van Duijnhoven, Fränzel J.B., additional, Van Guelpen, Bethany, additional, White, Emily, additional, Hsu, Li, additional, Moreno, Victor, additional, Peters, Ulrike, additional, Chan, Andrew T., additional, and Gauderman, W. James, additional

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

Author

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

Published
2024
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14. Germline genetic regulation of the colorectal tumor immune microenvironment

Author

Schmit, Stephanie L., primary, Tsai, Ya-Yu, additional, Bonner, Joseph D., additional, Sanz-Pamplona, Rebeca, additional, Joshi, Amit D., additional, Ugai, Tomotaka, additional, Lindsey, Sidney S., additional, Melas, Marilena, additional, McDonnell, Kevin J., additional, Idos, Gregory E., additional, Walker, Christopher P., additional, Qu, Chenxu, additional, Kast, W. Martin, additional, Da Silva, Diane M., additional, Glickman, Jonathan N., additional, Chan, Andrew T., additional, Giannakis, Marios, additional, Nowak, Jonathan A., additional, Rennert, Hedy S., additional, Robins, Harlan S., additional, Ogino, Shuji, additional, Greenson, Joel K., additional, Moreno, Victor, additional, Rennert, Gad, additional, and Gruber, Stephen B., additional

Published
2024
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15. Identification of potential mediators of the relationship between body mass index and colorectal cancer: a Mendelian randomization analysis

Author

Bouras, Emmanouil, primary, Gill, Dipender, additional, Zuber, Verena, additional, Murphy, Neil, additional, Dimou, Niki, additional, Aleksandrova, Krasimira, additional, Lewis, Sarah J, additional, Martin, Richard M, additional, Yarmolinsky, James, additional, Albanes, Demetrius, additional, Brenner, Hermann, additional, Castellví-Bel, Sergi, additional, Chan, Andrew T, additional, Cheng, Iona, additional, Gruber, Stephen, additional, Van Guelpen, Bethany, additional, Li, Christopher I, additional, Le Marchand, Loic, additional, Newcomb, Polly A, additional, Ogino, Shuji, additional, Pellatt, Andrew, additional, Schmit, Stephanie L, additional, Wolk, Alicja, additional, Wu, Anna H, additional, Peters, Ulrike, additional, Gunter, Marc J, additional, and Tsilidis, Konstantinos K, additional

Published
2024
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16. Supplemental Table 1 from Epidemiologic Factors in Relation to Colorectal Cancer Risk and Survival by Genotoxic Colibactin Mutational Signature

Author

Thomas, Claire E., primary, Georgeson, Peter, primary, Qu, Conghui, primary, Steinfelder, Robert S., primary, Buchanan, Daniel D., primary, Song, Mingyang, primary, Harrison, Tabitha A., primary, Um, Caroline Y., primary, Hullar, Meredith A., primary, Jenkins, Mark A., primary, Van Guelpen, Bethany, primary, Lynch, Brigid M., primary, Melaku, Yohannes Adama, primary, Huyghe, Jeroen R., primary, Aglago, Elom K., primary, Berndt, Sonja I., primary, Boardman, Lisa A., primary, Campbell, Peter T., primary, Cao, Yin, primary, Chan, Andrew T., primary, Drew, David A., primary, Figueiredo, Jane C., primary, French, Amy J., primary, Giannakis, Marios, primary, Goode, Ellen L., primary, Gruber, Stephen B., primary, Gsur, Andrea, primary, Gunter, Marc J., primary, Hoffmeister, Michael, primary, Hsu, Li, primary, Huang, Wen-Yi, primary, Moreno, Victor, primary, Murphy, Neil, primary, Newcomb, Polly A., primary, Newton, Christina C., primary, Nowak, Jonathan A., primary, Obón-Santacana, Mireia, primary, Ogino, Shuji, primary, Sun, Wei, primary, Toland, Amanda E., primary, Trinh, Quang M., primary, Ugai, Tomotaka, primary, Zaidi, Syed H., primary, Peters, Ulrike, primary, and Phipps, Amanda I., primary

Published
2024
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17. Supplemental Table 2 from Epidemiologic Factors in Relation to Colorectal Cancer Risk and Survival by Genotoxic Colibactin Mutational Signature

Author

Thomas, Claire E., primary, Georgeson, Peter, primary, Qu, Conghui, primary, Steinfelder, Robert S., primary, Buchanan, Daniel D., primary, Song, Mingyang, primary, Harrison, Tabitha A., primary, Um, Caroline Y., primary, Hullar, Meredith A., primary, Jenkins, Mark A., primary, Van Guelpen, Bethany, primary, Lynch, Brigid M., primary, Melaku, Yohannes Adama, primary, Huyghe, Jeroen R., primary, Aglago, Elom K., primary, Berndt, Sonja I., primary, Boardman, Lisa A., primary, Campbell, Peter T., primary, Cao, Yin, primary, Chan, Andrew T., primary, Drew, David A., primary, Figueiredo, Jane C., primary, French, Amy J., primary, Giannakis, Marios, primary, Goode, Ellen L., primary, Gruber, Stephen B., primary, Gsur, Andrea, primary, Gunter, Marc J., primary, Hoffmeister, Michael, primary, Hsu, Li, primary, Huang, Wen-Yi, primary, Moreno, Victor, primary, Murphy, Neil, primary, Newcomb, Polly A., primary, Newton, Christina C., primary, Nowak, Jonathan A., primary, Obón-Santacana, Mireia, primary, Ogino, Shuji, primary, Sun, Wei, primary, Toland, Amanda E., primary, Trinh, Quang M., primary, Ugai, Tomotaka, primary, Zaidi, Syed H., primary, Peters, Ulrike, primary, and Phipps, Amanda I., primary

Published
2024
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18. Data from Epidemiologic Factors in Relation to Colorectal Cancer Risk and Survival by Genotoxic Colibactin Mutational Signature

Author

Thomas, Claire E., primary, Georgeson, Peter, primary, Qu, Conghui, primary, Steinfelder, Robert S., primary, Buchanan, Daniel D., primary, Song, Mingyang, primary, Harrison, Tabitha A., primary, Um, Caroline Y., primary, Hullar, Meredith A., primary, Jenkins, Mark A., primary, Van Guelpen, Bethany, primary, Lynch, Brigid M., primary, Melaku, Yohannes Adama, primary, Huyghe, Jeroen R., primary, Aglago, Elom K., primary, Berndt, Sonja I., primary, Boardman, Lisa A., primary, Campbell, Peter T., primary, Cao, Yin, primary, Chan, Andrew T., primary, Drew, David A., primary, Figueiredo, Jane C., primary, French, Amy J., primary, Giannakis, Marios, primary, Goode, Ellen L., primary, Gruber, Stephen B., primary, Gsur, Andrea, primary, Gunter, Marc J., primary, Hoffmeister, Michael, primary, Hsu, Li, primary, Huang, Wen-Yi, primary, Moreno, Victor, primary, Murphy, Neil, primary, Newcomb, Polly A., primary, Newton, Christina C., primary, Nowak, Jonathan A., primary, Obón-Santacana, Mireia, primary, Ogino, Shuji, primary, Sun, Wei, primary, Toland, Amanda E., primary, Trinh, Quang M., primary, Ugai, Tomotaka, primary, Zaidi, Syed H., primary, Peters, Ulrike, primary, and Phipps, Amanda I., primary

Published
2024
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20. Metabolomic signatures of inflammation and metabolic dysregulation in relation to colorectal cancer risk

Author

Bever, Alaina M, primary, Hang, Dong, additional, Lee, Dong Hoon, additional, Tabung, Fred K, additional, Ugai, Tomotaka, additional, Ogino, Shuji, additional, Meyerhardt, Jeffrey A, additional, Chan, Andrew T, additional, Eliassen, A Heather, additional, Liang, Liming, additional, Stampfer, Meir J, additional, and Song, Mingyang, additional

Published
2024
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21. Epidemiologic Factors in Relation to Colorectal Cancer Risk and Survival by Genotoxic Colibactin Mutational Signature

Author

Thomas, Claire E., primary, Georgeson, Peter, additional, Qu, Conghui, additional, Steinfelder, Robert S., additional, Buchanan, Daniel D., additional, Song, Mingyang, additional, Harrison, Tabitha A., additional, Um, Caroline Y., additional, Hullar, Meredith A., additional, Jenkins, Mark A., additional, Van Guelpen, Bethany, additional, Lynch, Brigid M., additional, Melaku, Yohannes Adama, additional, Huyghe, Jeroen R., additional, Aglago, Elom K., additional, Berndt, Sonja I., additional, Boardman, Lisa A., additional, Campbell, Peter T., additional, Cao, Yin, additional, Chan, Andrew T., additional, Drew, David A., additional, Figueiredo, Jane C., additional, French, Amy J., additional, Giannakis, Marios, additional, Goode, Ellen L., additional, Gruber, Stephen B., additional, Gsur, Andrea, additional, Gunter, Marc J., additional, Hoffmeister, Michael, additional, Hsu, Li, additional, Huang, Wen-Yi, additional, Moreno, Victor, additional, Murphy, Neil, additional, Newcomb, Polly A., additional, Newton, Christina C., additional, Nowak, Jonathan A., additional, Obón-Santacana, Mireia, additional, Ogino, Shuji, additional, Sun, Wei, additional, Toland, Amanda E., additional, Trinh, Quang M., additional, Ugai, Tomotaka, additional, Zaidi, Syed H., additional, Peters, Ulrike, additional, and Phipps, Amanda I., additional

Published
2024
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22. Post‐diagnostic multivitamin supplement use and colorectal cancer survival: A prospective cohort study

Author

He, Ming‐ming, primary, Wang, Kai, additional, Lo, Chun‐Han, additional, Zhang, Yiwen, additional, Polychronidis, Georgios, additional, Knudsen, Markus D., additional, Zhong, Rong, additional, Ma, Yuan, additional, Wu, Kana, additional, Chan, Andrew T., additional, Giovannucci, Edward L., additional, Ogino, Shuji, additional, Ng, Kimmie, additional, Meyerhardt, Jeffrey A., additional, and Song, Mingyang, additional

Published
2024
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23. Weighting estimation in the cause‐specific Cox regression with partially missing causes of failure.

Author

Lee, Jooyoung, Ogino, Shuji, and Wang, Molin

Subjects
*PROPORTIONAL hazards models, *TUMOR markers, *MISSING data (Statistics), *MOLECULAR epidemiology
Abstract

Complex diseases are often analyzed using disease subtypes classified by multiple biomarkers to study pathogenic heterogeneity. In such molecular pathological epidemiology research, we consider a weighted Cox proportional hazard model to evaluate the effect of exposures on various disease subtypes under competing‐risk settings in the presence of partially or completely missing biomarkers. The asymptotic properties of the inverse and augmented inverse probability‐weighted estimating equation methods are studied with a general pattern of missing data. Simulation studies have been conducted to demonstrate the double robustness of the estimators. For illustration, we applied this method to examine the association between pack‐years of smoking before the age of 30 and the incidence of colorectal cancer subtypes defined by a combination of four tumor molecular biomarkers (statuses of microsatellite instability, CpG island methylator phenotype, BRAF mutation, and KRAS mutation) in the Nurses' Health Study cohort. [ABSTRACT FROM AUTHOR]

Published
2024
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28. Folate intake and colorectal cancer risk according to genetic subtypes defined by targeted tumor sequencing

Author

Aglago, Elom K., Qu, Conghui, Harlid, Sophia, Phipps, Amanda I., Steinfelder, Robert S., Ogino, Shuji, Thomas, Claire E., Hsu, Li, Toland, Amanda E., Brenner, Hermann, Berndt, Sonja I., Buchanan, Daniel D., Campbell, Peter T., Cao, Yin, Chan, Andrew T., Drew, David A., Figueiredo, Jane C., French, Amy J., Gallinger, Steven, Georgeson, Peter, Giannakis, Marios, Goode, Ellen L., Gruber, Stephen B., Gunter, Marc J., Harrison, Tabitha A., Hoffmeister, Michael, Huang, Wen-Yi, Hullar, Meredith AJ., Huyghe, Jeroen R., Jenkins, Mark A., Lynch, Brigid M., Moreno, Victor, Murphy, Neil, Newton, Christina C., Nowak, Jonathan A., Obón-Santacana, Mireia, Sun, Wei, Ugai, Tomotaka, Um, Caroline Y., Zaidi, Syed H., Tsilidis, Konstantinos K., van Guelpen, Bethany, and Peters, Ulrike

Abstract

Folate is involved in multiple genetic, epigenetic, and metabolic processes, and inadequate folate intake has been associated with an increased risk of cancer.

Published
2024
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29. Quantitative multiplexed analysis of IDO and ARG1 expression and myeloid cell infiltration in colorectal cancer

Author

Elomaa, Hanna, Härkönen, Jouni, Väyrynen, Sara A., Ahtiainen, Maarit, Ogino, Shuji, Nowak, Jonathan A., Lau, Mai Chan, Helminen, Olli, Wirta, Erkki-Ville, Seppälä, Toni T., Böhm, Jan, Mecklin, Jukka-Pekka, Kuopio, Teijo, and Väyrynen, Juha P.

Abstract

Indoleamine 2,3-dioxygenase (IDO) and Arginase-1 (ARG1) are amino acid metabolizing enzymes frequently highly expressed in cancer. Their expression may deplete essential amino acids, lead to immunosuppression, and promote cancer growth. Still, their expression patterns, prognostic significance, and spatial localization in the colorectal cancer microenvironment are incompletely understood. Using a custom 10-plex immunohistochemistry assay and supervised machine learning-based digital image analysis, we characterized IDO and ARG1 expression in monocytic cells, granulocytes, mast cells, and tumor cells in 833 colorectal cancer patients. We evaluated the prognostic value and spatial arrangement of IDO and ARG1 expressing myeloid cells and tumor cells. IDO was mainly expressed by monocytic cells but also by some tumor cells, whereas ARG1 was predominantly expressed by granulocytes. Higher density of IDO+monocytic cells was an independent prognostic factor for improved cancer-specific survival both in the tumor center (Ptrend=0.0002; HR for the highest ordinal category Q4 (vs Q1) 0.51, 95% CI 0.33–0.79) and the invasive margin (Ptrend=0.0015). Higher density of granulocytes was associated with prolonged cancer-specific survival in univariable models and higher FCGR3+ARG1+neutrophil density in the tumor center also in multivariable analysis (Ptrend=0.0020). Granulocytes were, on average, located closer to tumor cells than monocytic cells. Furthermore, IDO+monocytic cells and ARG1–granulocytes were closer than IDO–monocytic cells and ARG1+granulocytes, respectively. The mRNA expression of the IDO1gene was assessed in myeloid and tumor cells using publicly available single-cell RNA sequencing data for 62 colorectal cancers. IDO1was mainly expressed in monocytes and dendritic cells, and high IDO1activity in monocytes was associated with enriched immunostimulatory pathways. Our findings provided in-depth information about the infiltration patterns and prognostic value of cells expressing IDO and/or ARG1 in the colorectal cancer microenvironment highlighting the significance of host immune response in tumor progression.

Published
2024
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30. Improved Survival With Adjuvant Cyclooxygenase 2 Inhibition in PIK3CA -Activated Stage III Colon Cancer: CALGB/SWOG 80702 (Alliance).

Author

Nowak JA, Twombly T, Ma C, Shi Q, Haruki K, Fujiyoshi K, Väyrynen J, Zhao M, Knight J, Mane S, Shergill A, Kumar P, Couture F, Kuebler P, Krishnamurthi S, Tan B, Philip P, O'Reilly EM, Shields AF, Ogino S, Fuchs CS, and Meyerhardt JA

Abstract

Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical Trial Updates provide an opportunity to disseminate additional results from studies, published in JCO or elsewhere, for which the primary end point has already been reported. Observational studies have associated aspirin or cyclooxygenase 2 (COX-2) inhibitor usage either before or after colorectal cancer diagnosis with lower risk of recurrence and suggest that PIK3CA mutational status is predictive of better response to COX-2 inhibition. To prospectively test whether adding the COX-2 inhibitor celecoxib to standard adjuvant chemotherapy reduces the risk of recurrence and improves survival, the National Cancer Institute sponsored the CALGB/SWOG 80702 trial (ClinicalTrials.gov identifier: NCT01150045) for patients with stage III resected colon cancer. Although the primary hypothesis for all patients did not show a statistically significant improvement in disease-free survival (DFS) with celecoxib, subgroup analysis by PIK3CA mutational status was a preplanned study. PIK3CA gain-of-function mutations were detected in 259 of 1,197 tumors with available whole-exome sequencing data. When stratified by PIK3CA status, patients with PIK3CA gain-of-function mutations treated with celecoxib exhibited improved DFS (adjusted hazard ratio [HR], 0.56 [95% CI, 0.33 to 0.96]) compared with PIK3CA wildtype patients (adjusted HR, 0.89 [95% CI, 0.70 to 1.14]), although the interaction test was nonsignificant ( P interaction = .13). Overall survival was similarly improved for patients with PIK3CA gain-of-function mutations (adjusted HR, 0.44 [95% CI, 0.22 to 0.85]) compared with PIK3CA wildtype patients (adjusted HR, 0.94 [95% CI, 0.68 to 1.30]; P interaction = .04). Although the test for heterogeneity in DFS did not reach statistical significance, the results suggest potential utility of PIK3CA to consider selective usage of COX-2 inhibitors in addition to standard treatment for stage III colon cancer.

Published
2024
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31. Appendectomy and Long-term Colorectal Cancer Incidence, Overall and by Tumor Fusobacterium nucleatum Status.

Author

Kawamura H, Ugai T, Takashima Y, Okadome K, Shimizu T, Mima K, Akimoto N, Haruki K, Arima K, Zhao M, Väyrynen JP, Wu K, Zhang X, Ng K, Nowak JA, Meyerhardt JA, Giovannucci EL, Giannakis M, Chan AT, Huttenhower C, Garrett WS, Song M, and Ogino S

Abstract

Objective: To test hypotheses that appendectomy history might lower long-term colorectal cancer risk and that the risk reduction might be strong for tumors enriched with Fusobacterium nucleatum, bacterial species implicated in colorectal carcinogenesis., Background: The absence of the appendix, an immune system organ and a possible reservoir of certain pathogenic microbes, may affect the intestinal microbiome, thereby altering long-term colorectal cancer risk., Methods: Utilizing databases of prospective cohort studies, namely the Nurses' Health Study and the Health Professionals Follow-up Study, we examined the association of appendectomy history with colorectal cancer incidence overall and subclassified by the amount of tumor tissue Fusobacterium nucleatum​​ (Fusobacterium animalis). We used an inverse probability weighted multivariable-adjusted duplication-method Cox proportional hazards regression model., Results: During the follow-up of 139,406 participants (2,894,060 person-years), we documented 2811 incident colorectal cancer cases, of which 1065 cases provided tissue F. nucleatum analysis data. The multivariable-adjusted hazard ratio of appendectomy for overall colorectal cancer incidence was 0.92 (95% CI, 0.84-1.01). Appendectomy was associated with lower F. nucleatum-positive cancer incidence (multivariable-adjusted hazard ratio, 0.53; 95% CI, 0.33-0.85; P=0.0079), but not F. nucleatum-negative cancer incidence (multivariable-adjusted hazard ratio, 0.98; 95% CI, 0.83-1.14), suggesting a differential association by F. nucleatum status (Pheterogeneity=0.015). This differential association appeared to persist in various participant/patient strata including tumor location and microsatellite instability status., Conclusions: Appendectomy likely lowers the future long-term incidence of F. nucleatum-positive (but not F. nucleatum-negative) colorectal cancer. Our findings do not support the existing hypothesis that appendectomy may increase colorectal cancer risk., Competing Interests: A.T.C. previously served as a consultant for Bayer Healthcare and Pfizer Inc. M.G. was on an advisory board for AstraZeneca and receives research funding from Bristol-Myers Squibb. J.A.M. has served as an advisor/consultant to Merck Pharmaceuticals and COTA Healthcare. K.W. is currently a stakeholder and employee of Vertex Pharmaceuticals. This study was not funded by any of these commercial entities. The remaining authors report no conflicts of interest., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Published
2024
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32. Alcohol and colorectal cancer risk subclassified by mutational signatures of DNA mismatch repair deficiency.

Author

Fang A, Ugai T, Gurjao C, Zhong R, Liu Z, Zhang X, Wang P, Nowak J, Wang M, Giannakis M, Ogino S, Zhang X, and Giovannucci E

Abstract

Background: We examined whether the association between alcohol consumption and CRC incidence was stronger for tumors with higher contributions of defective MMR (dMMR)-related tumor mutational signatures (TMSs)., Methods: We used data from 227,916 men and women who participated in the Nurses' Health Study (1980-2016), the Nurses' Health Study II (1991-2017), and the Health Professionals Follow-up Study (1986-2016). Dietary data was collected every 4 years through validated food frequency questionnaires. Relative contributions of two dMMR-related TMSs (c-dMMRa/SBS15 and c-dMMRb/SBS26) were quantified using whole-exome sequencing data in a subset of incident CRC cases. Duplication-method Cox proportional hazards regression models were used to assess the association between alcohol consumption and the risk of CRC subtypes according to different contributions of the TMSs. All statistical tests were 2-sided., Results: We documented 825 incident CRC cases with available TMS data over 26-36 years of follow-up. The association between alcohol consumption and CRC incidence was stronger for tumors with higher contributions of c-dMMRb/SBS26 (P-heterogeneitytrend = 0.02) compared to tumors with lower contributions of this TMS. Compared with nondrinkers, drinkers with ≥15 g/d of alcohol had a high risk of c-dMMRb/SBS26-high CRC [multivariable-adjusted HR: 2.43 (95% CI: 1.55-3.82)], but not c-dMMRb/SBS26-low CRC [0.86 (95% CI: 0.57-1.28)] or c-dMMRb/SBS26-moderate CRC [1.14 (95% CI: 0.76-1.71)]. No significant differential associations were observed for c-dMMRa/SBS15 (P-heterogeneitytrend = 0.41)., Conclusions: High alcohol consumption was associated with an increased incidence of CRC containing higher contributions of c-dMMRb/SBS26, suggesting that alcohol consumption may be involved in colorectal carcinogenesis through the DNA mismatch repair pathway., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2024
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33. The Cancer Spectrum Theory.

Author

Lee HY, Song M, Stopsack KH, Peng C, Phipps AI, Wang M, Ogino S, Sasamoto N, and Ugai T

Subjects
Humans, Precision Medicine, Medical Oncology, Neoplasms genetics, Neoplasms pathology
Abstract

Summary: Biological characteristics of tumors are heterogeneous, forming spectra in terms of several factors such as age at onset, anatomic spatial localization, tumor subtyping, and the degree of tumor aggressiveness (encompassing a neoplastic property spectrum). Instead of blindly using dichotomized approaches, the application of the multicategorical and continuous analysis approaches to detailed cancer spectrum data can contribute to a better understanding of the etiology of cancer, ultimately leading to effective prevention and precision oncology. We provide examples of cancer spectra and emphasize the importance of integrating the cancer spectrum theory into large-scale population cancer research., (©2024 American Association for Cancer Research.)

Published
2024
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34. Metabolomic signatures of inflammation and metabolic dysregulation in relation to colorectal cancer risk.

Author

Bever AM, Hang D, Lee DH, Tabung FK, Ugai T, Ogino S, Meyerhardt JA, Chan AT, Eliassen AH, Liang L, Stampfer MJ, and Song M

Abstract

Background: Inflammation and metabolic dysregulation are associated with increased risk of colorectal cancer (CRC); the underlying mechanisms are not fully understood. We characterized metabolomic signatures of inflammation and metabolic dysregulation and evaluated the association of the signatures and individual metabolites with CRC risk., Methods: Among 684 incident CRC cases and 684 age-matched controls in the Nurses' Health Study (n = 818 women) and Health Professionals Follow-up Study (n = 550 men), we applied reduced rank and elastic net regression to 277 metabolites for markers of inflammation (CRP, IL6, TNFRSF1B, and GDF15) or metabolic dysregulation (body mass index, waist circumference, C-peptide, and adiponectin) to derive metabolomic signatures. We evaluated the association of the signatures and individual metabolites with CRC using multivariable conditional logistic regression. All statistical tests were 2-sided., Results: We derived a signature of 100 metabolites that explained 24% of variation in markers of inflammation and a signature of 73 metabolites that explained 27% of variation in markers of metabolic dysregulation. Among men, both signatures were associated with CRC (odds ratio per 1-standard deviation increase, inflammation = 1.34, 95% confidence interval 1.07 to 1.68; metabolic dysregulation = 1.25, 1.00 to 1.55); neither signature was associated with CRC in women. Eleven metabolites were individually associated with CRC and biomarkers of inflammation or metabolic dysregulation among either men or women., Conclusion: We derived metabolomic signatures and identified individual metabolites associated with inflammation, metabolic dysregulation, and CRC, highlighting several metabolites as promising candidates involved in the inflammatory and metabolic dysregulation pathways for CRC incidence., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2024
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35. Genotoxic colibactin mutational signature in colorectal cancer is associated with clinicopathological features, specific genomic alterations and better survival.

Author

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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