737 results on '"Bertrand, Kimberly A."'
Search Results
2. Body size and risk of multiple myeloma in the Black Women’s Health Study
- Author
-
Kataria, Yachana, Niharika Pillalamarri, Bala, Zirpoli, Gary, Szalat, Raphael, Palmer, Julie R., and Bertrand, Kimberly A.
- Published
- 2024
- Full Text
- View/download PDF
3. Vitamin D and monoclonal gammopathy of undetermined significance (MGUS) among U.S. Black women
- Author
-
Ruiz Lopez, Jorge N., McNeil, Grace E., Zirpoli, Gary, Palmer, Julie R., Kataria, Yachana, and Bertrand, Kimberly A.
- Published
- 2024
- Full Text
- View/download PDF
4. BMI and breast cancer risk around age at menopause
- Author
-
Von Holle, Ann, Adami, Hans-Olov, Baglietto, Laura, Berrington de Gonzalez, Amy, Bertrand, Kimberly A., Blot, William, Chen, Yu, DeHart, Jessica Clague, Dossus, Laure, Eliassen, A. Heather, Fournier, Agnes, Garcia-Closas, Montse, Giles, Graham, Guevara, Marcela, Hankinson, Susan E., Heath, Alicia, Jones, Michael E., Joshu, Corinne E., Kaaks, Rudolf, Kirsh, Victoria A., Kitahara, Cari M., Koh, Woon-Puay, Linet, Martha S., Park, Hannah Lui, Masala, Giovanna, Mellemkjaer, Lene, Milne, Roger L., O'Brien, Katie M., Palmer, Julie R., Riboli, Elio, Rohan, Thomas E., Shrubsole, Martha J., Sund, Malin, Tamimi, Rulla, Tin Tin, Sandar, Visvanathan, Kala, Vermeulen, Roel CH, Weiderpass, Elisabete, Willett, Walter C., Yuan, Jian-Min, Zeleniuch-Jacquotte, Anne, Nichols, Hazel B., Sandler, Dale P., Swerdlow, Anthony J., Schoemaker, Minouk J., and Weinberg, Clarice R.
- Published
- 2024
- Full Text
- View/download PDF
5. A model for predicting both breast cancer risk and non-breast cancer death among women > 55 years old
- Author
-
Schonberg, Mara A., Wolfson, Emily A., Eliassen, A. Heather, Bertrand, Kimberly A., Shvetsov, Yurii B., Rosner, Bernard A., Palmer, Julie R., and Ngo, Long H.
- Published
- 2023
- Full Text
- View/download PDF
6. Hypertensive conditions of pregnancy, preterm birth, and premenopausal breast cancer risk: a premenopausal breast cancer collaborative group analysis
- Author
-
Nichols, Hazel B., House, Melissa G., Yarosh, Rina, Mitra, Sara, Goldberg, Mandy, Bertrand, Kimberly A., Eliassen, A. Heather, Giles, Graham G., Jones, Michael E., Milne, Roger L., O’Brien, Katie M., Palmer, Julie R., Sandin, Sven, Willett, Walter C., Yin, Weiyao, Sandler, Dale P., Swerdlow, Anthony J., and Schoemaker, Minouk J.
- Published
- 2023
- Full Text
- View/download PDF
7. Hair relaxer use and risk of uterine cancer in the Black Women's Health Study
- Author
-
Bertrand, Kimberly A., Delp, Lauren, Coogan, Patricia F., Cozier, Yvette C., Lenzy, Yolanda M., Rosenberg, Lynn, and Palmer, Julie R.
- Published
- 2023
- Full Text
- View/download PDF
8. A Population-Based Study of Genes Previously Implicated in Breast Cancer
- Author
-
Hu, Chunling, Hart, Steven N, Gnanaolivu, Rohan, Huang, Hongyan, Lee, Kun Y, Na, Jie, Gao, Chi, Lilyquist, Jenna, Yadav, Siddhartha, Boddicker, Nicholas J, Samara, Raed, Klebba, Josh, Ambrosone, Christine B, Anton-Culver, Hoda, Auer, Paul, Bandera, Elisa V, Bernstein, Leslie, Bertrand, Kimberly A, Burnside, Elizabeth S, Carter, Brian D, Eliassen, Heather, Gapstur, Susan M, Gaudet, Mia, Haiman, Christopher, Hodge, James M, Hunter, David J, Jacobs, Eric J, John, Esther M, Kooperberg, Charles, Kurian, Allison W, Le Marchand, Loic, Lindstroem, Sara, Lindstrom, Tricia, Ma, Huiyan, Neuhausen, Susan, Newcomb, Polly A, O'Brien, Katie M, Olson, Janet E, Ong, Irene M, Pal, Tuya, Palmer, Julie R, Patel, Alpa V, Reid, Sonya, Rosenberg, Lynn, Sandler, Dale P, Scott, Christopher, Tamimi, Rulla, Taylor, Jack A, Trentham-Dietz, Amy, Vachon, Celine M, Weinberg, Clarice, Yao, Song, Ziogas, Argyrios, Weitzel, Jeffrey N, Goldgar, David E, Domchek, Susan M, Nathanson, Katherine L, Kraft, Peter, Polley, Eric C, and Couch, Fergus J
- Subjects
Breast Cancer ,Genetic Testing ,Prevention ,Cancer ,Clinical Research ,Genetics ,2.1 Biological and endogenous factors ,Aetiology ,4.1 Discovery and preclinical testing of markers and technologies ,Detection ,screening and diagnosis ,Adult ,Aged ,Aged ,80 and over ,Breast Neoplasms ,Case-Control Studies ,Female ,Genetic Predisposition to Disease ,Genetic Variation ,Humans ,Middle Aged ,Mutation ,Odds Ratio ,Risk ,Sequence Analysis ,DNA ,Young Adult ,Medical and Health Sciences ,General & Internal Medicine - Abstract
BackgroundPopulation-based estimates of the risk of breast cancer associated with germline pathogenic variants in cancer-predisposition genes are critically needed for risk assessment and management in women with inherited pathogenic variants.MethodsIn a population-based case-control study, we performed sequencing using a custom multigene amplicon-based panel to identify germline pathogenic variants in 28 cancer-predisposition genes among 32,247 women with breast cancer (case patients) and 32,544 unaffected women (controls) from population-based studies in the Cancer Risk Estimates Related to Susceptibility (CARRIERS) consortium. Associations between pathogenic variants in each gene and the risk of breast cancer were assessed.ResultsPathogenic variants in 12 established breast cancer-predisposition genes were detected in 5.03% of case patients and in 1.63% of controls. Pathogenic variants in BRCA1 and BRCA2 were associated with a high risk of breast cancer, with odds ratios of 7.62 (95% confidence interval [CI], 5.33 to 11.27) and 5.23 (95% CI, 4.09 to 6.77), respectively. Pathogenic variants in PALB2 were associated with a moderate risk (odds ratio, 3.83; 95% CI, 2.68 to 5.63). Pathogenic variants in BARD1, RAD51C, and RAD51D were associated with increased risks of estrogen receptor-negative breast cancer and triple-negative breast cancer, whereas pathogenic variants in ATM, CDH1, and CHEK2 were associated with an increased risk of estrogen receptor-positive breast cancer. Pathogenic variants in 16 candidate breast cancer-predisposition genes, including the c.657_661del5 founder pathogenic variant in NBN, were not associated with an increased risk of breast cancer.ConclusionsThis study provides estimates of the prevalence and risk of breast cancer associated with pathogenic variants in known breast cancer-predisposition genes in the U.S. population. These estimates can inform cancer testing and screening and improve clinical management strategies for women in the general population with inherited pathogenic variants in these genes. (Funded by the National Institutes of Health and the Breast Cancer Research Foundation.).
- Published
- 2021
9. Ethical, legal, and social implications (ELSI) and challenges in the design of a randomized controlled trial to test the online return of cancer genetic research results to U.S. Black women
- Author
-
Wang, Catharine, Bertrand, Kimberly A., Trevino-Talbot, Michelle, Flynn, Maureen, Ruderman, Maggie, Cabral, Howard J., Bowen, Deborah J., Hughes-Halbert, Chanita, and Palmer, Julie R.
- Published
- 2023
- Full Text
- View/download PDF
10. Abstract 14305: Experiences of Racism and Risk of Preeclampsia: Results From the Black Women’s Health Study
- Author
-
Ogunwole, Michelle, Bertrand, Kimberly A, Palmer, Julie R, Bennett, Wendy L, Zeng, Yong, Jennings, Jacky M, Boyer, Theresa, Amoah, Akua, and Thorpe, Roland J
- Published
- 2023
- Full Text
- View/download PDF
11. Contribution of Germline Predisposition Gene Mutations to Breast Cancer Risk in African American Women.
- Author
-
Palmer, Julie, Polley, Eric, Hu, Chunling, John, Esther, Haiman, Christopher, Hart, Steven, Gaudet, Mia, Pal, Tuya, Trentham-Dietz, Amy, Bernstein, Leslie, Ambrosone, Christine, Bandera, Elisa, Bertrand, Kimberly, Bethea, Traci, Gao, Chi, Gnanaolivu, Rohan, Huang, Hongyan, Lee, Kun, LeMarchand, Loic, Na, Jie, Sandler, Dale, Shah, Payal, Yadav, Siddhartha, Yang, William, Weitzel, Jeffrey, Domchek, Susan, Goldgar, David, Nathanson, Katherine, Kraft, Peter, Yao, Song, Couch, Fergus, and Anton-Culver, Hoda
- Subjects
Adolescent ,Adult ,Black or African American ,Aged ,Aged ,80 and over ,Breast Neoplasms ,Case-Control Studies ,Cohort Studies ,Female ,Genetic Predisposition to Disease ,Genetic Testing ,Genotype ,Germ-Line Mutation ,Humans ,Middle Aged ,Registries ,Risk Factors ,Young Adult - Abstract
BACKGROUND: The risks of breast cancer in African American (AA) women associated with inherited mutations in breast cancer predisposition genes are not well defined. Thus, whether multigene germline hereditary cancer testing panels are applicable to this population is unknown. We assessed associations between mutations in panel-based genes and breast cancer risk in 5054 AA women with breast cancer and 4993 unaffected AA women drawn from 10 epidemiologic studies. METHODS: Germline DNA samples were sequenced for mutations in 23 cancer predisposition genes using a QIAseq multiplex amplicon panel. Prevalence of mutations and odds ratios (ORs) for associations with breast cancer risk were estimated with adjustment for study design, age, and family history of breast cancer. RESULTS: Pathogenic mutations were identified in 10.3% of women with estrogen receptor (ER)-negative breast cancer, 5.2% of women with ER-positive breast cancer, and 2.3% of unaffected women. Mutations in BRCA1, BRCA2, and PALB2 were associated with high risks of breast cancer (OR = 47.55, 95% confidence interval [CI] = 10.43 to >100; OR = 7.25, 95% CI = 4.07 to 14.12; OR = 8.54, 95% CI = 3.67 to 24.95, respectively). RAD51D mutations were associated with high risk of ER-negative disease (OR = 7.82, 95% CI = 1.61 to 57.42). Moderate risks were observed for CHEK2, ATM, ERCC3, and FANCC mutations with ER-positive cancer, and RECQL mutations with all breast cancer. CONCLUSIONS: The study identifies genes that predispose to breast cancer in the AA population, demonstrates the validity of current breast cancer testing panels for use in AA women, and provides a basis for increased referral of AA patients for cancer genetic testing.
- Published
- 2020
12. Anthropometric traits and risk of multiple myeloma: a pooled prospective analysis
- Author
-
Bertrand, Kimberly A., Teras, Lauren R., Deubler, Emily L., Chao, Chun R., Rosner, Bernard A., Wang, Ke, Zhong, Charlie, Wang, Sophia S., and Birmann, Brenda M.
- Published
- 2022
- Full Text
- View/download PDF
13. Dioxin exposure and breast cancer risk in a prospective cohort study
- Author
-
VoPham, Trang, Bertrand, Kimberly A, Jones, Rena R, Deziel, Nicole C, DuPré, Natalie C, James, Peter, Liu, Ying, Vieira, Verónica M, Tamimi, Rulla M, Hart, Jaime E, Ward, Mary H, and Laden, Francine
- Subjects
Biological Sciences ,Environmental Sciences ,Chemical Sciences ,Prevention ,Cancer ,Breast Cancer ,2.2 Factors relating to the physical environment ,Aetiology ,Breast Neoplasms ,Dioxins ,Female ,Humans ,Polychlorinated Dibenzodioxins ,Prospective Studies ,Risk ,Dioxin ,Environmental exposure ,Breast cancer ,Epidemiology ,Toxicology ,Biological sciences ,Chemical sciences ,Environmental sciences - Abstract
BackgroundDioxins are persistent organic pollutants generated from industrial combustion processes such as waste incineration. To date, results from epidemiologic studies of dioxin exposure and breast cancer risk have been mixed.ObjectivesTo prospectively examine the association between ambient dioxin exposure using a nationwide spatial database of industrial dioxin-emitting facilities and invasive breast cancer risk in the Nurses' Health Study II (NHSII).MethodsNHSII includes female registered nurses in the US who have completed self-administered biennial questionnaires since 1989. Incident invasive breast cancer diagnoses were self-reported and confirmed by medical record review. Dioxin exposure was estimated based on residential proximity, duration of residence, and emissions from facilities located within 3, 5, and 10 km around geocoded residential addresses updated throughout follow-up. Cox regression models adjusted for breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsFrom 1989 to 2013, 3840 invasive breast cancer cases occurred among 112,397 participants. There was no association between residential proximity to any dioxin facilities (all facilities combined) and breast cancer risk overall. However, women who resided within 10 km of any municipal solid waste incinerator (MSWI) compared to none had increased breast cancer risk (adjusted HR = 1.15, 95% CI: 1.03, 1.28), with stronger associations noted for women who lived within 5 km (adjusted HR = 1.25, 95% CI: 1.04, 1.52). Positive associations were also observed for longer duration of residence and higher dioxin emissions from MSWIs within 3, 5, and 10 km. There were no clear differences in patterns of association for ER + vs. ER-breast cancer or by menopausal status.DiscussionResults from this study support positive associations between dioxin exposure from MSWIs and invasive breast cancer risk.
- Published
- 2020
14. Contribution of socioeconomic and environmental factors to geographic disparities in breast cancer risk in the Nurses' Health Study II.
- Author
-
Vieira, Verónica M, VoPham, Trang, Bertrand, Kimberly A, James, Peter, DuPré, Natalie, Tamimi, Rulla M, Laden, Francine, and Hart, Jaime E
- Subjects
Breast Cancer ,Cancer ,Prevention ,Aging ,Clinical Research ,2.2 Factors relating to the physical environment - Abstract
BackgroundEvidence of geographic disparities in breast cancer incidence within the U.S. and spatial analyses can provide insight into the potential contribution of environmental exposures or other geographically-varying factors to these disparities.MethodsWe applied generalized additive models (GAMs) to smooth geocoded residential coordinates while adjusting for covariates. Our analysis included 3,478 breast cancer cases among 24,519 control women from the Nurses' Health Study II (NHSII). We first examined associations with residential location during adolescence (high school address) or early adulthood (address in 1991). We then assessed the contribution from known individual-level risk factors, measures of socioeconomic status (SES), and occupational and environmental factors that vary spatially and have been linked to breast cancer. Secondary analyses by estrogen receptor (ER) and menopausal status were also conducted.ResultsWe identified geographic patterns of breast cancer risk associated with location during adolescence, with increased risk apparent in Michigan, the Northwest, and the New York City area, that shifted to southern New England when addresses during early adulthood were analyzed. Similar results were observed after adjustment for individual- and area-level factors, although spatial associations were no longer statistically significant.ConclusionBreast cancer risk is not spatially uniform across the U.S. and incidence patterns varied depending on the timing during life of the residence considered. Geographic disparities persisted even after accounting for established and suspected breast cancer risk factors, suggesting that unmeasured environmental or lifestyle risk factors may explain geographic variation in risk in different parts of the country.
- Published
- 2020
15. Hypertensive diseases of pregnancy and risk of breast cancer in the Black Women’s Health Study
- Author
-
Bigham, Zahna, Robles, Yvonne, Freund, Karen M., Palmer, Julie R., and Bertrand, Kimberly A.
- Published
- 2022
- Full Text
- View/download PDF
16. Coffee consumption and risk of endometrial cancer: a pooled analysis of individual participant data in the Epidemiology of Endometrial Cancer Consortium (E2C2)
- Author
-
Crous-Bou, Marta, Du, Mengmeng, Gunter, Marc J, Setiawan, Veronica W, Schouten, Leo J, Shu, Xiao-ou, Wentzensen, Nicolas, Bertrand, Kimberly A, Cook, Linda S, Friedenreich, Christine M, Gapstur, Susan M, Goodman, Marc T, Ibiebele, Torukiri I, La Vecchia, Carlo, Levi, Fabio, Liao, Linda M, Negri, Eva, McCann, Susan E, O’Connell, Kelly, Palmer, Julie R, Patel, Alpa V, Ponte, Jeanette, Reynolds, Peggy, Sacerdote, Carlotta, Sinha, Rashmi, Spurdle, Amanda B, Trabert, Britton, van den Brandt, Piet A, Webb, Penelope M, Petruzella, Stacey, Olson, Sara H, and De Vivo, Immaculata
- Published
- 2022
- Full Text
- View/download PDF
17. Ultraviolet radiation exposure and breast cancer risk in the Nurses’ Health Study II
- Author
-
VoPham, Trang, Bertrand, Kimberly A, DuPré, Natalie C, James, Peter, Vieira, Verónica M, Tamimi, Rulla M, Laden, Francine, and Hart, Jaime E
- Subjects
Health Services and Systems ,Biomedical and Clinical Sciences ,Health Sciences ,Oncology and Carcinogenesis ,Prevention ,Clinical Research ,Cancer ,Aging ,Breast Cancer - Abstract
Ultraviolet (UV) radiation exposure, the primary source of vitamin D for most people, may reduce breast cancer risk. To date, epidemiologic studies have shown inconsistent results. The Nurses' Health Study II is a U.S. nationwide prospective cohort of female registered nurses. A UV exposure model was linked with geocoded residential address histories. Early-life UV exposure was estimated based on the state of residence at birth, age 15, and age 30. Self-reported breast cancer was confirmed from medical records. Time-varying Cox regression models adjusted for established breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). From 1989 to 2013, 3,959 invasive breast cancer cases occurred among 112,447 participants. Higher UV exposure during adulthood was not associated with invasive breast cancer risk overall (adjusted HR comparing highest to lowest quintile = 1.00, 95% CI: 0.90, 1.11, p for trend = 0.64) or according to estrogen receptor (ER) status. There were suggestive inverse associations between ER- breast cancer and early-life UV exposure at birth (adjusted HR = 0.94, 95% CI: 0.88, 1.01 per interquartile range increase [15.7 mW/m2]), age 15 (adjusted HR = 0.96, 95% CI: 0.89, 1.04 per 18.0 mW/m2), and age 30 (adjusted HR = 0.90, 95% CI: 0.82, 1.00 per 27.7 mW/m2). Ambient UV exposure during adulthood was not associated with risk of invasive breast cancer overall or by ER status. However, we observed suggestive inverse associations between early-life UV exposure and ER- breast cancer risk.
- Published
- 2019
18. Exposure to hazardous air pollutants and risk of incident breast cancer in the Nurses’ Health Study II
- Author
-
Hart, Jaime E, Bertrand, Kimberly A, DuPre, Natalie, James, Peter, Vieira, Verónica M, VoPham, Trang, Mittleman, Maggie R, Tamimi, Rulla M, and Laden, Francine
- Subjects
Health Services and Systems ,Health Sciences ,Prevention ,Cancer ,Clinical Research ,Breast Cancer ,Estrogen ,Aetiology ,2.2 Factors relating to the physical environment ,Adult ,Air Pollutants ,Breast Neoplasms ,Environmental Exposure ,Female ,Hazardous Substances ,Humans ,Incidence ,Middle Aged ,Prospective Studies ,Risk Factors ,United States ,Air pollution ,Hazardous air pollutants ,Breast cancer ,Public Health and Health Services ,Toxicology ,Epidemiology ,Public health - Abstract
BackgroundFindings from a recent prospective cohort study in California suggested increased risk of breast cancer associated with higher exposure to certain carcinogenic and estrogen-disrupting hazardous air pollutants (HAPs). However, to date, no nationwide studies have evaluated these possible associations. Our objective was to examine the impacts of mammary carcinogen and estrogen disrupting HAPs on risk of invasive breast cancer in a nationwide cohort.MethodsWe assigned HAPs from the US Environmental Protection Agency's 2002 National Air Toxics Assessment to 109,239 members of the nationwide, prospective Nurses' Health Study II (NHSII). Risk of overall invasive, estrogen receptor (ER)-positive (ER+), and ER-negative (ER-) breast cancer with increasing quartiles of exposure were assessed in time-varying multivariable proportional hazards models, adjusted for traditional breast cancer risk factors.ResultsA total of 3321 invasive cases occurred (2160 ER+, 558 ER-) during follow-up 1989-2011. Overall, there was no consistent pattern of elevated risk of the HAPs with risk of breast cancer. Suggestive elevations were only seen with increasing 1,2-dibromo-3-chloropropane exposures (multivariable adjusted HR of overall breast cancer = 1.12, 95% CI: 0.98-1.29; ER+ breast cancer HR = 1.09; 95% CI: 0.92, 1.30; ER- breast cancer HR = 1.14; 95% CI: 0.81, 1.61; each in the top exposure quartile compared to the lowest).ConclusionsExposures to HAPs during adulthood were not consistently associated with an increased risk of overall or estrogen-receptor subtypes of invasive breast cancer in this nationwide cohort of women.
- Published
- 2018
19. Racial and Socioeconomic Disparities in Breast Cancer Outcomes within the AJCC Pathologic Prognostic Staging System
- Author
-
Kantor, Olga, Wang, Monica L., Bertrand, Kimberly, Pierce, Lori, Freedman, Rachel A., Chavez-MacGregor, Mariana, King, Tari A., and Mittendorf, Elizabeth A.
- Published
- 2022
- Full Text
- View/download PDF
20. The association of age at menarche and adult height with mammographic density in the International Consortium of Mammographic Density
- Author
-
Ward, Sarah V., Burton, Anya, Tamimi, Rulla M., Pereira, Ana, Garmendia, Maria Luisa, Pollan, Marina, Boyd, Norman, dos-Santos-Silva, Isabel, Maskarinec, Gertraud, Perez-Gomez, Beatriz, Vachon, Celine, Miao, Hui, Lajous, Martín, López-Ridaura, Ruy, Bertrand, Kimberly, Kwong, Ava, Ursin, Giske, Lee, Eunjung, Ma, Huiyan, Vinnicombe, Sarah, Moss, Sue, Allen, Steve, Ndumia, Rose, Vinayak, Sudhir, Teo, Soo-Hwang, Mariapun, Shivaani, Peplonska, Beata, Bukowska-Damska, Agnieszka, Nagata, Chisato, Hopper, John, Giles, Graham, Ozmen, Vahit, Aribal, Mustafa Erkin, Schüz, Joachim, Van Gils, Carla H., Wanders, Johanna O. P., Sirous, Reza, Sirous, Mehri, Hipwell, John, Kim, Jisun, Lee, Jong Won, Dickens, Caroline, Hartman, Mikael, Chia, Kee-Seng, Scott, Christopher, Chiarelli, Anna M., Linton, Linda, Flugelman, Anath Arzee, Salem, Dorria, Kamal, Rasha, McCormack, Valerie, and Stone, Jennifer
- Published
- 2022
- Full Text
- View/download PDF
21. Childhood adiposity, serum metabolites and breast density in young women
- Author
-
Dorgan, Joanne F., Baer, Heather J., Bertrand, Kimberly A., LeBlanc, Erin S., Jung, Seungyoun, Magder, Laurence S., Snetselaar, Linda G., Stevens, Victor J., Zhang, Yuji, and Van Horn, Linda
- Published
- 2022
- Full Text
- View/download PDF
22. Benign and Malignant Outcomes in the Offspring of Females Exposed In Utero to Diethylstilbestrol (DES): An Update from the NCI Third Generation Study.
- Author
-
Titus, Linda, Hatch, Elizabeth E., Bertrand, Kimberly A., Palmer, Julie R., Strohsnitter, William C., Huo, Dezheng, Curry, Michael, Hyer, Marianne, Aagaard, Kjersti, Gierach, Gretchen L., and Troisi, Rebecca
- Subjects
BREAST tumor risk factors ,ADENOCARCINOMA ,RISK assessment ,PRENATAL exposure delayed effects ,MATERNAL exposure ,CERVIX uteri diseases ,RESEARCH funding ,DESCRIPTIVE statistics ,DYSPLASIA ,CONFIDENCE intervals ,DATA analysis software ,DIETHYLSTILBESTROL ,TESTIS tumors ,PROPORTIONAL hazards models ,DISEASE risk factors ,FETUS - Abstract
Simple Summary: Females prenatally exposed to diethylstilbestrol have an elevated risk of severe cervical dysplasia and some cancers, while testicular cancer is increased in males. We assessed these associations in the prenatally exposed female's offspring (third generation). Based on third-generation females' self-reports, diethylstilbestrol exposure was not associated with risks of overall cancer, breast cancer, or severe cervical dysplasia. Borderline ovarian cancer risk in exposed vs. unexposed was elevated but compatible with chance. Based on mothers' reports, diethylstilbestrol exposure did not increase the risk of overall or other cancers in third-generation females. Overall cancer risk in exposed males appeared elevated but compatible with chance. Testicular cancer risk was not elevated in exposed males, and there were no prostate cancers reported. These data do not provide evidence that diethylstilbestrol is associated with cancer risk in third-generation females or males. The third generation is relatively young and requires follow-up to assess risk as the cohort ages. Background: Females exposed prenatally to diethylstilbestrol (DES) have an elevated risk of cervical dysplasia, breast cancer, and clear cell adenocarcinoma (CCA) of the cervix/vagina. Testicular cancer risk is increased in prenatally exposed males. Epigenetic changes may mediate the transmission of DES effects to the next ("third") generation of offspring. Methods: Using data self-reported by third-generation females, we assessed DES in relation to the risk of cancer and benign breast and reproductive tract conditions. Using data from prenatally DES-exposed and unexposed mothers, we assessed DES in relation to cancer risk in their female and male offspring. Cancer risk was assessed by standardized incidence ratios (SIR) and 95% confidence intervals (CI); the risks of benign and malignant diagnoses were assessed by hazard ratios (HR) and 95% CI. Results: In self-reported data, DES exposure was not associated with an increased risk of overall cancer (HR 0.83; CI 0.36–1.90), breast cancer, or severe cervical dysplasia. No females reported CCA. The risk of borderline ovarian cancer appeared elevated, but the HR was imprecise (3.46; CI 0.37–32.42). Based on mothers' reports, DES exposure did not increase the risk of overall cancer (HR 0.80; CI 0.49–1.32) or of other cancers in third-generation females. Overall cancer risk in exposed males appeared elevated (HR 1.41; CI 0.70–2.86), but the CI was wide. The risk of testicular cancer was not elevated in exposed males; no cases of prostate cancer were reported. Conclusions: To date, there is little evidence that DES is associated with cancer risk in third-generation females or males, but these individuals are relatively young, and further follow-up is needed. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
23. Does mammographic density mediate risk factor associations with breast cancer? An analysis by tumor characteristics
- Author
-
Rice, Megan S, Tamimi, Rulla M, Bertrand, Kimberly A, Scott, Christopher G, Jensen, Matthew R, Norman, Aaron D, Visscher, Daniel W, Chen, Yunn-Yi, Brandt, Kathleen R, Couch, Fergus J, Shepherd, John A, Fan, Bo, Wu, Fang-Fang, Ma, Lin, Collins, Laura C, Cummings, Steven R, Kerlikowske, Karla, and Vachon, Celine M
- Subjects
Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Cancer ,Clinical Research ,Breast Cancer ,Prevention ,Estrogen ,Aging ,Adult ,Aged ,Biomarkers ,Tumor ,Breast ,Breast Density ,Breast Neoplasms ,Female ,Humans ,Mammography ,Middle Aged ,Pregnancy ,Receptor ,ErbB-2 ,Receptors ,Estrogen ,Receptors ,Progesterone ,Risk Factors ,Mammographic density ,Breast cancer ,Receptor ,erbB-2 ,Clinical Sciences ,Oncology & Carcinogenesis ,Clinical sciences ,Oncology and carcinogenesis - Abstract
BackgroundThough mammographic density (MD) has been proposed as an intermediate marker of breast cancer risk, few studies have examined whether the associations between breast cancer risk factors and risk are mediated by MD, particularly by tumor characteristics.MethodsOur study population included 3392 cases (1105 premenopausal) and 8882 (3192 premenopausal) controls from four case-control studies. For established risk factors, we estimated the percent of the total risk factor association with breast cancer that was mediated by percent MD (secondarily, by dense area and non-dense area) for invasive breast cancer as well as for subtypes defined by the estrogen receptor (ER+/ER-), progesterone receptor (PR+/PR-), and HER2 (HER2+/HER2-). Analyses were conducted separately in pre- and postmenopausal women.ResultsPositive associations between prior breast biopsy and risk of invasive breast cancer as well as all subtypes were partially mediated by percent MD in pre- and postmenopausal women (percent mediated = 11-27%, p ≤ 0.02). In postmenopausal women, nulliparity and hormone therapy use were positively associated with invasive, ER+ , PR+ , and HER2- breast cancer; percent MD partially mediated these associations (percent mediated ≥ 31%, p ≤ 0.02). Further, among postmenopausal women, percent MD partially mediated the positive association between later age at first birth and invasive as well as ER+ breast cancer (percent mediated = 16%, p ≤ 0.05).ConclusionPercent MD partially mediated the associations between breast biopsy, nulliparity, age at first birth, and hormone therapy with risk of breast cancer, particularly among postmenopausal women, suggesting that these risk factors at least partially influence breast cancer risk through changes in breast tissue composition.
- Published
- 2018
24. Polyclonal human antibodies against glycans bearing red meat-derived non-human sialic acid N-glycolylneuraminic acid are stable, reproducible, complex and vary between individuals: Total antibody levels are associated with colorectal cancer risk
- Author
-
Samraj, Annie N, Bertrand, Kimberly A, Luben, Robert, Khedri, Zahra, Yu, Hai, Nguyen, Dzung, Gregg, Christopher J, Diaz, Sandra L, Sawyer, Sherilyn, Chen, Xi, Eliassen, Heather, Padler-Karavani, Vered, Wu, Kana, Khaw, Kay-Tee, Willett, Walter, and Varki, Ajit
- Subjects
Biological Sciences ,Biomedical and Clinical Sciences ,Immunology ,Prevention ,Digestive Diseases ,Nutrition ,Cancer ,Colo-Rectal Cancer ,Clinical Research ,Adult ,Aged ,Antibodies ,Atherosclerosis ,Autoantigens ,Colorectal Neoplasms ,Diabetes Mellitus ,Type 2 ,Epitopes ,Female ,Humans ,Middle Aged ,N-Acetylneuraminic Acid ,Neuraminic Acids ,Polysaccharides ,Red Meat ,Risk Factors ,General Science & Technology - Abstract
BackgroundN-glycolylneuraminic acid (Neu5Gc) is a non-human red-meat-derived sialic acid immunogenic to humans. Neu5Gc can be metabolically incorporated into glycan chains on human endothelial and epithelial surfaces. This represents the first example of a "xeno-autoantigen", against which circulating human "xeno-autoantibodies" can react. The resulting inflammation ("xenosialitis") has been demonstrated in human-like Neu5Gc-deficient mice and contributed to carcinoma progression via antibody-mediated inflammation. Anti-Neu5Gc antibodies have potential as biomarkers for diseases associated with red meat consumption such as carcinomas, atherosclerosis, and type 2 diabetes.MethodsELISA assays measured antibodies against Neu5Gc or Neu5Gc-glycans in plasma or serum samples from the Nurses' Health Studies, the Health Professionals Follow-up Study, and the European Prospective Investigation into Cancer and Nutrition, including inter-assay reproducibility, stability with delayed sample processing, and within-person reproducibility over 1-3 years in archived samples. We also assessed associations between antibody levels and coronary artery disease risk (CAD) or red meat intake. A glycan microarray was used to detected antibodies against multiple Neu5Gc-glycan epitopes. A nested case-control study design assessed the association between total anti-Neu5Gc antibodies detected in the glycan array assay and the risk of colorectal cancer (CRC).ResultsELISA assays showed a wide range of anti-Neu5Gc responses and good inter-assay reproducibility, stability with delayed sample processing, and within-person reproducibility over time, but these antibody levels did not correlate with CAD risk or red meat intake. Antibodies against Neu5Gc alone or against individual Neu5Gc-bearing epitopes were also not associated with colorectal cancer (CRC) risk. However, a sialoglycan microarray study demonstrated positive association with CRC risk when the total antibody responses against all Neu5Gc-glycans were combined. Individuals in the top quartile of total anti-Neu5Gc IgG antibody concentrations had nearly three times the risk compared to those in the bottom quartile (Multivariate Odds Ratio comparing top to bottom quartile: 2.98, 95% CI: 0.80, 11.1; P for trend = 0.02).ConclusionsFurther work harnessing the utility of these anti-Neu5Gc antibodies as biomarkers in red meat-associated diseases must consider diversity in individual antibody profiles against different Neu5Gc-bearing glycans. Traditional ELISA assays for antibodies directed against Neu5Gc alone, or against specific Neu5Gc-glycans may not be adequate to define risk associations. Our finding of a positive association of total anti-Neu5Gc antibodies with CRC risk also warrants confirmation in larger prospective studies.
- Published
- 2018
25. Environmental radon exposure and breast cancer risk in the Nurses’ Health Study II
- Author
-
VoPham, Trang, DuPré, Natalie, Tamimi, Rulla M, James, Peter, Bertrand, Kimberly A, Vieira, Veronica, Laden, Francine, and Hart, Jaime E
- Subjects
Health Services and Systems ,Health Sciences ,Cancer ,Breast Cancer ,Prevention ,Adult ,Breast Neoplasms ,Female ,Humans ,Incidence ,Prospective Studies ,Radiation Exposure ,Radioactive Pollutants ,Radon ,Risk Factors ,United States ,Breast cancer ,Ionizing radiation ,Public Health and Health Services ,Toxicology ,Epidemiology ,Public health - Abstract
BackgroundRadon and its decay products, a source of ionizing radiation, are primarily inhaled and can deliver a radiation dose to breast tissue, where they may continue to decay and emit DNA damage-inducing particles. Few studies have examined the relationship between radon and breast cancer.MethodsThe Nurses' Health Study II (NHSII) includes U.S. female registered nurses who completed biennial questionnaires since 1989. Self-reported breast cancer was confirmed from medical records. County-level radon exposures were linked with geocoded residential addresses updated throughout follow-up. Time-varying Cox regression models adjusted for established breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsFrom 1989 to 2013, 3966 invasive breast cancer cases occurred among 112,639 participants. Increasing radon exposure was not associated with breast cancer risk overall (adjusted HR comparing highest to lowest quintile = 1.06, 95% CI: 0.94, 1.21, p for trend = 0.30). However, women in the highest quintile of exposure (≥74.9 Bq/m3) had a suggested elevated risk of ER-/PR- breast cancer compared to women in the lowest quintile (
- Published
- 2017
26. Hypertension and risk of endometrial cancer: a pooled analysis in the Epidemiology of Endometrial Cancer Consortium (E2C2)
- Author
-
Habeshian, Talar S., primary, Peeri, Noah C., additional, De Vivo, Immaculata, additional, Schouten, Leo J., additional, Shu, Xiao-Ou, additional, Cote, Michele L., additional, Bertrand, Kimberly A., additional, Chen, Yu, additional, Clarke, Megan A., additional, Clendenen, Tess V., additional, Cook, Linda S., additional, Costas, Laura, additional, Dal Maso, Luigino, additional, Freudenheim, Jo L., additional, Friedenreich, Christine M., additional, Gallagher, Grace, additional, Gierach, Gretchen L., additional, Goodman, Marc T., additional, Jordan, Susan J., additional, La Vecchia, Carlo, additional, Lacey, James V., additional, Levi, Fabio, additional, Liao, Linda M., additional, Lipworth, Loren, additional, Lu, Lingeng, additional, Matías-Guiu, Xavier, additional, Moysich, Kirsten B., additional, Mutter, George L., additional, Na, Renhua, additional, Naduparambil, Jeffin, additional, Negri, Eva, additional, O'Connell, Kelli, additional, O'Mara, Tracy A., additional, Onieva Hernández, Irene, additional, Palmer, Julie R., additional, Parazzini, Fabio, additional, Patel, Alpa V., additional, Penney, Kathryn L., additional, Prizment, Anna E., additional, Ricceri, Fulvio, additional, Risch, Harvey A., additional, Sacerdote, Carlotta, additional, Sandin, Sven, additional, Stolzenberg-Solomon, Rachael Z., additional, van den Brandt, Piet A., additional, Webb, Penelope M., additional, Wentzensen, Nicolas, additional, Wijayabahu, Akemi T., additional, Wilkens, Lynne R., additional, Xu, Wanghong, additional, Yu, Herbert, additional, Zeleniuch-Jacquotte, Anne, additional, Zheng, Wei, additional, Du, Mengmeng, additional, and Setiawan, Veronica Wendy., additional
- Published
- 2024
- Full Text
- View/download PDF
27. An Update on Prenatal Diethylstilbestrol Exposure and High-Grade Squamous Intraepithelial Lesions of the Lower Genital Tract
- Author
-
Troisi, Rebecca, primary, Bertrand, Kimberly, additional, Hatch, Elizabeth E., additional, Strohsnitter, William C., additional, Aagaard, Kjersti, additional, Robboy, Stanley J., additional, Gierach, Gretchen, additional, and Titus, Linda, additional
- Published
- 2024
- Full Text
- View/download PDF
28. Deciphering racial disparities in multiple myeloma outcomes
- Author
-
Bertrand, Kimberly A., primary and Szalat, Raphael, additional
- Published
- 2024
- Full Text
- View/download PDF
29. Interaction of mammographic breast density with menopausal status and postmenopausal hormone use in relation to the risk of aggressive breast cancer subtypes.
- Author
-
Chen, Yunn-Yi, Ma, Lin, Beck, Andrew, Cummings, Steven, Kerlikowske, Karla, Vachon, Celine, Yaghjyan, Lusine, Tamimi, Rulla, Bertrand, Kimberly, Scott, Christopher, Jensen, Matthew, Pankratz, V, Brandt, Kathy, Visscher, Daniel, Norman, Aaron, Couch, Fergus, Shepherd, John, and Fan, Bo
- Subjects
Breast cancer subtypes ,Breast density ,Postmenopausal hormone therapy ,Tumor aggressiveness ,Adult ,Breast ,Breast Density ,Breast Neoplasms ,Case-Control Studies ,Disease Progression ,Estrogen Replacement Therapy ,Female ,Humans ,Menopause ,Middle Aged ,Odds Ratio ,Population Surveillance ,Risk - Abstract
PURPOSE: We examined the associations of mammographic breast density with breast cancer risk by tumor aggressiveness and by menopausal status and current postmenopausal hormone therapy. METHODS: This study included 2596 invasive breast cancer cases and 4059 controls selected from participants of four nested case-control studies within four established cohorts: the Mayo Mammography Health Study, the Nurses Health Study, Nurses Health Study II, and San Francisco Mammography Registry. Percent breast density (PD), absolute dense (DA), and non-dense areas (NDA) were assessed from digitized film-screen mammograms using a computer-assisted threshold technique and standardized across studies. We used polytomous logistic regression to quantify the associations of breast density with breast cancer risk by tumor aggressiveness (defined as presence of at least two of the following tumor characteristics: size ≥2 cm, grade 2/3, ER-negative status, or positive nodes), stratified by menopausal status and current hormone therapy. RESULTS: Overall, the positive association of PD and borderline inverse association of NDA with breast cancer risk was stronger in aggressive vs. non-aggressive tumors (≥51 vs. 11-25% OR 2.50, 95% CI 1.94-3.22 vs. OR 2.03, 95% CI 1.70-2.43, p-heterogeneity = 0.03; NDA 4th vs. 2nd quartile OR 0.54, 95% CI 0.41-0.70 vs. OR 0.71, 95% CI 0.59-0.85, p-heterogeneity = 0.07). However, there were no differences in the association of DA with breast cancer by aggressive status. In the stratified analysis, there was also evidence of a stronger association of PD and NDA with aggressive tumors among postmenopausal women and, in particular, current estrogen+progesterone users (≥51 vs. 11-25% OR 3.24, 95% CI 1.75-6.00 vs. OR 1.93, 95% CI 1.25-2.98, p-heterogeneity = 0.01; NDA 4th vs. 2nd quartile OR 0.43, 95% CI 0.21-0.85 vs. OR 0.56, 95% CI 0.35-0.89, p-heterogeneity = 0.01), even though the interaction was not significant. CONCLUSION: Our findings suggest that associations of mammographic density with breast cancer risk differ by tumor aggressiveness. While there was no strong evidence that these associations differed by menopausal status or hormone therapy, they did appear more prominent among current estrogen+progesterone users.
- Published
- 2017
30. Outdoor Light at Night and Breast Cancer Incidence in the Nurses Health Study II.
- Author
-
James, Peter, Bertrand, Kimberly, Hart, Jaime, Schernhammer, Eva, Tamimi, Rulla, and Laden, Francine
- Subjects
Adult ,Breast Neoplasms ,Environmental Exposure ,Female ,Humans ,Incidence ,Lighting ,Middle Aged ,Prospective Studies ,Risk Factors - Abstract
BACKGROUND: Animal and epidemiologic studies suggest that exposure to light at night (LAN) may disrupt circadian patterns and decrease nocturnal secretion of melatonin, which may disturb estrogen regulation, leading to increased breast cancer risk. OBJECTIVES: We examined the association between residential outdoor LAN and breast cancer incidence using data from the nationwide U.S.-based Nurses Health Study II cohort. METHODS: We followed 109,672 women from 1989 through 2013. Cumulative LAN exposure was estimated using time-varying satellite data for a composite of persistent nighttime illumination at ∼1 km2 scale for each residence during follow-up. Incident invasive breast cancer cases were confirmed by medical record review. We used Cox proportional hazard models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for anthropometric, reproductive, lifestyle, and socioeconomic risk factors. RESULTS: Over 2,187,425 person-years, we identified 3,549 incident breast cancer cases. Based on a fully adjusted model, the estimated HR for incident breast cancer with an interquartile range (IQR) (31.6 nW/cm2/sr) increase in cumulative average outdoor LAN was 1.05 (95% CI: 1.00, 1.11). An association between LAN and breast cancer appeared to be limited to women who were premenopausal at the time of a case [HR=1.07 (95% CI: 1.01, 1.14) based on 1,973 cases vs. HR=1.00 (95% CI: 0.91, 1.09) based on 1,172 cases in postmenopausal women; p-interaction=0.08]. The LAN-breast cancer association was observed only in past and current smokers at the end of follow-up [HR=1.00 (95% CI: 0.94, 1.07) based on 2,215 cases in never smokers; HR=1.10 (95% CI: 1.01, 1.19) based on 1,034 cases in past smokers vs. HR=1.21 (95% CI: 1.07, 1.37) for 300 cases in current smokers; p-interaction=0.08]. CONCLUSIONS: Although further work is required to confirm our results and to clarify potential mechanisms, our findings suggest that exposure to residential outdoor light at night may contribute to invasive breast cancer risk. https://doi.org/10.1289/EHP935.
- Published
- 2017
31. Association of mammographic density measures and breast cancer “intrinsic” molecular subtypes
- Author
-
Kleinstern, Geffen, Scott, Christopher G., Tamimi, Rulla M., Jensen, Matthew R., Pankratz, V. Shane, Bertrand, Kimberly A., Norman, Aaron D., Visscher, Daniel W., Couch, Fergus J., Brandt, Kathleen, Shepherd, John, Wu, Fang-Fang, Chen, Yunn-Yi, Cummings, Steven R., Winham, Stacey, Kerlikowske, Karla, and Vachon, Celine M.
- Published
- 2021
- Full Text
- View/download PDF
32. Risk factors for estrogen receptor positive ductal carcinoma in situ of the breast in African American women
- Author
-
Bertrand, Kimberly A., Bethea, Traci N., Rosenberg, Lynn, Bandera, Elisa V., Khoury, Thaer, Troester, Melissa A., Ambrosone, Christine B., and Palmer, Julie R.
- Published
- 2020
- Full Text
- View/download PDF
33. Long-term Particulate Matter Exposures during Adulthood and Risk of Breast Cancer Incidence in the Nurses' Health Study II Prospective Cohort
- Author
-
Hart, Jaime E, Bertrand, Kimberly A, DuPre, Natalie, James, Peter, Vieira, Verónica M, Tamimi, Rulla M, and Laden, Francine
- Subjects
Biomedical and Clinical Sciences ,Epidemiology ,Health Services and Systems ,Health Sciences ,Oncology and Carcinogenesis ,Breast Cancer ,Climate-Related Exposures and Conditions ,Clinical Research ,Cancer ,Aging ,Prevention ,Aetiology ,2.2 Factors relating to the physical environment ,Good Health and Well Being ,Adult ,Air Pollutants ,Air Pollution ,Breast Neoplasms ,Female ,Humans ,Incidence ,Middle Aged ,Nurses ,Particulate Matter ,Proportional Hazards Models ,Prospective Studies ,Risk Factors ,Self Report ,Vehicle Emissions ,Medical and Health Sciences ,Biomedical and clinical sciences ,Health sciences - Abstract
BackgroundThere is increasing concern that environmental exposures, such as air pollution, may be related to increasing rates of breast cancer; however, results from cohort studies have been mixed. We examined the association between particulate matter (PM) and measures of distance to roadway with the risk of incident breast cancer in the prospective nationwide Nurses' Health Study II (NHSII) cohort.MethodsIncident invasive breast cancer from 1993 to 2011 (N = 3,416) was assessed among 115,921 women in the NHSII cohort. Time-varying Cox proportional hazards models were used to calculate HRs and 95% confidence intervals (95% CI) for increases in ambient exposures to PM10, PM2.5-10, and PM2.5 and residential roadway proximity categories.ResultsIn multivariable adjusted models, there was little evidence of an increased risk of breast cancer (or any of the receptor-specific subtypes) overall or by menopausal status with PM exposure. There was, however, a suggestion of increased risks among women living
- Published
- 2016
34. Early Life Body Fatness, Serum Anti-Müllerian Hormone, and Breast Density in Young Adult Women
- Author
-
Bertrand, Kimberly A, Baer, Heather J, Orav, E John, Klifa, Catherine, Kumar, Ajay, Hylton, Nola M, LeBlanc, Erin S, Snetselaar, Linda G, Van Horn, Linda, and Dorgan, Joanne F
- Subjects
Biomedical and Clinical Sciences ,Health Sciences ,Oncology and Carcinogenesis ,Pediatric ,Clinical Research ,Obesity ,Nutrition ,Cancer ,Breast Cancer ,Prevention ,Adipose Tissue ,Adolescent ,Adult ,Age Factors ,Anti-Mullerian Hormone ,Biomarkers ,Tumor ,Body Mass Index ,Breast Density ,Breast Neoplasms ,Child ,Enzyme-Linked Immunosorbent Assay ,Female ,Follow-Up Studies ,Humans ,Magnetic Resonance Imaging ,Risk Factors ,Young Adult ,Medical and Health Sciences ,Epidemiology ,Biomedical and clinical sciences ,Health sciences - Abstract
BackgroundEmerging evidence suggests positive associations between serum anti-Müllerian hormone (AMH), a marker of ovarian function, and breast cancer risk. Body size at young ages may influence AMH levels, but few studies have examined this. Also, no studies have examined the relation of AMH levels with breast density, a strong predictor of breast cancer risk.MethodsWe examined associations of early life body fatness, AMH concentrations, and breast density among 172 women in the Dietary Intervention Study in Children (DISC). Height and weight were measured at baseline (ages 8-10) and throughout adolescence. Serum AMH concentrations and breast density were assessed at ages 25-29 at the DISC 2006 Follow-up visit. We used linear mixed effects models to quantify associations of AMH (dependent variable) with quartiles of age-specific youth body mass index (BMI) Z-scores (independent variable). We assessed cross-sectional associations of breast density (dependent variable) with AMH concentration (independent variable).ResultsNeither early life BMI nor current adult BMI was associated with AMH concentrations. There were no associations between AMH and percent or absolute dense breast volume. In contrast, women with higher AMH concentrations had significantly lower absolute nondense breast volume (Ptrend < 0.01).ConclusionsWe found no evidence that current or early life BMI influences AMH concentrations in later life. Women with higher concentrations of AMH had similar percent and absolute dense breast volume, but lower nondense volume.ImpactThese results suggest that AMH may be associated with lower absolute nondense breast volume; however, future prospective studies are needed to establish temporality. Cancer Epidemiol Biomarkers Prev; 25(7); 1151-7. ©2016 AACR.
- Published
- 2016
35. Genetically predicted longer telomere length is associated with increased risk of B-cell lymphoma subtypes
- Author
-
Machiela, Mitchell J, Lan, Qing, Slager, Susan L, Vermeulen, Roel CH, Teras, Lauren R, Camp, Nicola J, Cerhan, James R, Spinelli, John J, Wang, Sophia S, Nieters, Alexandra, Vijai, Joseph, Yeager, Meredith, Wang, Zhaoming, Ghesquières, Hervé, McKay, James, Conde, Lucia, de Bakker, Paul IW, Cox, David G, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Giles, Graham G, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Purdue, Mark P, Vajdic, Claire M, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Tilly, Hervé, Haioun, Corinne, Molina, Thierry J, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Roos, Göran, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Boeing, Heiner, Tjønneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, De Vivo, Immaculata, Giovannucci, Edward, Kraft, Peter, and Huang, Jinyan
- Subjects
Clinical Research ,Rare Diseases ,Genetics ,Cancer ,Hematology ,Lymphoma ,Adolescent ,Adult ,Age Factors ,Aged ,Aged ,80 and over ,Female ,Genetic Association Studies ,Genetic Predisposition to Disease ,Humans ,Lymphoma ,B-Cell ,Male ,Middle Aged ,Prospective Studies ,Telomere ,Biological Sciences ,Medical and Health Sciences ,Genetics & Heredity - Abstract
Evidence from a small number of studies suggests that longer telomere length measured in peripheral leukocytes is associated with an increased risk of non-Hodgkin lymphoma (NHL). However, these studies may be biased by reverse causation, confounded by unmeasured environmental exposures and might miss time points for which prospective telomere measurement would best reveal a relationship between telomere length and NHL risk. We performed an analysis of genetically inferred telomere length and NHL risk in a study of 10 102 NHL cases of the four most common B-cell histologic types and 9562 controls using a genetic risk score (GRS) comprising nine telomere length-associated single-nucleotide polymorphisms. This approach uses existing genotype data and estimates telomere length by weighing the number of telomere length-associated variant alleles an individual carries with the published change in kb of telomere length. The analysis of the telomere length GRS resulted in an association between longer telomere length and increased NHL risk [four B-cell histologic types combined; odds ratio (OR) = 1.49, 95% CI 1.22-1.82,P-value = 8.5 × 10(-5)]. Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL subtype contributing to this association (OR = 2.60, 95% CI 1.93-3.51,P-value = 4.0 × 10(-10)). Significant interactions were observed across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the follicular lymphoma subtype. Our results indicate that a genetic background that favors longer telomere length may increase NHL risk, particularly risk of CLL/SLL, and are consistent with earlier studies relating longer telomere length with increased NHL risk.
- Published
- 2016
36. International Pooled Analysis of Leisure-Time Physical Activity and Premenopausal Breast Cancer in Women From 19 Cohorts
- Author
-
Timmins, Iain R., primary, Jones, Michael E., additional, O'Brien, Katie M., additional, Adami, Hans-Olov, additional, Aune, Dagfinn, additional, Baglietto, Laura, additional, Bertrand, Kimberly A., additional, Brantley, Kristen D., additional, Chen, Yu, additional, Clague DeHart, Jessica, additional, Clendenen, Tess V., additional, Dossus, Laure, additional, Eliassen, A. Heather, additional, Fletcher, Olivia, additional, Fournier, Agnès, additional, Håkansson, Niclas, additional, Hankinson, Susan E., additional, Houlston, Richard S., additional, Joshu, Corinne E., additional, Kirsh, Victoria A., additional, Kitahara, Cari M., additional, Koh, Woon-Puay, additional, Linet, Martha S., additional, Park, Hannah Lui, additional, Lynch, Brigid M., additional, May, Anne M., additional, Mellemkjær, Lene, additional, Milne, Roger L., additional, Palmer, Julie R., additional, Ricceri, Fulvio, additional, Rohan, Thomas E., additional, Ruddy, Kathryn J., additional, Sánchez, Maria-Jose, additional, Shu, Xiao-Ou, additional, Smith-Byrne, Karl, additional, Steindorf, Karen, additional, Sund, Malin, additional, Vachon, Celine M., additional, Vatten, Lars J., additional, Visvanathan, Kala, additional, Weiderpass, Elisabete, additional, Willett, Walter C., additional, Wolk, Alicja, additional, Yuan, Jian-Min, additional, Zheng, Wei, additional, Nichols, Hazel B., additional, Sandler, Dale P., additional, Swerdlow, Anthony J., additional, and Schoemaker, Minouk J., additional
- Published
- 2023
- Full Text
- View/download PDF
37. Enhancing Mammography and Empowering Solutions for Breast Cancer Disparities
- Author
-
Tehranifar, Parisa, primary and Bertrand, Kimberly A., additional
- Published
- 2023
- Full Text
- View/download PDF
38. Circulating lipids, mammographic density, and risk of breast cancer in the Nurses’ Health Study and Nurses’ Health Study II
- Author
-
Lucht, Sarah A., Eliassen, A. Heather, Bertrand, Kimberly A., Ahern, Thomas P., Borgquist, Signe, Rosner, Bernard, Hankinson, Susan E., and Tamimi, Rulla M.
- Published
- 2019
39. Pre- and perinatal factors and incidence of breast cancer in the Black Women’s Health Study
- Author
-
Barber, Lauren E., Bertrand, Kimberly A., Rosenberg, Lynn, Battaglia, Tracy A., and Palmer, Julie R.
- Published
- 2019
40. 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, De Vivo, Immaculata, 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, 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 KC, 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, and Davis, Faith G
- Subjects
Tobacco ,Clinical Research ,Urologic Diseases ,Lung ,Genetics ,Rare Diseases ,Lung Cancer ,Human Genome ,Hematology ,Cancer ,Tobacco Smoke and Health ,Prevention ,Lymphoma ,Adult ,Aged ,Asian People ,Bone Neoplasms ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Kidney Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lung Neoplasms ,Lymphoma ,Large B-Cell ,Diffuse ,Male ,Middle Aged ,Neoplasms ,Osteosarcoma ,Polymorphism ,Single Nucleotide ,Smoking ,Testicular Neoplasms ,Tissue Array Analysis ,Urinary Bladder Neoplasms ,White People ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
41. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen 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, De Vivo, Immaculata, 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, 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 KC, 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, and Davis, Faith G
- Subjects
Humans ,Neoplasms ,Osteosarcoma ,Bone Neoplasms ,Testicular Neoplasms ,Lung Neoplasms ,Kidney Neoplasms ,Genetic Predisposition to Disease ,Tissue Array Analysis ,Smoking ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Middle Aged ,Asian Continental Ancestry Group ,European Continental Ancestry Group ,Female ,Male ,Urinary Bladder Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Genome-Wide Association Study ,Polymorphism ,Single Nucleotide ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Oncology And Carcinogenesis ,Oncology & Carcinogenesis ,Oncology and Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
42. Automated percent mammographic density, mammographic texture variation, and risk of breast cancer: a nested case-control study
- Author
-
Warner, Erica T., Rice, Megan S., Zeleznik, Oana A., Fowler, Erin E., Murthy, Divya, Vachon, Celine M., Bertrand, Kimberly A., Rosner, Bernard A., Heine, John, and Tamimi, Rulla M.
- Published
- 2021
- Full Text
- View/download PDF
43. Body fatness during childhood and adolescence and breast density in young women: a prospective analysis.
- Author
-
Bertrand, Kimberly, Baer, Heather, Orav, E, Klifa, Catherine, Shepherd, John, Van Horn, Linda, Snetselaar, Linda, Stevens, Victor, Hylton, Nola, and Dorgan, Joanne
- Subjects
Adipose Tissue ,Adiposity ,Adult ,Age Factors ,Body Mass Index ,Breast Density ,Breast Neoplasms ,Child ,Female ,Follow-Up Studies ,Humans ,Magnetic Resonance Imaging ,Mammary Glands ,Human ,Prospective Studies - Abstract
INTRODUCTION: Overweight and obesity in childhood and adolescence are associated with reduced breast cancer risk, independent of adult body mass index (BMI). These associations may be mediated through breast density. METHODS: We prospectively examined associations of early life body fatness with adult breast density measured by MRI in 182 women in the Dietary Intervention Study in Children (DISC) who were ages 25-29 at follow-up. Height, weight, and other factors were measured at baseline (ages 8-10) and annual clinic visits through adolescence. We used linear mixed-effects models to quantify associations of percent breast density and dense and non-dense breast volume at ages 25-29 with quartiles of age-specific youth body mass index (BMI) Z-scores, adjusting for clinic, treatment group, current adult BMI, and other well-established risk factors for breast cancer and predictors of breast density. RESULTS: We observed inverse associations between age-specific BMI Z-scores at all youth clinic visits and percent breast density, adjusting for current adult BMI and other covariates (all p values
- Published
- 2015
44. Dense and Nondense Mammographic Area and Risk of Breast Cancer by Age and Tumor Characteristics
- Author
-
Bertrand, Kimberly A, Scott, Christopher G, Tamimi, Rulla M, Jensen, Matthew R, Pankratz, V Shane, Norman, Aaron D, Visscher, Daniel W, Couch, Fergus J, Shepherd, John, Chen, Yunn-Yi, Fan, Bo, Wu, Fang-Fang, Ma, Lin, Beck, Andrew H, Cummings, Steven R, Kerlikowske, Karla, and Vachon, Celine M
- Subjects
Health Services and Systems ,Biomedical and Clinical Sciences ,Health Sciences ,Oncology and Carcinogenesis ,Breast Cancer ,Cancer ,Aging ,Clinical Research ,Adult ,Age Factors ,Breast Density ,Breast Neoplasms ,Female ,Humans ,Mammary Glands ,Human ,Middle Aged ,Radiography ,Receptor ,ErbB-2 ,Receptors ,Estrogen ,Risk Factors ,Young Adult ,Receptor ,erbB-2 ,Medical and Health Sciences ,Epidemiology ,Biomedical and clinical sciences ,Health sciences - Abstract
BackgroundMammographic density (MD) is a strong breast cancer risk factor. We previously reported associations of percent mammographic density (PMD) with larger and node-positive tumors across all ages, and estrogen receptor (ER)-negative status among women ages
- Published
- 2015
45. A genome-wide association study of marginal zone lymphoma shows association to the HLA region.
- Author
-
Vijai, Joseph, Wang, Zhaoming, Berndt, Sonja I, Skibola, Christine F, Slager, Susan L, de Sanjose, Silvia, Melbye, Mads, Glimelius, Bengt, Bracci, Paige M, Conde, Lucia, Birmann, Brenda M, Wang, Sophia S, Brooks-Wilson, Angela R, Lan, Qing, de Bakker, Paul IW, Vermeulen, Roel CH, Portlock, Carol, Ansell, Stephen M, Link, Brian K, Riby, Jacques, North, Kari E, Gu, Jian, Hjalgrim, Henrik, Cozen, Wendy, Becker, Nikolaus, Teras, Lauren R, Spinelli, John J, Turner, Jenny, Zhang, Yawei, Purdue, Mark P, Giles, Graham G, Kelly, Rachel S, Zeleniuch-Jacquotte, Anne, Ennas, Maria Grazia, Monnereau, Alain, Bertrand, Kimberly A, Albanes, Demetrius, Lightfoot, Tracy, Yeager, Meredith, Chung, Charles C, Burdett, Laurie, Hutchinson, Amy, Lawrence, Charles, Montalvan, Rebecca, Liang, Liming, Huang, Jinyan, Ma, Baoshan, Villano, Danylo J, Maria, Ann, Corines, Marina, Thomas, Tinu, Novak, Anne J, Dogan, Ahmet, Liebow, Mark, Thompson, Carrie A, Witzig, Thomas E, Habermann, Thomas M, Weiner, George J, Smith, Martyn T, Holly, Elizabeth A, Jackson, Rebecca D, Tinker, Lesley F, Ye, Yuanqing, Adami, Hans-Olov, Smedby, Karin E, De Roos, Anneclaire J, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Diver, W Ryan, Vajdic, Claire M, Armstrong, Bruce K, Kricker, Anne, Zheng, Tongzhang, Holford, Theodore R, Severi, Gianluca, Vineis, Paolo, Ferri, Giovanni M, Ricco, Rosalia, Miligi, Lucia, Clavel, Jacqueline, Giovannucci, Edward, Kraft, Peter, Virtamo, Jarmo, Smith, Alex, Kane, Eleanor, Roman, Eve, Chiu, Brian CH, Fraumeni, Joseph F, Wu, Xifeng, Cerhan, James R, Offit, Kenneth, and Chanock, Stephen J
- Subjects
Humans ,Membrane Glycoproteins ,Computational Biology ,Major Histocompatibility Complex ,Genotype ,Polymorphism ,Single Nucleotide ,European Continental Ancestry Group ,Lymphoma ,B-Cell ,Marginal Zone ,Genome-Wide Association Study ,Butyrophilins ,Polymorphism ,Single Nucleotide ,Lymphoma ,B-Cell ,Marginal Zone - Abstract
Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.
- Published
- 2015
46. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma
- Author
-
Cerhan, James R, Berndt, Sonja I, Vijai, Joseph, Ghesquières, Hervé, McKay, James, Wang, Sophia S, Wang, Zhaoming, Yeager, Meredith, Conde, Lucia, de Bakker, Paul IW, Nieters, Alexandra, Cox, David, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Lan, Qing, Severi, Gianluca, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Teras, Lauren R, Purdue, Mark P, Vajdic, Claire M, Spinelli, John J, Giles, Graham G, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Weiner, George J, Veron, Amelie S, Zelenika, Diana, Tilly, Hervé, Haioun, Corinne, Molina, Thierry Jo, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Kricker, Anne, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Vermeulen, Roel CH, Boeing, Heiner, Tjonneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, and Birmann, Brenda M
- Subjects
Human Genome ,Rare Diseases ,Genetics ,Cancer ,Hematology ,Lymphoma ,Aetiology ,2.1 Biological and endogenous factors ,Chromosome Mapping ,Computational Biology ,Genetic Loci ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Genotype ,Humans ,Likelihood Functions ,Lymphoma ,Large B-Cell ,Diffuse ,Polymorphism ,Single Nucleotide ,Quantitative Trait Loci ,White People ,Biological Sciences ,Medical and Health Sciences ,Developmental Biology - Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
- Published
- 2014
47. Genome-wide Association Study Identifies Five Susceptibility Loci for Follicular Lymphoma outside the HLA Region
- Author
-
Skibola, Christine F, Berndt, Sonja I, Vijai, Joseph, Conde, Lucia, Wang, Zhaoming, Yeager, Meredith, de Bakker, Paul IW, Birmann, Brenda M, Vajdic, Claire M, Foo, Jia-Nee, Bracci, Paige M, Vermeulen, Roel CH, Slager, Susan L, de Sanjose, Silvia, Wang, Sophia S, Linet, Martha S, Salles, Gilles, Lan, Qing, Severi, Gianluca, Hjalgrim, Henrik, Lightfoot, Tracy, Melbye, Mads, Gu, Jian, Ghesquières, Hervé, Link, Brian K, Morton, Lindsay M, Holly, Elizabeth A, Smith, Alex, Tinker, Lesley F, Teras, Lauren R, Kricker, Anne, Becker, Nikolaus, Purdue, Mark P, Spinelli, John J, Zhang, Yawei, Giles, Graham G, Vineis, Paolo, Monnereau, Alain, Bertrand, Kimberly A, Albanes, Demetrius, Zeleniuch-Jacquotte, Anne, Gabbas, Attilio, Chung, Charles C, Burdett, Laurie, Hutchinson, Amy, Lawrence, Charles, Montalvan, Rebecca, Liang, Liming, Huang, Jinyan, Ma, Baoshan, Liu, Jianjun, Adami, Hans-Olov, Glimelius, Bengt, Ye, Yuanqing, Nowakowski, Grzegorz S, Dogan, Ahmet, Thompson, Carrie A, Habermann, Thomas M, Novak, Anne J, Liebow, Mark, Witzig, Thomas E, Weiner, George J, Schenk, Maryjean, Hartge, Patricia, De Roos, Anneclaire J, Cozen, Wendy, Zhi, Degui, Akers, Nicholas K, Riby, Jacques, Smith, Martyn T, Lacher, Mortimer, Villano, Danylo J, Maria, Ann, Roman, Eve, Kane, Eleanor, Jackson, Rebecca D, North, Kari E, Diver, W Ryan, Turner, Jenny, Armstrong, Bruce K, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, McKay, James, Brooks-Wilson, Angela R, Zheng, Tongzhang, Holford, Theodore R, Chamosa, Saioa, Kaaks, Rudolph, Kelly, Rachel S, Ohlsson, Bodil, Travis, Ruth C, Weiderpass, Elisabete, Clavel, Jacqueline, Giovannucci, Edward, Kraft, Peter, and Virtamo, Jarmo
- Subjects
Hematology ,Cancer ,Clinical Research ,Human Genome ,Lymphoma ,Genetics ,Rare Diseases ,2.1 Biological and endogenous factors ,Aetiology ,Alleles ,Biomarkers ,Tumor ,Case-Control Studies ,Chromosomes ,Human ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,HLA Antigens ,Haplotypes ,Humans ,Lymphoma ,Follicular ,Polymorphism ,Single Nucleotide ,Biological Sciences ,Medical and Health Sciences ,Genetics & Heredity - Abstract
Genome-wide association studies (GWASs) of follicular lymphoma (FL) have previously identified human leukocyte antigen (HLA) gene variants. To identify additional FL susceptibility loci, we conducted a large-scale two-stage GWAS in 4,523 case subjects and 13,344 control subjects of European ancestry. Five non-HLA loci were associated with FL risk: 11q23.3 (rs4938573, p = 5.79 × 10(-20)) near CXCR5; 11q24.3 (rs4937362, p = 6.76 × 10(-11)) near ETS1; 3q28 (rs6444305, p = 1.10 × 10(-10)) in LPP; 18q21.33 (rs17749561, p = 8.28 × 10(-10)) near BCL2; and 8q24.21 (rs13254990, p = 1.06 × 10(-8)) near PVT1. In an analysis of the HLA region, we identified four linked HLA-DRβ1 multiallelic amino acids at positions 11, 13, 28, and 30 that were associated with FL risk (pomnibus = 4.20 × 10(-67) to 2.67 × 10(-70)). Additional independent signals included rs17203612 in HLA class II (odds ratio [OR(per-allele)] = 1.44; p = 4.59 × 10(-16)) and rs3130437 in HLA class I (OR(per-allele) = 1.23; p = 8.23 × 10(-9)). Our findings further expand the number of loci associated with FL and provide evidence that multiple common variants outside the HLA region make a significant contribution to FL risk.
- Published
- 2014
48. ASO Visual Abstract: Racial and Socioeconomic Disparities in Breast Cancer Outcomes within the AJCC Pathologic Prognostic Staging System
- Author
-
Kantor, Olga, Wang, Monica L., Bertrand, Kimberly, Pierce, Lori, Freedman, Rachel A., Chavez-MacGregor, Mariana, King, Tari A., and Mittendorf, Elizabeth A.
- Published
- 2021
- Full Text
- View/download PDF
49. International Pooled Analysis of Leisure-Time Physical Activity and Premenopausal Breast Cancer in Women From 19 Cohorts.
- Author
-
Timmins, Iain R., Jones, Michael E., O'Brien, Katie M., Adami, Hans-Olov, Aune, Dagfinn, Baglietto, Laura, Bertrand, Kimberly A., Brantley, Kristen D., Chen, Yu, Clague DeHart, Jessica, Clendenen, Tess V., Dossus, Laure, Eliassen, A. Heather, Fletcher, Olivia, Fournier, Agnès, Håkansson, Niclas, Hankinson, Susan E., Houlston, Richard S., Joshu, Corinne E., and Kirsh, Victoria A.
- Published
- 2024
- Full Text
- View/download PDF
50. Validating a model for predicting breast cancer and nonbreast cancer death in women aged 55 years and older.
- Author
-
Wolfson, Emily A, Schonberg, Mara A, Eliassen, A Heather, Bertrand, Kimberly A, Shvetsov, Yurii B, Rosner, Bernard A, Palmer, Julie R, LaCroix, Andrea Z, Chlebowski, Rowan T, Nelson, Rebecca A, and Ngo, Long H
- Subjects
BREAST cancer ,CANCER patients ,BREAST imaging ,ONCOLOGY nursing ,DISEASE risk factors ,SURVIVAL analysis (Biometry) ,WOMEN'S health - Abstract
Background To support mammography screening decision making, we developed a competing-risk model to estimate 5-year breast cancer risk and 10-year nonbreast cancer death for women aged 55 years and older using Nurses' Health Study data and examined model performance in the Black Women's Health Study (BWHS). Here, we examine model performance in predicting 10-year outcomes in the BWHS, Women's Health Initiative-Extension Study (WHI-ES), and Multiethnic Cohort (MEC) and compare model performance to existing breast cancer prediction models. Methods We used competing-risk regression and Royston and Altman methods for validating survival models to calculate our model's calibration and discrimination (C index) in BWHS (n = 17 380), WHI-ES (n = 106 894), and MEC (n = 49 668). The Nurses' Health Study development cohort (n = 48 102) regression coefficients were applied to the validation cohorts. We compared our model's performance with breast cancer risk assessment tool (Gail) and International Breast Cancer Intervention Study (IBIS) models by computing breast cancer risk estimates and C statistics. Results When predicting 10-year breast cancer risk, our model's C index was 0.569 in BWHS, 0.572 in WHI-ES, and 0.576 in MEC. The Gail model's C statistic was 0.554 in BWHS, 0.564 in WHI-ES, and 0.551 in MEC; IBIS's C statistic was 0.547 in BWHS, 0.552 in WHI-ES, and 0.562 in MEC. The Gail model underpredicted breast cancer risk in WHI-ES; IBIS underpredicted breast cancer risk in WHI-ES and in MEC but overpredicted breast cancer risk in BWHS. Our model calibrated well. Our model's C index for predicting 10-year nonbreast cancer death was 0.760 in WHI-ES and 0.763 in MEC. Conclusions Our competing-risk model performs as well as existing breast cancer prediction models in diverse cohorts and predicts nonbreast cancer death. We are developing a website to disseminate our model. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.