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Start Over Author "Severi, Gianluca" Journal journal of the national cancer institute
20 results on '"Severi, Gianluca"'

1. A Prospective Study of the Immune System Activation Biomarker Neopterin and Colorectal Cancer Risk

Author

Aleksandrova, Krasimira, Chuang, Shu-Chun, Boeing, Heiner, Zuo, Hui, Tell, Grethe S, Pischon, Tobias, Jenab, Mazda, Bueno-de-Mesquita, Bas, Vollset, Stein Emil, Midttun, Øivind, Ueland, Per Magne, Fedirko, Veronika, Johansson, Mattias, Weiderpass, Elisabete, Severi, Gianluca, Racine, Antoine, Boutron-Ruault, Marie-Christine, Kaaks, Rudolf, Kühn, Tilman, Tjønneland, Anne, Overvad, Kim, Quirós, J Ramón, Jakszyn, Paula, Sánchez, María-José, Dorronsoro, Miren, Chirlaque, Maria-Dolores, Ardanaz, Eva, Khaw, Kay-Tee, Wareham, Nicholas J, Travis, Ruth C, Trichopoulou, Antonia, Lagiou, Pagona, Trichopoulos, Dimitrios, Palli, Domenico, Sieri, Sabina, Tumino, Rosario, Panico, Salvatore, May, Anne M, Palmqvist, Richard, Ljuslinder, Ingrid, Kong, So Yeon J, Freisling, Heinz, Gunter, Marc J, Lu, Yunxia, Cross, Amanda J, Riboli, Elio, and Vineis, Paolo

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Colo-Rectal Cancer, Cancer, Clinical Research, Digestive Diseases, Adult, Aged, Biomarkers, Tumor, Case-Control Studies, Chromatography, Liquid, Colonic Neoplasms, Colorectal Neoplasms, Europe, Female, Humans, Immunity, Cellular, Male, Middle Aged, Neopterin, Odds Ratio, Prospective Studies, Rectal Neoplasms, Sensitivity and Specificity, T-Lymphocytes, Helper-Inducer, Tandem Mass Spectrometry, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Neopterin may be relevant for colorectal cancer (CRC) development, as a biomarker of cellular immune activity exerting pleiotropic effects on cellular ageing, oxidative stress, and inflammation. So far, the association between prediagnostic neopterin and colon and rectal cancer risk has not been evaluated in human populations. A nested case-control study was conducted within the European Prospective Investigation into Cancer and Nutrition cohort using data on plasma concentrations of total neopterin (T-N, sum of neopterin and 7,8-dihydroneopterin) in 830 incident CRC case patients (561 colon and 269 rectal) matched within risk sets to 830 control participants. A subsequent replication study used data from the Hordaland Health Study, where 173 CRC case patients have been diagnosed among 6594 healthy participants over 12 years of follow-up. After multivariable adjustment for a priori chosen CRC risk factors, a "U-shaped" association of T-N with CRC was revealed. Compared with the second quintile of the T-N distribution, the relative risks for the first, third, fourth, and fifth quintiles were 2.37 (95% CI = 1.66 to 3.39), 1.24 (95% CI = 0.87 to 1.77), 1.55 (95% CI = 1.08 to 2.22), and 2.31 (95% CI = 1.63 to 3.27), respectively. Replication of these associations within the Hordaland Health Study yielded similar results. No differences have been observed when the associations were explored by colon and rectal cancer site (two-sided P difference = .87) and after excluding case patients diagnosed within the first four follow-up years. These novel findings provide evidence of the role of both suppressed and activated cell-mediated immunity as reflected by prediagnostic T-N concentrations in the development of CRC.

Published
2015

2. Associations of breast cancer risk factors with tumor subtypes: a pooled analysis from the Breast Cancer Association Consortium studies.

Author

Yang, Xiaohong R, Chang-Claude, Jenny, Goode, Ellen L, Couch, Fergus J, Nevanlinna, Heli, Milne, Roger L, Gaudet, Mia, Schmidt, Marjanka K, Broeks, Annegien, Cox, Angela, Fasching, Peter A, Hein, Rebecca, Spurdle, Amanda B, Blows, Fiona, Driver, Kristy, Flesch-Janys, Dieter, Heinz, Judith, Sinn, Peter, Vrieling, Alina, Heikkinen, Tuomas, Aittomäki, Kristiina, Heikkilä, Päivi, Blomqvist, Carl, Lissowska, Jolanta, Peplonska, Beata, Chanock, Stephen, Figueroa, Jonine, Brinton, Louise, Hall, Per, Czene, Kamila, Humphreys, Keith, Darabi, Hatef, Liu, Jianjun, Van 't Veer, Laura J, van Leeuwen, Flora E, Andrulis, Irene L, Glendon, Gord, Knight, Julia A, Mulligan, Anna Marie, O'Malley, Frances P, Weerasooriya, Nayana, John, Esther M, Beckmann, Matthias W, Hartmann, Arndt, Weihbrecht, Sebastian B, Wachter, David L, Jud, Sebastian M, Loehberg, Christian R, Baglietto, Laura, English, Dallas R, Giles, Graham G, McLean, Catriona A, Severi, Gianluca, Lambrechts, Diether, Vandorpe, Thijs, Weltens, Caroline, Paridaens, Robert, Smeets, Ann, Neven, Patrick, Wildiers, Hans, Wang, Xianshu, Olson, Janet E, Cafourek, Victoria, Fredericksen, Zachary, Kosel, Matthew, Vachon, Celine, Cramp, Helen E, Connley, Daniel, Cross, Simon S, Balasubramanian, Sabapathy P, Reed, Malcolm WR, Dörk, Thilo, Bremer, Michael, Meyer, Andreas, Karstens, Johann H, Ay, Aysun, Park-Simon, Tjoung-Won, Hillemanns, Peter, Arias Pérez, Jose Ignacio, Menéndez Rodríguez, Primitiva, Zamora, Pilar, Benítez, Javier, Ko, Yon-Dschun, Fischer, Hans-Peter, Hamann, Ute, Pesch, Beate, Brüning, Thomas, Justenhoven, Christina, Brauch, Hiltrud, Eccles, Diana M, Tapper, William J, Gerty, Sue M, Sawyer, Elinor J, Tomlinson, Ian P, Jones, Angela, Kerin, Michael, Miller, Nicola, McInerney, Niall, Anton-Culver, Hoda, and Ziogas, Argyrios

Subjects
Humans, Breast Neoplasms, Obesity, Receptor, erbB-2, Receptors, Estrogen, Receptors, Progesterone, Body Mass Index, Logistic Models, Odds Ratio, Risk Factors, Case-Control Studies, Age Factors, Parity, Parturition, Menarche, Female, Keratin-5, ErbB Receptors, Biomarkers, Tumor, Receptor, ErbB-2, Prevention, Cancer, Aging, Breast Cancer, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

BackgroundPrevious studies have suggested that breast cancer risk factors are associated with estrogen receptor (ER) and progesterone receptor (PR) expression status of the tumors.MethodsWe pooled tumor marker and epidemiological risk factor data from 35,568 invasive breast cancer case patients from 34 studies participating in the Breast Cancer Association Consortium. Logistic regression models were used in case-case analyses to estimate associations between epidemiological risk factors and tumor subtypes, and case-control analyses to estimate associations between epidemiological risk factors and the risk of developing specific tumor subtypes in 12 population-based studies. All statistical tests were two-sided.ResultsIn case-case analyses, of the epidemiological risk factors examined, early age at menarche (≤12 years) was less frequent in case patients with PR(-) than PR(+) tumors (P = .001). Nulliparity (P = 3 × 10(-6)) and increasing age at first birth (P = 2 × 10(-9)) were less frequent in ER(-) than in ER(+) tumors. Obesity (body mass index [BMI] ≥ 30 kg/m(2)) in younger women (≤50 years) was more frequent in ER(-)/PR(-) than in ER(+)/PR(+) tumors (P = 1 × 10(-7)), whereas obesity in older women (>50 years) was less frequent in PR(-) than in PR(+) tumors (P = 6 × 10(-4)). The triple-negative (ER(-)/PR(-)/HER2(-)) or core basal phenotype (CBP; triple-negative and cytokeratins [CK]5/6(+) and/or epidermal growth factor receptor [EGFR](+)) accounted for much of the heterogeneity in parity-related variables and BMI in younger women. Case-control analyses showed that nulliparity, increasing age at first birth, and obesity in younger women showed the expected associations with the risk of ER(+) or PR(+) tumors but not triple-negative (nulliparity vs parity, odds ratio [OR] = 0.94, 95% confidence interval [CI] = 0.75 to 1.19, P = .61; 5-year increase in age at first full-term birth, OR = 0.95, 95% CI = 0.86 to 1.05, P = .34; obesity in younger women, OR = 1.36, 95% CI = 0.95 to 1.94, P = .09) or CBP tumors.ConclusionsThis study shows that reproductive factors and BMI are most clearly associated with hormone receptor-positive tumors and suggest that triple-negative or CBP tumors may have distinct etiology.

Published
2011

3. Association Between a Germline OCA2 Polymorphism at Chromosome 15q13.1 and Estrogen Receptor–Negative Breast Cancer Survival

Author

Azzato, Elizabeth M, Tyrer, Jonathan, Fasching, Peter A, Beckmann, Matthias W, Ekici, Arif B, Schulz-Wendtland, Rüdiger, Bojesen, Stig E, Nordestgaard, Børge G, Flyger, Henrik, Milne, Roger L, Arias, José Ignacio, Menéndez, Primitiva, Benítez, Javier, Chang-Claude, Jenny, Hein, Rebecca, Wang-Gohrke, Shan, Nevanlinna, Heli, Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Margolin, Sara, Mannermaa, Arto, Kosma, Veli-Matti, Kataja, Vesa, Beesley, Jonathan, Chen, Xiaoqing, Chenevix-Trench, Georgia, Couch, Fergus J, Olson, Janet E, Fredericksen, Zachary S, Wang, Xianshu, Giles, Graham G, Severi, Gianluca, Baglietto, Laura, Southey, Melissa C, Devilee, Peter, Tollenaar, Rob AEM, Seynaeve, Caroline, García-Closas, Montserrat, Lissowska, Jolanta, Sherman, Mark E, Bolton, Kelly L, Hall, Per, Czene, Kamila, Cox, Angela, Brock, Ian W, Elliott, Graeme C, Reed, Malcolm WR, Greenberg, David, Anton-Culver, Hoda, Ziogas, Argyrios, Humphreys, Manjeet, Easton, Douglas F, Caporaso, Neil E, and Pharoah, Paul DP

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Genetics, Breast Cancer, Human Genome, Cancer, Adult, Aged, Alleles, Biomarkers, Tumor, Breast Neoplasms, Chromosomes, Human, Pair 15, Female, Genotype, Germ-Line Mutation, Humans, Membrane Transport Proteins, Middle Aged, Polymorphism, Single Nucleotide, Proportional Hazards Models, Receptors, Estrogen, Research Design, Risk Assessment, Risk Factors, Survival Analysis, Kathleen Cuningham Foundation Consortium for Research into Familial Breast Cancer, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundTraditional prognostic factors for survival and treatment response of patients with breast cancer do not fully account for observed survival variation. We used available genotype data from a previously conducted two-stage, breast cancer susceptibility genome-wide association study (ie, Studies of Epidemiology and Risk factors in Cancer Heredity [SEARCH]) to investigate associations between variation in germline DNA and overall survival.MethodsWe evaluated possible associations between overall survival after a breast cancer diagnosis and 10 621 germline single-nucleotide polymorphisms (SNPs) from up to 3761 patients with invasive breast cancer (including 647 deaths and 26 978 person-years at risk) that were genotyped previously in the SEARCH study with high-density oligonucleotide microarrays (ie, hypothesis-generating set). Associations with all-cause mortality were assessed for each SNP by use of Cox regression analysis, generating a per rare allele hazard ratio (HR). To validate putative associations, we used patient genotype information that had been obtained with 5' nuclease assay or mass spectrometry and overall survival information for up to 14 096 patients with invasive breast cancer (including 2303 deaths and 70 019 person-years at risk) from 15 international case-control studies (ie, validation set). Fixed-effects meta-analysis was used to generate an overall effect estimate in the validation dataset and in combined SEARCH and validation datasets. All statistical tests were two-sided.ResultsIn the hypothesis-generating dataset, SNP rs4778137 (C>G) of the OCA2 gene at 15q13.1 was statistically significantly associated with overall survival among patients with estrogen receptor-negative tumors, with the rare G allele being associated with increased overall survival (HR of death per rare allele carried = 0.56, 95% confidence interval [CI] = 0.41 to 0.75, P = 9.2 x 10(-5)). This association was also observed in the validation dataset (HR of death per rare allele carried = 0.88, 95% CI = 0.78 to 0.99, P = .03) and in the combined dataset (HR of death per rare allele carried = 0.82, 95% CI = 0.73 to 0.92, P = 5 x 10(-4)).ConclusionThe rare G allele of the OCA2 polymorphism, rs4778137, may be associated with improved overall survival among patients with estrogen receptor-negative breast cancer.

Published
2010

4. Risk of Estrogen Receptor–Positive and –Negative Breast Cancer and Single–Nucleotide Polymorphism 2q35-rs13387042

Author

Milne, Roger L, Benítez, Javier, Nevanlinna, Heli, Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Arias, José Ignacio, Zamora, M Pilar, Burwinkel, Barbara, Bartram, Claus R, Meindl, Alfons, Schmutzler, Rita K, Cox, Angela, Brock, Ian, Elliott, Graeme, Reed, Malcolm WR, Southey, Melissa C, Smith, Letitia, Spurdle, Amanda B, Hopper, John L, Couch, Fergus J, Olson, Janet E, Wang, Xianshu, Fredericksen, Zachary, Schürmann, Peter, Bremer, Michael, Hillemanns, Peter, Dörk, Thilo, Devilee, Peter, van Asperen, Christie J, Tollenaar, Rob AEM, Seynaeve, Caroline, Hall, Per, Czene, Kamila, Liu, Jianjun, Li, Yuqing, Ahmed, Shahana, Dunning, Alison M, Maranian, Melanie, Pharoah, Paul DP, Chenevix-Trench, Georgia, Beesley, Jonathan, Investigators, kConFab, Group, AOCS, Bogdanova, Natalia V, Antonenkova, Natalia N, Zalutsky, Iosif V, Anton-Culver, Hoda, Ziogas, Argyrios, Brauch, Hiltrud, Justenhoven, Christina, Ko, Yon-Dschun, Haas, Susanne, Fasching, Peter A, Strick, Reiner, Ekici, Arif B, Beckmann, Matthias W, Giles, Graham G, Severi, Gianluca, Baglietto, Laura, English, Dallas R, Fletcher, Olivia, Johnson, Nichola, dos Santos Silva, Isabel, Peto, Julian, Turnbull, Clare, Hines, Sarah, Renwick, Anthony, Rahman, Nazneen, Nordestgaard, Børge G, Bojesen, Stig E, Flyger, Henrik, Kang, Daehee, Yoo, Keun-Young, Noh, Dong-Young, Mannermaa, Arto, Kataja, Vesa, Kosma, Veli-Matti, García-Closas, Montserrat, Chanock, Stephen, Lissowska, Jolanta, Brinton, Louise A, Chang-Claude, Jenny, Wang-Gohrke, Shan, Shen, Chen-Yang, Wang, Hui-Chun, Yu, Jyh-Cherng, Chen, Sou-Tong, Bermisheva, Marina, Nikolaeva, Tatjana, Khusnutdinova, Elza, Humphreys, Manjeet K, Morrison, Jonathan, Platte, Radka, Easton, Douglas F, and Consortium, on behalf of the Breast Cancer Association

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Breast Cancer, Clinical Research, Cancer, Human Genome, Estrogen, Adult, Aged, Asian People, Biomarkers, Tumor, Breast Neoplasms, Carcinoma, Ductal, Breast, Carcinoma, Intraductal, Noninfiltrating, Case-Control Studies, Confidence Intervals, Confounding Factors, Epidemiologic, Female, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Linkage Disequilibrium, Middle Aged, Neoplasms, Hormone-Dependent, Odds Ratio, Polymorphism, Single Nucleotide, Receptors, Estrogen, Receptors, Progesterone, White People, kConFab Investigators, AOCS Group, Breast Cancer Association Consortium, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundA recent genome-wide association study identified single-nucleotide polymorphism (SNP) 2q35-rs13387042 as a marker of susceptibility to estrogen receptor (ER)-positive breast cancer. We attempted to confirm this association using the Breast Cancer Association Consortium.Methods2q35-rs13387042 SNP was genotyped for 31 510 women with invasive breast cancer, 1101 women with ductal carcinoma in situ, and 35 969 female control subjects from 25 studies. Odds ratios (ORs) were estimated by logistic regression, adjusted for study. Heterogeneity in odds ratios by each of age, ethnicity, and study was assessed by fitting interaction terms. Heterogeneity by each of invasiveness, family history, bilaterality, and hormone receptor status was assessed by subclassifying case patients and applying polytomous logistic regression. All statistical tests were two-sided.ResultsWe found strong evidence of association between rs13387042 and breast cancer in white women of European origin (per-allele OR = 1.12, 95% confidence interval [CI] = 1.09 to 1.15; P(trend) = 1.0 x 10(-19)). The odds ratio was lower than that previously reported (P = .02) and did not vary by age or ethnicity (all P > or = .2). However, it was higher when the analysis was restricted to case patients who were selected for a strong family history (P = .02). An association was observed for both ER-positive (OR = 1.14, 95% CI = 1.10 to 1.17; P = 10(-15)) and ER-negative disease (OR = 1.10, 95% CI = 1.04 to 1.15; P = .0003) and both progesterone receptor (PR)-positive (OR = 1.15, 95% CI = 1.11 to 1.19; P = 5 x 10(-14)) and PR-negative disease (OR = 1.10, 95% CI = 1.06 to 1.15; P = .00002).ConclusionThe rs13387042 is associated with both ER-positive and ER-negative breast cancer in European women.

Published
2009

5. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types

Author

Sampson, Joshua N., Wheeler, William A., Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I., Lan, Qing, Abnet, Christian C., Amundadottir, Laufey T., Figueroa, Jonine D., Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A., Taylor, Philip R., Vivo, Immaculata De, McGlynn, Katherine A., Purdue, Mark P., Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Jr., Andrulis, Irene L., Angelucci, Emanuele, Ansell, Stephen M., Arici, Cecilia, Armstrong, Bruce K., Arslan, Alan A., Austin, Melissa A., Baris, Dalsu, Barkauskas, Donald A., Bassig, Bryan A., Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A., Birmann, Brenda M., Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M., Brinton, Louise, Brooks-Wilson, Angela R., Bueno-de-Mesquita, H. Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John K. C., Chang, Ellen T., Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C., Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S., Comperat, Eva, Conde, Lucia, Connors, Joseph M., Conti, David, Cortessis, Victoria K., Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, Davis, Faith G., Ding, Ti, Diver, W. Ryan, Dorronsoro, Miren, Dossus, Laure, Duell, Eric J., Ennas, Maria Grazia, Erickson, Ralph L., Feychting, Maria, Flanagan, Adrienne M., Foretova, Lenka, Fraumeni, Joseph F., Jr, Freedman, Neal D., Beane Freeman, Laura E., Fuchs, Charles, Gago-Dominguez, Manuela, Gallinger, Steven, Gao, Yu-Tang, Gapstur, Susan M., Garcia-Closas, Montserrat, García-Closas, Reina, Gascoyne, Randy D., Gastier-Foster, Julie, Gaudet, Mia M., Gaziano, J. Michael, Giffen, Carol, Giles, Graham G., Giovannucci, Edward, Glimelius, Bengt, Goggins, Michael, Gokgoz, Nalan, Goldstein, Alisa M., Gorlick, Richard, Gross, Myron, Grubb, Robert, III, Gu, Jian, Guan, Peng, Gunter, Marc, Guo, Huan, Habermann, Thomas M., Haiman, Christopher A., Halai, Dina, Hallmans, Goran, Hassan, Manal, Hattinger, Claudia, He, Qincheng, He, Xingzhou, Helzlsouer, Kathy, Henderson, Brian, Henriksson, Roger, Hjalgrim, Henrik, Hoffman-Bolton, Judith, Hohensee, Chancellor, Holford, Theodore R., Holly, Elizabeth A., Hong, Yun-Chul, Hoover, Robert N., Horn-Ross, Pamela L., Hosain, G. M. Monawar, Hosgood, H. Dean, III, Hsiao, Chin-Fu, Hu, Nan, Hu, Wei, Hu, Zhibin, Huang, Ming-Shyan, Huerta, Jose-Maria, Hung, Jen-Yu, Hutchinson, Amy, Inskip, Peter D., Jackson, Rebecca D., Jacobs, Eric J., Jenab, Mazda, Jeon, Hyo-Sung, Ji, Bu-Tian, Jin, Guangfu, Jin, Li, Johansen, Christoffer, Johnson, Alison, Jung, Yoo Jin, Kaaks, Rudolph, Kamineni, Aruna, Kane, Eleanor, Kang, Chang Hyun, Karagas, Margaret R., Kelly, Rachel S., Khaw, Kay-Tee, Kim, Christopher, Kim, Hee Nam, Kim, Jin Hee, Kim, Jun Suk, Kim, Yeul Hong, Kim, Young Tae, Kim, Young-Chul, Kitahara, Cari M., Klein, Alison P., Klein, Robert J., Kogevinas, Manolis, Kohno, Takashi, Kolonel, Laurence N., Kooperberg, Charles, Kricker, Anne, Krogh, Vittorio, Kunitoh, Hideo, Kurtz, Robert C., Kweon, Sun-Seog, LaCroix, Andrea, Lawrence, Charles, Lecanda, Fernando, Lee, Victor Ho Fun, Li, Donghui, Li, Haixin, Li, Jihua, Li, Yao-Jen, Li, Yuqing, Liao, Linda M., Liebow, Mark, Lightfoot, Tracy, Lim, Wei-Yen, Lin, Chien-Chung, Lin, Dongxin, Lindstrom, Sara, Linet, Martha S., Link, Brian K., Liu, Chenwei, Liu, Jianjun, Liu, Li, Ljungberg, Börje, Lloreta, Josep, Lollo, Simonetta Di, Lu, Daru, Lund, Eiluv, Malats, Nuria, Mannisto, Satu, Marchand, Loic Le, Marina, Neyssa, Masala, Giovanna, Mastrangelo, Giuseppe, Matsuo, Keitaro, Maynadie, Marc, McKay, James, McKean-Cowdin, Roberta, Melbye, Mads, Melin, Beatrice S., Michaud, Dominique S., Mitsudomi, Tetsuya, Monnereau, Alain, Montalvan, Rebecca, Moore, Lee E., Mortensen, Lotte Maxild, Nieters, Alexandra, North, Kari E., Novak, Anne J., Oberg, Ann L., Offit, Kenneth, Oh, In-Jae, Olson, Sara H., Palli, Domenico, Pao, William, Park, In Kyu, Park, Jae Yong, Park, Kyong Hwa, Patiño-Garcia, Ana, Pavanello, Sofia, Peeters, Petra H. M., Perng, Reury-Perng, Peters, Ulrike, Petersen, Gloria M., Picci, Piero, Pike, Malcolm C., Porru, Stefano, Prescott, Jennifer, Prokunina-Olsson, Ludmila, Qian, Biyun, Qiao, You-Lin, Rais, Marco, Riboli, Elio, Riby, Jacques, Risch, Harvey A., Rizzato, Cosmeri, Rodabough, Rebecca, Roman, Eve, Roupret, Morgan, Ruder, Avima M., Sanjose, Silvia de, Scelo, Ghislaine, Schned, Alan, Schumacher, Fredrick, Schwartz, Kendra, Schwenn, Molly, Scotlandi, Katia, Seow, Adeline, Serra, Consol, Serra, Massimo, Sesso, Howard D., Setiawan, Veronica Wendy, Severi, Gianluca, Severson, Richard K., Shanafelt, Tait D., Shen, Hongbing, Shen, Wei, Shin, Min-Ho, Shiraishi, Kouya, Shu, Xiao-Ou, Siddiq, Afshan, Sierrasesúmaga, Luis, Sihoe, Alan Dart Loon, Skibola, Christine F., Smith, Alex, Smith, Martyn T., Southey, Melissa C., Spinelli, John J., Staines, Anthony, Stampfer, Meir, Stern, Marianna C., Stevens, Victoria L., Stolzenberg-Solomon, Rachael S., Su, Jian, Su, Wu-Chou, Sund, Malin, Sung, Jae Sook, Sung, Sook Whan, Tan, Wen, Tang, Wei, Tardón, Adonina, Thomas, David, Thompson, Carrie A., Tinker, Lesley F., Tirabosco, Roberto, Tjønneland, Anne, Travis, Ruth C., Trichopoulos, Dimitrios, Tsai, Fang-Yu, Tsai, Ying-Huang, Tucker, Margaret, Turner, Jenny, Vajdic, Claire M., Vermeulen, Roel C. H., Villano, Danylo J., Vineis, Paolo, Virtamo, Jarmo, Visvanathan, Kala, Wactawski-Wende, Jean, Wang, Chaoyu, Wang, Chih-Liang, Wang, Jiu-Cun, Wang, Junwen, Wei, Fusheng, Weiderpass, Elisabete, Weiner, George J., Weinstein, Stephanie, Wentzensen, Nicolas, White, Emily, Witzig, Thomas E., Wolpin, Brian M., Wong, Maria Pik, Wu, Chen, Wu, Guoping, Wu, Junjie, Wu, Tangchun, Wu, Wei, Wu, Xifeng, Wu, Yi-Long, Wunder, Jay S., Xiang, Yong-Bing, Xu, Jun, Xu, Ping, Yang, Pan-Chyr, Yang, Tsung-Ying, Ye, Yuanqing, Yin, Zhihua, Yokota, Jun, Yoon, Ho-Il, Yu, Chong-Jen, Yu, Herbert, Yu, Kai, Yuan, Jian-Min, Zelenetz, Andrew, Zeleniuch-Jacquotte, Anne, Zhang, Xu-Chao, Zhang, Yawei, Zhao, Xueying, Zhao, Zhenhong, Zheng, Hong, Zheng, Tongzhang, Zheng, Wei, Zhou, Baosen, Zhu, Meng, Zucca, Mariagrazia, Boca, Simina M., Cerhan, James R., Ferri, Giovanni M., Hartge, Patricia, Hsiung, Chao Agnes, Magnani, Corrado, Miligi, Lucia, Morton, Lindsay M., Smedby, Karin E., Teras, Lauren R., Vijai, Joseph, Wang, Sophia S., Brennan, Paul, Caporaso, Neil E., Hunter, David J., Kraft, Peter, Rothman, Nathaniel, Silverman, Debra T., Slager, Susan L., Chanock, Stephen J., and Chatterjee, Nilanjan

Published
2015
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6. Circulating Biomarkers of One-Carbon Metabolism in Relation to Renal Cell Carcinoma Incidence and Survival

Author

Johansson, Mattias, Fanidi, Anouar, Muller, David C., Bassett, Julie K., Midttun, Øivind, Vollset, Stein Emil, Travis, Ruth C., Palli, Domenico, Mattiello, Amalia, Sieri, Sabina, Trichopoulou, Antonia, Lagiou, Pagona, Trichopoulos, Dimitrios, Ljungberg, Börje, Hallmans, Göran, Weiderpass, Elisabete, Skeie, Guri, González, Carlos A., Dorronsoro, Miren, Peeters, Petra H., Bueno-de-Mesquita, H. B(as)., Ros, Martine M., Boutron Ruault, Marie-Christine, Fagherazzi, Guy, Clavel, Françoise, Sánchez, María-José, Gurrea, Aurelio Barricarte, Navarro, Carmen, Quiros, J. Ramon, Overvad, Kim, Tjønneland, Anne, Aleksandrova, Krassimira, Vineis, Paolo, Gunter, Marc J., Kaaks, Rudolf, Giles, Graham, Relton, Caroline, Riboli, Elio, Boeing, Heiner, Ueland, Per Magne, Severi, Gianluca, and Brennan, Paul

Published
2014
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7. Circulating Fatty Acids and Prostate Cancer Risk: Individual Participant Meta-Analysis of Prospective Studies

Author

Crowe, Francesca L., Appleby, Paul N., Travis, Ruth C., Barnett, Matt, Brasky, Theodore M., Bueno-de-Mesquita, Bas H., Chajes, Veronique, Chavarro, Jorge E., Chirlaque, Maria-Dolores, English, Dallas R., Gibson, Robert A., Giles, Graham G., Goodman, Gary E., Henning, Susanne M., Kaaks, Rudolf, King, Irena B., Kolonel, Lawrence N., Kristal, Alan R., Neuhouser, Marian L., Park, Song-Yi, Severi, Gianluca, Siddiq, Afshan, Stampfer, Meir J., Stattin, Pär, Tangen, Catherine M., Tjønneland, Anne, Trichopoulos, Dimitrios, Tumino, Rosario, Wilkens, Lynne R., Key, Timothy J., and Allen, Naomi E.

Published
2014
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13. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types

Author

Sampson, Joshua N., primary, Wheeler, William A., additional, Yeager, Meredith, additional, Panagiotou, Orestis, additional, Wang, Zhaoming, additional, Berndt, Sonja I., additional, Lan, Qing, additional, Abnet, Christian C., additional, Amundadottir, Laufey T., additional, Figueroa, Jonine D., additional, Landi, Maria Teresa, additional, Mirabello, Lisa, additional, Savage, Sharon A., additional, Taylor, Philip R., additional, Vivo, Immaculata De, additional, McGlynn, Katherine A., additional, Purdue, Mark P., additional, Rajaraman, Preetha, additional, Adami, Hans-Olov, additional, Ahlbom, Anders, additional, Albanes, Demetrius, additional, Amary, Maria Fernanda, additional, An, She-Juan, additional, Andersson, Ulrika, additional, Andriole, Gerald, additional, Andrulis, Irene L., additional, Angelucci, Emanuele, additional, Ansell, Stephen M., additional, Arici, Cecilia, additional, Armstrong, Bruce K., additional, Arslan, Alan A., additional, Austin, Melissa A., additional, Baris, Dalsu, additional, Barkauskas, Donald A., additional, Bassig, Bryan A., additional, Becker, Nikolaus, additional, Benavente, Yolanda, additional, Benhamou, Simone, additional, Berg, Christine, additional, Van Den Berg, David, additional, Bernstein, Leslie, additional, Bertrand, Kimberly A., additional, Birmann, Brenda M., additional, Black, Amanda, additional, Boeing, Heiner, additional, Boffetta, Paolo, additional, Boutron-Ruault, Marie-Christine, additional, Bracci, Paige M., additional, Brinton, Louise, additional, Brooks-Wilson, Angela R., additional, Bueno-de-Mesquita, H. Bas, additional, Burdett, Laurie, additional, Buring, Julie, additional, Butler, Mary Ann, additional, Cai, Qiuyin, additional, Cancel-Tassin, Geraldine, additional, Canzian, Federico, additional, Carrato, Alfredo, additional, Carreon, Tania, additional, Carta, Angela, additional, Chan, John K. C., additional, Chang, Ellen T., additional, Chang, Gee-Chen, additional, Chang, I-Shou, additional, Chang, Jiang, additional, Chang-Claude, Jenny, additional, Chen, Chien-Jen, additional, Chen, Chih-Yi, additional, Chen, Chu, additional, Chen, Chung-Hsing, additional, Chen, Constance, additional, Chen, Hongyan, additional, Chen, Kexin, additional, Chen, Kuan-Yu, additional, Chen, Kun-Chieh, additional, Chen, Ying, additional, Chen, Ying-Hsiang, additional, Chen, Yi-Song, additional, Chen, Yuh-Min, additional, Chien, Li-Hsin, additional, Chirlaque, María-Dolores, additional, Choi, Jin Eun, additional, Choi, Yi Young, additional, Chow, Wong-Ho, additional, Chung, Charles C., additional, Clavel, Jacqueline, additional, Clavel-Chapelon, Françoise, additional, Cocco, Pierluigi, additional, Colt, Joanne S., additional, Comperat, Eva, additional, Conde, Lucia, additional, Connors, Joseph M., additional, Conti, David, additional, Cortessis, Victoria K., additional, Cotterchio, Michelle, additional, Cozen, Wendy, additional, Crouch, Simon, additional, Crous-Bou, Marta, additional, Cussenot, Olivier, additional, Davis, Faith G., additional, Ding, Ti, additional, Diver, W. Ryan, additional, Dorronsoro, Miren, additional, Dossus, Laure, additional, Duell, Eric J., additional, Ennas, Maria Grazia, additional, Erickson, Ralph L., additional, Feychting, Maria, additional, Flanagan, Adrienne M., additional, Foretova, Lenka, additional, Fraumeni, Joseph F., additional, Freedman, Neal D., additional, Beane Freeman, Laura E., additional, Fuchs, Charles, additional, Gago-Dominguez, Manuela, additional, Gallinger, Steven, additional, Gao, Yu-Tang, additional, Gapstur, Susan M., additional, Garcia-Closas, Montserrat, additional, García-Closas, Reina, additional, Gascoyne, Randy D., additional, Gastier-Foster, Julie, additional, Gaudet, Mia M., additional, Gaziano, J. Michael, additional, Giffen, Carol, additional, Giles, Graham G., additional, Giovannucci, Edward, additional, Glimelius, Bengt, additional, Goggins, Michael, additional, Gokgoz, Nalan, additional, Goldstein, Alisa M., additional, Gorlick, Richard, additional, Gross, Myron, additional, Grubb, Robert, additional, Gu, Jian, additional, Guan, Peng, additional, Gunter, Marc, additional, Guo, Huan, additional, Habermann, Thomas M., additional, Haiman, Christopher A., additional, Halai, Dina, additional, Hallmans, Goran, additional, Hassan, Manal, additional, Hattinger, Claudia, additional, He, Qincheng, additional, He, Xingzhou, additional, Helzlsouer, Kathy, additional, Henderson, Brian, additional, Henriksson, Roger, additional, Hjalgrim, Henrik, additional, Hoffman-Bolton, Judith, additional, Hohensee, Chancellor, additional, Holford, Theodore R., additional, Holly, Elizabeth A., additional, Hong, Yun-Chul, additional, Hoover, Robert N., additional, Horn-Ross, Pamela L., additional, Hosain, G. M. Monawar, additional, Hosgood, H. Dean, additional, Hsiao, Chin-Fu, additional, Hu, Nan, additional, Hu, Wei, additional, Hu, Zhibin, additional, Huang, Ming-Shyan, additional, Huerta, Jose-Maria, additional, Hung, Jen-Yu, additional, Hutchinson, Amy, additional, Inskip, Peter D., additional, Jackson, Rebecca D., additional, Jacobs, Eric J., additional, Jenab, Mazda, additional, Jeon, Hyo-Sung, additional, Ji, Bu-Tian, additional, Jin, Guangfu, additional, Jin, Li, additional, Johansen, Christoffer, additional, Johnson, Alison, additional, Jung, Yoo Jin, additional, Kaaks, Rudolph, additional, Kamineni, Aruna, additional, Kane, Eleanor, additional, Kang, Chang Hyun, additional, Karagas, Margaret R., additional, Kelly, Rachel S., additional, Khaw, Kay-Tee, additional, Kim, Christopher, additional, Kim, Hee Nam, additional, Kim, Jin Hee, additional, Kim, Jun Suk, additional, Kim, Yeul Hong, additional, Kim, Young Tae, additional, Kim, Young-Chul, additional, Kitahara, Cari M., additional, Klein, Alison P., additional, Klein, Robert J., additional, Kogevinas, Manolis, additional, Kohno, Takashi, additional, Kolonel, Laurence N., additional, Kooperberg, Charles, additional, Kricker, Anne, additional, Krogh, Vittorio, additional, Kunitoh, Hideo, additional, Kurtz, Robert C., additional, Kweon, Sun-Seog, additional, LaCroix, Andrea, additional, Lawrence, Charles, additional, Lecanda, Fernando, additional, Lee, Victor Ho Fun, additional, Li, Donghui, additional, Li, Haixin, additional, Li, Jihua, additional, Li, Yao-Jen, additional, Li, Yuqing, additional, Liao, Linda M., additional, Liebow, Mark, additional, Lightfoot, Tracy, additional, Lim, Wei-Yen, additional, Lin, Chien-Chung, additional, Lin, Dongxin, additional, Lindstrom, Sara, additional, Linet, Martha S., additional, Link, Brian K., additional, Liu, Chenwei, additional, Liu, Jianjun, additional, Liu, Li, additional, Ljungberg, Börje, additional, Lloreta, Josep, additional, Lollo, Simonetta Di, additional, Lu, Daru, additional, Lund, Eiluv, additional, Malats, Nuria, additional, Mannisto, Satu, additional, Marchand, Loic Le, additional, Marina, Neyssa, additional, Masala, Giovanna, additional, Mastrangelo, Giuseppe, additional, Matsuo, Keitaro, additional, Maynadie, Marc, additional, McKay, James, additional, McKean-Cowdin, Roberta, additional, Melbye, Mads, additional, Melin, Beatrice S., additional, Michaud, Dominique S., additional, Mitsudomi, Tetsuya, additional, Monnereau, Alain, additional, Montalvan, Rebecca, additional, Moore, Lee E., additional, Mortensen, Lotte Maxild, additional, Nieters, Alexandra, additional, North, Kari E., additional, Novak, Anne J., additional, Oberg, Ann L., additional, Offit, Kenneth, additional, Oh, In-Jae, additional, Olson, Sara H., additional, Palli, Domenico, additional, Pao, William, additional, Park, In Kyu, additional, Park, Jae Yong, additional, Park, Kyong Hwa, additional, Patiño-Garcia, Ana, additional, Pavanello, Sofia, additional, Peeters, Petra H. M., additional, Perng, Reury-Perng, additional, Peters, Ulrike, additional, Petersen, Gloria M., additional, Picci, Piero, additional, Pike, Malcolm C., additional, Porru, Stefano, additional, Prescott, Jennifer, additional, Prokunina-Olsson, Ludmila, additional, Qian, Biyun, additional, Qiao, You-Lin, additional, Rais, Marco, additional, Riboli, Elio, additional, Riby, Jacques, additional, Risch, Harvey A., additional, Rizzato, Cosmeri, additional, Rodabough, Rebecca, additional, Roman, Eve, additional, Roupret, Morgan, additional, Ruder, Avima M., additional, Sanjose, Silvia de, additional, Scelo, Ghislaine, additional, Schned, Alan, additional, Schumacher, Fredrick, additional, Schwartz, Kendra, additional, Schwenn, Molly, additional, Scotlandi, Katia, additional, Seow, Adeline, additional, Serra, Consol, additional, Serra, Massimo, additional, Sesso, Howard D., additional, Setiawan, Veronica Wendy, additional, Severi, Gianluca, additional, Severson, Richard K., additional, Shanafelt, Tait D., additional, Shen, Hongbing, additional, Shen, Wei, additional, Shin, Min-Ho, additional, Shiraishi, Kouya, additional, Shu, Xiao-Ou, additional, Siddiq, Afshan, additional, Sierrasesúmaga, Luis, additional, Sihoe, Alan Dart Loon, additional, Skibola, Christine F., additional, Smith, Alex, additional, Smith, Martyn T., additional, Southey, Melissa C., additional, Spinelli, John J., additional, Staines, Anthony, additional, Stampfer, Meir, additional, Stern, Marianna C., additional, Stevens, Victoria L., additional, Stolzenberg-Solomon, Rachael S., additional, Su, Jian, additional, Su, Wu-Chou, additional, Sund, Malin, additional, Sung, Jae Sook, additional, Sung, Sook Whan, additional, Tan, Wen, additional, Tang, Wei, additional, Tardón, Adonina, additional, Thomas, David, additional, Thompson, Carrie A., additional, Tinker, Lesley F., additional, Tirabosco, Roberto, additional, Tjønneland, Anne, additional, Travis, Ruth C., additional, Trichopoulos, Dimitrios, additional, Tsai, Fang-Yu, additional, Tsai, Ying-Huang, additional, Tucker, Margaret, additional, Turner, Jenny, additional, Vajdic, Claire M., additional, Vermeulen, Roel C. H., additional, Villano, Danylo J., additional, Vineis, Paolo, additional, Virtamo, Jarmo, additional, Visvanathan, Kala, additional, Wactawski-Wende, Jean, additional, Wang, Chaoyu, additional, Wang, Chih-Liang, additional, Wang, Jiu-Cun, additional, Wang, Junwen, additional, Wei, Fusheng, additional, Weiderpass, Elisabete, additional, Weiner, George J., additional, Weinstein, Stephanie, additional, Wentzensen, Nicolas, additional, White, Emily, additional, Witzig, Thomas E., additional, Wolpin, Brian M., additional, Wong, Maria Pik, additional, Wu, Chen, additional, Wu, Guoping, additional, Wu, Junjie, additional, Wu, Tangchun, additional, Wu, Wei, additional, Wu, Xifeng, additional, Wu, Yi-Long, additional, Wunder, Jay S., additional, Xiang, Yong-Bing, additional, Xu, Jun, additional, Xu, Ping, additional, Yang, Pan-Chyr, additional, Yang, Tsung-Ying, additional, Ye, Yuanqing, additional, Yin, Zhihua, additional, Yokota, Jun, additional, Yoon, Ho-Il, additional, Yu, Chong-Jen, additional, Yu, Herbert, additional, Yu, Kai, additional, Yuan, Jian-Min, additional, Zelenetz, Andrew, additional, Zeleniuch-Jacquotte, Anne, additional, Zhang, Xu-Chao, additional, Zhang, Yawei, additional, Zhao, Xueying, additional, Zhao, Zhenhong, additional, Zheng, Hong, additional, Zheng, Tongzhang, additional, Zheng, Wei, additional, Zhou, Baosen, additional, Zhu, Meng, additional, Zucca, Mariagrazia, additional, Boca, Simina M., additional, Cerhan, James R., additional, Ferri, Giovanni M., additional, Hartge, Patricia, additional, Hsiung, Chao Agnes, additional, Magnani, Corrado, additional, Miligi, Lucia, additional, Morton, Lindsay M., additional, Smedby, Karin E., additional, Teras, Lauren R., additional, Vijai, Joseph, additional, Wang, Sophia S., additional, Brennan, Paul, additional, Caporaso, Neil E., additional, Hunter, David J., additional, Kraft, Peter, additional, Rothman, Nathaniel, additional, Silverman, Debra T., additional, Slager, Susan L., additional, Chanock, Stephen J., additional, and Chatterjee, Nilanjan, additional

Published
2015
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14. Lung cancer risk discrimination of prediagnostic proteomics measurements compared with existing prediction tools.

Author

Feng X, Wu WY, Onwuka JU, Haider Z, Alcala K, Smith-Byrne K, Zahed H, Guida F, Wang R, Bassett JK, Stevens V, Wang Y, Weinstein S, Freedman ND, Chen C, Tinker L, Nøst TH, Koh WP, Muller D, Colorado-Yohar SM, Tumino R, Hung RJ, Amos CI, Lin X, Zhang X, Arslan AA, Sánchez MJ, Sørgjerd EP, Severi G, Hveem K, Brennan P, Langhammer A, Milne RL, Yuan JM, Melin B, Johansson M, Robbins HA, and Johansson M

Subjects
Humans, Risk Assessment, Case-Control Studies, Prospective Studies, Lung, Early Detection of Cancer, Proteomics, Lung Neoplasms diagnosis, Lung Neoplasms epidemiology
Abstract

Background: We sought to develop a proteomics-based risk model for lung cancer and evaluate its risk-discriminatory performance in comparison with a smoking-based risk model (PLCOm2012) and a commercially available autoantibody biomarker test., Methods: We designed a case-control study nested in 6 prospective cohorts, including 624 lung cancer participants who donated blood samples at most 3 years prior to lung cancer diagnosis and 624 smoking-matched cancer free participants who were assayed for 302 proteins. We used 470 case-control pairs from 4 cohorts to select proteins and train a protein-based risk model. We subsequently used 154 case-control pairs from 2 cohorts to compare the risk-discriminatory performance of the protein-based model with that of the Early Cancer Detection Test (EarlyCDT)-Lung and the PLCOm2012 model using receiver operating characteristics analysis and by estimating models' sensitivity. All tests were 2-sided., Results: The area under the curve for the protein-based risk model in the validation sample was 0.75 (95% confidence interval [CI] = 0.70 to 0.81) compared with 0.64 (95% CI = 0.57 to 0.70) for the PLCOm2012 model (Pdifference = .001). The EarlyCDT-Lung had a sensitivity of 14% (95% CI = 8.2% to 19%) and a specificity of 86% (95% CI = 81% to 92%) for incident lung cancer. At the same specificity of 86%, the sensitivity for the protein-based risk model was estimated at 49% (95% CI = 41% to 57%) and 30% (95% CI = 23% to 37%) for the PLCOm2012 model., Conclusion: Circulating proteins showed promise in predicting incident lung cancer and outperformed a standard risk prediction model and the commercialized EarlyCDT-Lung., (© The Author(s) 2023. Published by Oxford University Press.)

Published
2023
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15. Use of menopausal hormone therapy and ovarian cancer risk in a French cohort study.

Author

Fournier A, Cairat M, Severi G, Gunter MJ, Rinaldi S, and Dossus L

Subjects
Humans, Female, Cohort Studies, Dydrogesterone, Prospective Studies, Postmenopause, Risk Factors, Progestins adverse effects, Estrogens adverse effects, Menopause, Progesterone adverse effects, Ovarian Neoplasms chemically induced, Ovarian Neoplasms epidemiology, Ovarian Neoplasms drug therapy
Abstract

Background: Epidemiological studies have found that menopausal hormone therapy (MHT) use is associated with an increased ovarian cancer risk. However, whether different MHT types confer the same level of risk is unclear. We estimated the associations between different MHT types and the risk of ovarian cancer in a prospective cohort., Methods: The study population included 75 606 postmenopausal women from the E3N cohort. Exposure to MHT was identified from self-reports in biennial questionnaires between 1992 and 2004 and from drug claim data matched to the cohort between 2004 and 2014. Hazard ratios and 95% confidence intervals (CIs) of ovarian cancer were estimated using multivariable Cox proportional hazards models with MHT as a time-varying exposure. Tests of statistical significance were 2-sided., Results: Over an average 15.3 years follow-up, 416 ovarian cancers were diagnosed. Hazard ratios of ovarian cancer associated with ever use of estrogens combined with progesterone or dydrogesterone and ever use of estrogens combined with other progestagen were equal to 1.28 (95% CI = 1.04 to 1.57) and 0.81 (95% CI = 0.65 to 1.00), respectively (Phomogeneity = .003), compared with never use. The hazard ratio for unopposed estrogen use was 1.09 (95% CI = 0.82 to 1.46). We found no trend according to duration of use or time since last use except for estrogens combined with progesterone or dydrogesterone, which showed decreasing risk with increasing time since last use., Conclusion: Different MHT types may impact ovarian cancer risk differentially. The possibility that MHT containing progestagens other than progesterone or dydrogesterone may confer some protection should be evaluated in other epidemiological studies., (© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2023
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16. A Transcriptome-Wide Association Study Identifies Novel Candidate Susceptibility Genes for Pancreatic Cancer.

Author

Zhong J, Jermusyk A, Wu L, Hoskins JW, Collins I, Mocci E, Zhang M, Song L, Chung CC, Zhang T, Xiao W, Albanes D, Andreotti G, Arslan AA, Babic A, Bamlet WR, Beane-Freeman L, Berndt S, Borgida A, Bracci PM, Brais L, Brennan P, Bueno-de-Mesquita B, Buring J, Canzian F, Childs EJ, Cotterchio M, Du M, Duell EJ, Fuchs C, Gallinger S, Gaziano JM, Giles GG, Giovannucci E, Goggins M, Goodman GE, Goodman PJ, Haiman C, Hartge P, Hasan M, Helzlsouer KJ, Holly EA, Klein EA, Kogevinas M, Kurtz RJ, LeMarchand L, Malats N, Männistö S, Milne R, Neale RE, Ng K, Obazee O, Oberg AL, Orlow I, Patel AV, Peters U, Porta M, Rothman N, Scelo G, Sesso HD, Severi G, Sieri S, Silverman D, Sund M, Tjønneland A, Thornquist MD, Tobias GS, Trichopoulou A, Van Den Eeden SK, Visvanathan K, Wactawski-Wende J, Wentzensen N, White E, Yu H, Yuan C, Zeleniuch-Jacquotte A, Hoover R, Brown K, Kooperberg C, Risch HA, Jacobs EJ, Li D, Yu K, Shu XO, Chanock SJ, Wolpin BM, Stolzenberg-Solomon RZ, Chatterjee N, Klein AP, Smith JP, Kraft P, Shi J, Petersen GM, Zheng W, and Amundadottir LT

Subjects
Databases, Genetic, Gene Expression, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Transcriptome, Pancreatic Neoplasms genetics
Abstract

Background: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown., Methods: To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples)., Results: We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate < .05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22: RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction., Conclusions: By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation., (Published by Oxford University Press 2020. This work is written by US Government employees and is in the public domain in the US.)

Published
2020
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17. Prediagnostic Plasma Bile Acid Levels and Colon Cancer Risk: A Prospective Study.

Author

Kühn T, Stepien M, López-Nogueroles M, Damms-Machado A, Sookthai D, Johnson T, Roca M, Hüsing A, Maldonado SG, Cross AJ, Murphy N, Freisling H, Rinaldi S, Scalbert A, Fedirko V, Severi G, Boutron-Ruault MC, Mancini FR, Sowah SA, Boeing H, Jakszyn P, Sánchez MJ, Merino S, Colorado-Yohar S, Barricarte A, Khaw KT, Schmidt JA, Perez-Cornago A, Trichopoulou A, Karakatsani A, Thriskos P, Palli D, Agnoli C, Tumino R, Sacerdote C, Panico S, Bueno-de-Mesquita B, van Gils CH, Heath AK, Gunter MJ, Riboli E, Lahoz A, Jenab M, and Kaaks R

Subjects
Adult, Aged, Case-Control Studies, Cohort Studies, Colonic Neoplasms diagnosis, Colonic Neoplasms epidemiology, Female, Humans, Male, Middle Aged, Risk, Spain epidemiology, Bile Acids and Salts blood, Colonic Neoplasms blood
Abstract

Background: Bile acids have been proposed to promote colon carcinogenesis. However, there are limited prospective data on circulating bile acid levels and colon cancer risk in humans., Methods: Associations between prediagnostic plasma levels of 17 primary, secondary, and tertiary bile acid metabolites (conjugated and unconjugated) and colon cancer risk were evaluated in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Bile acid levels were quantified by tandem mass spectrometry in samples from 569 incident colon cancer cases and 569 matched controls. Multivariable logistic regression analyses were used to estimate odds ratios (ORs) for colon cancer risk across quartiles of bile acid concentrations., Results: Positive associations were observed between colon cancer risk and plasma levels of seven conjugated bile acid metabolites: the primary bile acids glycocholic acid (ORquartile 4 vs quartile 1= 2.22, 95% confidence interval [CI] = 1.52 to 3.26), taurocholic acid (OR = 1.78, 95% CI = 1.23 to 2.58), glycochenodeoxycholic acid (OR = 1.68, 95% CI = 1.13 to 2.48), taurochenodeoxycholic acid (OR = 1.62, 95% CI = 1.11 to 2.36), and glycohyocholic acid (OR = 1.65, 95% CI = 1.13 to 2.40), and the secondary bile acids glycodeoxycholic acid (OR = 1.68, 95% CI = 1.12 to 2.54) and taurodeoxycholic acid (OR = 1.54, 95% CI = 1.02 to 2.31). By contrast, unconjugated bile acids and tertiary bile acids were not associated with risk., Conclusions: This prospective study showed that prediagnostic levels of certain conjugated primary and secondary bile acids were positively associated with risk of colon cancer. Our findings support experimental data to suggest that a high bile acid load is colon cancer promotive., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2020
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18. Agnostic Pathway/Gene Set Analysis of Genome-Wide Association Data Identifies Associations for Pancreatic Cancer.

Author

Walsh N, Zhang H, Hyland PL, Yang Q, Mocci E, Zhang M, Childs EJ, Collins I, Wang Z, Arslan AA, Beane-Freeman L, Bracci PM, Brennan P, Canzian F, Duell EJ, Gallinger S, Giles GG, Goggins M, Goodman GE, Goodman PJ, Hung RJ, Kooperberg C, Kurtz RC, Malats N, LeMarchand L, Neale RE, Olson SH, Scelo G, Shu XO, Van Den Eeden SK, Visvanathan K, White E, Zheng W, Albanes D, Andreotti G, Babic A, Bamlet WR, Berndt SI, Borgida A, Boutron-Ruault MC, Brais L, Brennan P, Bueno-de-Mesquita B, Buring J, Chaffee KG, Chanock S, Cleary S, Cotterchio M, Foretova L, Fuchs C, M Gaziano JM, Giovannucci E, Goggins M, Hackert T, Haiman C, Hartge P, Hasan M, Helzlsouer KJ, Herman J, Holcatova I, Holly EA, Hoover R, Hung RJ, Janout V, Klein EA, Kurtz RC, Laheru D, Lee IM, Lu L, Malats N, Mannisto S, Milne RL, Oberg AL, Orlow I, Patel AV, Peters U, Porta M, Real FX, Rothman N, Sesso HD, Severi G, Silverman D, Strobel O, Sund M, Thornquist MD, Tobias GS, Wactawski-Wende J, Wareham N, Weiderpass E, Wentzensen N, Wheeler W, Yu H, Zeleniuch-Jacquotte A, Kraft P, Li D, Jacobs EJ, Petersen GM, Wolpin BM, Risch HA, Amundadottir LT, Yu K, Klein AP, and Stolzenberg-Solomon RZ

Subjects
Case-Control Studies, Genetic Predisposition to Disease, Humans, Models, Statistical, Polymorphism, Single Nucleotide, Carcinoma, Pancreatic Ductal genetics, Genome-Wide Association Study methods, Pancreatic Neoplasms genetics
Abstract

Background: Genome-wide association studies (GWAS) identify associations of individual single-nucleotide polymorphisms (SNPs) with cancer risk but usually only explain a fraction of the inherited variability. Pathway analysis of genetic variants is a powerful tool to identify networks of susceptibility genes., Methods: We conducted a large agnostic pathway-based meta-analysis of GWAS data using the summary-based adaptive rank truncated product method to identify gene sets and pathways associated with pancreatic ductal adenocarcinoma (PDAC) in 9040 cases and 12 496 controls. We performed expression quantitative trait loci (eQTL) analysis and functional annotation of the top SNPs in genes contributing to the top associated pathways and gene sets. All statistical tests were two-sided., Results: We identified 14 pathways and gene sets associated with PDAC at a false discovery rate of less than 0.05. After Bonferroni correction (P ≤ 1.3 × 10-5), the strongest associations were detected in five pathways and gene sets, including maturity-onset diabetes of the young, regulation of beta-cell development, role of epidermal growth factor (EGF) receptor transactivation by G protein-coupled receptors in cardiac hypertrophy pathways, and the Nikolsky breast cancer chr17q11-q21 amplicon and Pujana ATM Pearson correlation coefficient (PCC) network gene sets. We identified and validated rs876493 and three correlating SNPs (PGAP3) and rs3124737 (CASP7) from the Pujana ATM PCC gene set as eQTLs in two normal derived pancreas tissue datasets., Conclusion: Our agnostic pathway and gene set analysis integrated with functional annotation and eQTL analysis provides insight into genes and pathways that may be biologically relevant for risk of PDAC, including those not previously identified., (Published by Oxford University Press 2018. This work is written by US Government employees and is in the public domain in the US.)

Published
2019
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19. Novel Common Genetic Susceptibility Loci for Colorectal Cancer.

Author

Schmit SL, Edlund CK, Schumacher FR, Gong J, Harrison TA, Huyghe JR, Qu C, Melas M, Van Den Berg DJ, Wang H, Tring S, Plummer SJ, Albanes D, Alonso MH, Amos CI, Anton K, Aragaki AK, Arndt V, Barry EL, Berndt SI, Bezieau S, Bien S, Bloomer A, Boehm J, Boutron-Ruault MC, Brenner H, Brezina S, Buchanan DD, Butterbach K, Caan BJ, Campbell PT, Carlson CS, Castelao JE, Chan AT, Chang-Claude J, Chanock SJ, Cheng I, Cheng YW, Chin LS, Church JM, Church T, Coetzee GA, Cotterchio M, Cruz Correa M, Curtis KR, Duggan D, Easton DF, English D, Feskens EJM, Fischer R, FitzGerald LM, Fortini BK, Fritsche LG, Fuchs CS, Gago-Dominguez M, Gala M, Gallinger SJ, Gauderman WJ, Giles GG, Giovannucci EL, Gogarten SM, Gonzalez-Villalpando C, Gonzalez-Villalpando EM, Grady WM, Greenson JK, Gsur A, Gunter M, Haiman CA, Hampe J, Harlid S, Harju JF, Hayes RB, Hofer P, Hoffmeister M, Hopper JL, Huang SC, Huerta JM, Hudson TJ, Hunter DJ, Idos GE, Iwasaki M, Jackson RD, Jacobs EJ, Jee SH, Jenkins MA, Jia WH, Jiao S, Joshi AD, Kolonel LN, Kono S, Kooperberg C, Krogh V, Kuehn T, Küry S, LaCroix A, Laurie CA, Lejbkowicz F, Lemire M, Lenz HJ, Levine D, Li CI, Li L, Lieb W, Lin Y, Lindor NM, Liu YR, Loupakis F, Lu Y, Luh F, Ma J, Mancao C, Manion FJ, Markowitz SD, Martin V, Matsuda K, Matsuo K, McDonnell KJ, McNeil CE, Milne R, Molina AJ, Mukherjee B, Murphy N, Newcomb PA, Offit K, Omichessan H, Palli D, Cotoré JPP, Pérez-Mayoral J, Pharoah PD, Potter JD, Qu C, Raskin L, Rennert G, Rennert HS, Riggs BM, Schafmayer C, Schoen RE, Sellers TA, Seminara D, Severi G, Shi W, Shibata D, Shu XO, Siegel EM, Slattery ML, Southey M, Stadler ZK, Stern MC, Stintzing S, Taverna D, Thibodeau SN, Thomas DC, Trichopoulou A, Tsugane S, Ulrich CM, van Duijnhoven FJB, van Guelpan B, Vijai J, Virtamo J, Weinstein SJ, White E, Win AK, Wolk A, Woods M, Wu AH, Wu K, Xiang YB, Yen Y, Zanke BW, Zeng YX, Zhang B, Zubair N, Kweon SS, Figueiredo JC, Zheng W, Marchand LL, Lindblom A, Moreno V, Peters U, Casey G, Hsu L, Conti DV, and Gruber SB

Subjects
Case-Control Studies, Ethnicity statistics & numerical data, Follow-Up Studies, Genotype, Humans, Prognosis, United States epidemiology, Colorectal Neoplasms epidemiology, Colorectal Neoplasms genetics, Ethnicity genetics, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Polymorphism, Single Nucleotide
Abstract

Background: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk., Methods: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided., Results: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0., Conclusions: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screening., (© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2019
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20. Circulating Folate, Vitamin B6, and Methionine in Relation to Lung Cancer Risk in the Lung Cancer Cohort Consortium (LC3).

Author

Fanidi A, Muller DC, Yuan JM, Stevens VL, Weinstein SJ, Albanes D, Prentice R, Thomsen CA, Pettinger M, Cai Q, Blot WJ, Wu J, Arslan AA, Zeleniuch-Jacquotte A, McCullough ML, Le Marchand L, Wilkens LR, Haiman CA, Zhang X, Han J, Stampfer MJ, Smith-Warner SA, Giovannucci E, Giles GG, Hodge AM, Severi G, Johansson M, Grankvist K, Langhammer A, Krokstad S, Næss M, Wang R, Gao YT, Butler LM, Koh WP, Shu XO, Xiang YB, Li H, Zheng W, Lan Q, Visvanathan K, Bolton JH, Ueland PM, Midttun Ø, Ulvik A, Caporaso NE, Purdue M, Ziegler RG, Freedman ND, Buring JE, Lee IM, Sesso HD, Gaziano JM, Manjer J, Ericson U, Relton C, Brennan P, and Johansson M

Subjects
Adult, Aged, Aged, 80 and over, Asia epidemiology, Australia epidemiology, Case-Control Studies, Cotinine blood, Europe epidemiology, Female, Humans, Incidence, Lung Neoplasms blood, Male, Middle Aged, Prospective Studies, Protective Factors, Risk Factors, Sex Factors, Smoking blood, Smoking epidemiology, United States epidemiology, Folic Acid blood, Lung Neoplasms epidemiology, Methionine blood, Vitamin B 6 blood
Abstract

Background: Circulating concentrations of B vitamins and factors related to one-carbon metabolism have been found to be strongly inversely associated with lung cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The extent to which these associations are present in other study populations is unknown., Methods: Within 20 prospective cohorts from the National Cancer Institute Cohort Consortium, a nested case-control study was designed including 5364 incident lung cancer case patients and 5364 control subjects who were individually matched to case patients by age, sex, cohort, and smoking status. Centralized biochemical analyses were performed to measure circulating concentrations of vitamin B6, folate, and methionine, as well as cotinine as an indicator of recent tobacco exposure. The association between these biomarkers and lung cancer risk was evaluated using conditional logistic regression models., Results: Participants with higher circulating concentrations of vitamin B6 and folate had a modestly decreased risk of lung cancer risk overall, the odds ratios when comparing the top and bottom fourths (OR 4vs1 ) being 0.88 (95% confidence interval [CI] = 0.78 to 1.00) and 0.86 (95% CI = 0.74 to 0.99), respectively. We found stronger associations among men (vitamin B6: OR 4vs1 = 0.74, 95% CI = 0.62 to 0.89; folate: OR 4vs1 = 0.75, 95% CI = 0.61 to 0.93) and ever smokers (vitamin B6: OR 4vs1 = 0.78, 95% CI = 0.67 to 0.91; folate: OR 4vs1 = 0.87, 95% CI = 0.73 to 1.03). We further noted that the association of folate was restricted to Europe/Australia and Asia, whereas no clear association was observed for the United States. Circulating concentrations of methionine were not associated with lung cancer risk overall or in important subgroups., Conclusions: Although confounding by tobacco exposure or reverse causation cannot be ruled out, these study results are compatible with a small decrease in lung cancer risk in ever smokers who avoid low concentrations of circulating folate and vitamin B6., (© The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Published
2018
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