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  • 1. Fanidi, Anouar
    et al.
    Carreras-Torres, Robert
    Larose, Tricia L.
    Yuan, Jian-Min
    Stevens, Victoria L.
    Weinstein, Stephanie J.
    Albanes, Demetrius
    Prentice, Ross
    Pettinger, Mary
    Cai, Qiuyin
    Blot, William J.
    Arslan, Alan A.
    Zeleniuch-Jacquotte, Anne
    McCullough, Marjorie L.
    Le Marchand, Loic
    Wilkens, Lynne R.
    Haiman, Christopher A.
    Zhang, Xuehong
    Stampfer, Meir J.
    Smith-Warner, Stephanie A.
    Giovannucci, Edward
    Giles, Graham G.
    Hodge, Allison M.
    Severi, Gianluca
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Langhammer, Arnulf
    Brumpton, Ben M.
    Wang, Renwei
    Gao, Yu-Tang
    Ericson, Ulrika
    Bojesen, Stig E.
    Arnold, Susanne M.
    Koh, Woon-Puay
    Shu, Xiao-Ou
    Xiang, Yong-Bing
    Li, Honglan
    Zheng, Wei
    Lan, Qing
    Visvanathan, Kala
    Hoffman-Bolton, Judith
    Ueland, Per M.
    Midttun, Oivind
    Caporaso, Neil E.
    Purdue, Mark
    Freedman, Neal D.
    Buring, Julie E.
    Lee, I-Min
    Sesso, Howard D.
    Gaziano, J. Michael
    Manjer, Jonas
    Relton, Caroline L.
    Hung, Rayjean J.
    Amos, Chris, I
    Johansson, Mattias
    Brennan, Paul
    Is high vitamin B12 status a cause of lung cancer?2019In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 145, no 6, p. 1499-1503Article in journal (Refereed)
    Abstract [en]

    Vitamin B supplementation can have side effects for human health, including cancer risk. We aimed to elucidate the role of vitamin B12 in lung cancer etiology via direct measurements of pre‐diagnostic circulating vitamin B12 concentrations in a nested case–control study, complemented with a Mendelian randomization (MR) approach in an independent case–control sample. We used pre‐diagnostic biomarker data from 5183 case–control pairs nested within 20 prospective cohorts, and genetic data from 29,266 cases and 56,450 controls. Exposures included directly measured circulating vitamin B12 in pre‐diagnostic blood samples from the nested case–control study, and 8 single nucleotide polymorphisms associated with vitamin B12 concentrations in the MR study. Our main outcome of interest was increased risk for lung cancer, overall and by histological subtype, per increase in circulating vitamin B12 concentrations. We found circulating vitamin B12 to be positively associated with overall lung cancer risk in a dose response fashion (odds ratio for a doubling in B12 [ORlog2B12] = 1.15, 95% confidence interval (95%CI) = 1.06–1.25). The MR analysis based on 8 genetic variants also indicated that genetically determined higher vitamin B12 concentrations were positively associated with overall lung cancer risk (OR per 150 pmol/L standard deviation increase in B12 [ORSD] = 1.08, 95%CI = 1.00–1.16). Considering the consistency of these two independent and complementary analyses, these findings support the hypothesis that high vitamin B12 status increases the risk of lung cancer.

  • 2. Fortner, Renee T.
    et al.
    Poole, Elizabeth M.
    Wentzensen, Nicolas A.
    Trabert, Britton
    White, Emily
    Arslan, Alan A.
    Patel, Alpa, V
    Setiawan, V. Wendy
    Visvanathan, Kala
    Weiderpass, Elisabete
    Adami, Hans-Olov
    Black, Amanda
    Bernstein, Leslie
    Brinton, Louise A.
    Buring, Julie
    Clendenen, Tess, V
    Fournier, Agnes
    Fraser, Gary
    Gapstur, Susan M.
    Gaudet, Mia M.
    Giles, Graham G.
    Gram, Inger T.
    Hartge, Patricia
    Hoffman-Bolton, Judith
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Kaaks, Rudolf
    Kirsh, Victoria A.
    Knutsen, Synnove
    Koh, Woon-Puay
    Lacey, James V., Jr.
    Lee, I-Min
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Merritt, Melissa A.
    Milne, Roger L.
    Onland-Moret, N. Charlotte
    Peters, Ulrike
    Poynter, Jenny N.
    Rinaldi, Sabina
    Robien, Kim
    Rohan, Thomas
    Sanchez, Maria-Jose
    Schairer, Catherine
    Schouten, Leo J.
    Tjonneland, Anne
    Townsend, Mary K.
    Travis, Ruth C.
    Trichopoulou, Antonia
    van den Brandt, Piet A.
    Vineis, Paolo
    Wilkens, Lynne
    Wolk, Alicja
    Yang, Hannah P.
    Zeleniuch-Jacquotte, Anne
    Tworoger, Shelley S.
    Ovarian cancer risk factors by tumor aggressiveness: an analysis from the Ovarian Cancer Cohort Consortium2019In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 145, no 1, p. 58-69Article in journal (Refereed)
    Abstract [en]

    Ovarian cancer risk factors differ by histotype; however, within subtype, there is substantial variability in outcomes. We hypothesized that risk factor profiles may influence tumor aggressiveness, defined by time between diagnosis and death, independent of histology. Among 1.3 million women from 21 prospective cohorts, 4,584 invasive epithelial ovarian cancers were identified and classified as highly aggressive (death in <1 year, n = 864), very aggressive (death in 1 to < 3 years, n = 1,390), moderately aggressive (death in 3 to < 5 years, n = 639), and less aggressive (lived 5+ years, n = 1,691). Using competing risks Cox proportional hazards regression, we assessed heterogeneity of associations by tumor aggressiveness for all cases and among serous and endometrioid/clear cell tumors. Associations between parity (phet = 0.01), family history of ovarian cancer (phet = 0.02), body mass index (BMI; phet ≤ 0.04) and smoking (phet < 0.01) and ovarian cancer risk differed by aggressiveness. A first/single pregnancy, relative to nulliparity, was inversely associated with highly aggressive disease (HR: 0.72; 95% CI [0.58–0.88]), no association was observed for subsequent pregnancies (per pregnancy, 0.97 [0.92–1.02]). In contrast, first and subsequent pregnancies were similarly associated with less aggressive disease (0.87 for both). Family history of ovarian cancer was only associated with risk of less aggressive disease (1.94 [1.47–2.55]). High BMI (≥35 vs. 20 to < 25 kg/m2, 1.93 [1.46–2.56] and current smoking (vs. never, 1.30 [1.07–1.57]) were associated with increased risk of highly aggressive disease. Results were similar within histotypes. Ovarian cancer risk factors may be directly associated with subtypes defined by tumor aggressiveness, rather than through differential effects on histology. Studies to assess biological pathways are warranted.

  • 3. Huang, Joyce Y.
    et al.
    Larose, Tricia L.
    Luu, Hung N.
    Wang, Renwei
    Fanidi, Anouar
    Alcala, Karine
    Stevens, Victoria L.
    Weinstein, Stephanie J.
    Albanes, Demetrius
    Caporaso, Neil E.
    Purdue, Mark P.
    Ziegler, Regina G.
    Freedman, Neal D.
    Lan, Qing
    Prentice, Ross L.
    Pettinger, Mary
    Thomson, Cynthia A.
    Cai, Qiuyin
    Wu, Jie
    Blot, William J.
    Shu, Xiao-Ou
    Zheng, Wei
    Arslan, Alan A.
    Zeleniuch-Jacquotte, Anne
    Le Marchand, Loic
    Wilkens, Lynn R.
    Haiman, Christopher A.
    Zhang, Xuehong
    Stampfer, Meir J.
    Giles, Graham G.
    Hodge, Allison M.
    Severi, Gianluca
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Langhammer, Arnulf
    Hveem, Kristian
    Xiang, Yong-Bing
    Li, Hong-Lan
    Gao, Yu-Tang
    Visvanathan, Kala
    Ueland, Per M.
    Midttun, Oivind
    Ulvi, Arve
    Buring, Julie E.
    Lee, I-Min
    SeSS, Howard D.
    Gaziano, J. Michael
    Manjer, Jonas
    Relton, Caroline
    Koh, Woon-Puay
    Brennan, Paul
    Johansson, Mattias
    Yuan, Jian-Min
    Han, Jiali
    Circulating markers of cellular immune activation in prediagnostic blood sample and lung cancer risk in the Lung Cancer Cohort Consortium (LC3)2019In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215Article in journal (Refereed)
    Abstract [en]

    Cell-mediated immune suppression may play an important role in lung carcinogenesis. We investigated the associations for circulating levels of tryptophan, kynurenine, kynurenine:tryptophan ratio (KTR), quinolinic acid (QA) and neopterin as markers of immune regulation and inflammation with lung cancer risk in 5,364 smoking-matched case-control pairs from 20 prospective cohorts included in the international Lung Cancer Cohort Consortium. All biomarkers were quantified by mass spectrometry-based methods in serum/plasma samples collected on average 6 years before lung cancer diagnosis. Odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer associated with individual biomarkers were calculated using conditional logistic regression with adjustment for circulating cotinine. Compared to the lowest quintile, the highest quintiles of kynurenine, KTR, QA and neopterin were associated with a 20-30% higher risk, and tryptophan with a 15% lower risk of lung cancer (all p(trend) < 0.05). The strongest associations were seen for current smokers, where the adjusted ORs (95% CIs) of lung cancer for the highest quintile of KTR, QA and neopterin were 1.42 (1.15-1.75), 1.42 (1.14-1.76) and 1.45 (1.13-1.86), respectively. A stronger association was also seen for KTR and QA with risk of lung squamous cell carcinoma followed by adenocarcinoma, and for lung cancer diagnosed within the first 2 years after blood draw. This study demonstrated that components of the tryptophan-kynurenine pathway with immunomodulatory effects are associated with risk of lung cancer overall, especially for current smokers. Further research is needed to evaluate the role of these biomarkers in lung carcinogenesis and progression.

  • 4. Jung, Seungyoun
    et al.
    Allen, Naomi
    Arslan, Alan A.
    Baglietto, Laura
    Barricarte, Aurelio
    Brinton, Louise A.
    Egleston, Brian L.
    Falk, Roni T.
    Fortner, Renée T.
    Helzlsouer, Kathy J.
    Gao, Yutang
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Kaaks, Rudolph
    Krogh, Vittorio
    Merritt, Melissa A.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Onland-Moret, N. Charlotte
    Rinaldi, Sabina
    Schock, Helena
    Shu, Xiao-Ou
    Sluss, Patrick M.
    Staats, Paul N.
    Sacerdote, Carlotta
    Travis, Ruth C.
    Tjønneland, Anne
    Trichopoulou, Antonia
    Tworoger, Shelley S.
    Visvanathan, Kala
    Weiderpass, Elisabete
    Zeleniuch-Jacquotte, Anne
    Dorgan, Joanne F.
    Anti‐Müllerian hormone and risk of ovarian cancer in nine cohorts2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 142, no 2, p. 262-270Article in journal (Refereed)
    Abstract [en]

    Animal and experimental data suggest that anti‐Müllerian hormone (AMH) serves as a marker of ovarian reserve and inhibits the growth of ovarian tumors. However, few epidemiologic studies have examined the association between AMH and ovarian cancer risk. We conducted a nested case‐control study of 302 ovarian cancer cases and 336 matched controls from nine cohorts. Prediagnostic blood samples of premenopausal women were assayed for AMH using a picoAMH enzyme‐linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable‐adjusted conditional logistic regression. AMH concentration was not associated with overall ovarian cancer risk. The multivariable‐adjusted OR (95% CI), comparing the highest to the lowest quartile of AMH, was 0.99 (0.59–1.67) (Ptrend: 0.91). The association did not differ by age at blood draw or oral contraceptive use (all Pheterogeneity: ≥0.26). There also was no evidence for heterogeneity of risk for tumors defined by histologic developmental pathway, stage, and grade, and by age at diagnosis and time between blood draw and diagnosis (all Pheterogeneity: ≥0.39). In conclusion, this analysis of mostly late premenopausal women from nine cohorts does not support the hypothesized inverse association between prediagnostic circulating levels of AMH and risk of ovarian cancer.

  • 5. Klein, Alison P.
    et al.
    Wolpin, Brian M.
    Risch, Harvey A.
    Stolzenberg-Solomon, Rachael Z.
    Mocci, Evelina
    Zhang, Mingfeng
    Canzian, Federico
    Childs, Erica J.
    Hoskins, Jason W.
    Jermusyk, Ashley
    Zhong, Jun
    Chen, Fei
    Albanes, Demetrius
    Andreotti, Gabriella
    Arslan, Alan A.
    Babic, Ana
    Bamlet, William R.
    Beane-Freeman, Laura
    Berndt, Sonja I.
    Blackford, Amanda
    Borges, Michael
    Borgida, Ayelet
    Bracci, Paige M.
    Brais, Lauren
    Brennan, Paul
    Brenner, Hermann
    Bueno-de-Mesquita, Bas
    Buring, Julie
    Campa, Daniele
    Capurso, Gabriele
    Cavestro, Giulia Martina
    Chaffee, Kari G.
    Chung, Charles C.
    Cleary, Sean
    Cotterchio, Michelle
    Dijk, Frederike
    Duell, Eric J.
    Foretova, Lenka
    Fuchs, Charles
    Funel, Niccola
    Gallinger, Steven
    Gaziano, J. Michael M.
    Gazouli, Maria
    Giles, Graham G.
    Giovannucci, Edward
    Goggins, Michael
    Goodman, Gary E.
    Goodman, Phyllis J.
    Hackert, Thilo
    Haiman, Christopher
    Hartge, Patricia
    Hasan, Manal
    Hegyi, Peter
    Helzlsouer, Kathy J.
    Herman, Joseph
    Holcatova, Ivana
    Holly, Elizabeth A.
    Hoover, Robert
    Hung, Rayjean J.
    Jacobs, Eric J.
    Jamroziak, Krzysztof
    Janout, Vladimir
    Kaaks, Rudolf
    Khaw, Kay-Tee
    Klein, Eric A.
    Kogevinas, Manolis
    Kooperberg, Charles
    Kulke, Matthew H.
    Kupcinskas, Juozas
    Kurtz, Robert J.
    Laheru, Daniel
    Landi, Stefano
    Lawlor, Rita T.
    Lee, I. -Min
    LeMarchand, Loic
    Lu, Lingeng
    Malats, Nuria
    Mambrini, Andrea
    Mannisto, Satu
    Milne, Roger L.
    Mohelnikova-Duchonova, Beatrice
    Neale, Rachel E.
    Neoptolemos, John P.
    Oberg, Ann L.
    Olson, Sara H.
    Orlow, Irene
    Pasquali, Claudio
    Patel, Alpa V.
    Peters, Ulrike
    Pezzilli, Raffaele
    Porta, Miquel
    Real, Francisco X.
    Rothman, Nathaniel
    Scelo, Ghislaine
    Sesso, Howard D.
    Severi, Gianluca
    Shu, Xiao-Ou
    Silverman, Debra
    Smith, Jill P.
    Soucek, Pavel
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Talar-Wojnarowska, Renata
    Tavano, Francesca
    Thornquist, Mark D.
    Tobias, Geoffrey S.
    Van Den Eeden, Stephen K.
    Vashist, Yogesh
    Visvanathan, Kala
    Vodicka, Pavel
    Wactawski-Wende, Jean
    Wang, Zhaoming
    Wentzensen, Nicolas
    White, Emily
    Yu, Herbert
    Yu, Kai
    Zeleniuch-Jacquotte, Anne
    Zheng, Wei
    Kraft, Peter
    Li, Donghui
    Chanock, Stephen
    Obazee, Ofure
    Petersen, Gloria M.
    Amundadottir, Laufey T.
    Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer2018In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 9, article id 556Article in journal (Refereed)
    Abstract [en]

    In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 x 10(-8)). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PAN-DoRA) consortium yields new genome-wide significant loci: rs13303010 at 1p36.33 (NOC2L, P = 8.36 x 10(-14)), rs2941471 at 8q21.11 (HNF4G, P = 6.60 x 10(-10)), rs4795218 at 17q12 (HNF1B, P = 1.32 x 10(-8)), and rs1517037 at 18q21.32 (GRP, P = 3.28 x 10(-8)). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene.

  • 6. Larose, Tricia L.
    et al.
    Guida, Florence
    Fanidi, Anouar
    Langhammer, Arnulf
    Kveem, Kristian
    Stevens, Victoria L.
    Jacobs, Eric J.
    Smith-Warner, Stephanie A.
    Giovannucci, Edward
    Albanes, Demetrius
    Weinstein, Stephanie J.
    Freedman, Neal D.
    Prentice, Ross
    Pettinger, Mary
    Thomson, Cynthia A.
    Cai, Qiuyin
    Wu, Jie
    Blot, William J.
    Arslan, Alan A.
    Zeleniuch-Jacquotte, Anne
    Le Marchand, Loic
    Wilkens, Lynne R.
    Haiman, Christopher A.
    Zhang, Xuehong
    Stampfer, Meir J.
    Hodge, Allison M.
    Giles, Graham G.
    Severi, Gianluca
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Wang, Renwei
    Yuan, Jian-Min
    Gao, Yu-Tang
    Koh, Woon-Puay
    Shu, Xiao-Ou
    Zheng, Wei
    Xiang, Yong-Bing
    Li, Honglan
    Lan, Qing
    Visvanathan, Kala
    Bolton, Judith Hoffman
    Ueland, Per Magne
    Midttun, Oivind
    Caporaso, Neil
    Purdue, Mark
    Sesso, Howard D.
    Buring, Julie E.
    Lee, I-Min
    Gaziano, J. Michael
    Manjer, Jonas
    Brunnstrom, Hans
    Brennan, Paul
    Johansson, Mattias
    Circulating cotinine concentrations and lung cancer risk in the Lung Cancer Cohort Consortium (LC3)2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 6, p. 1760-1771Article in journal (Refereed)
    Abstract [en]

    Background: Self-reported smoking is the principal measure used to assess lung cancer risk in epidemiological studies. We evaluated if circulating cotinine—a nicotine metabolite and biomarker of recent tobacco exposure—provides additional information on lung cancer risk.

    Methods: The study was conducted in the Lung Cancer Cohort Consortium (LC3) involving 20 prospective cohort studies. Pre-diagnostic serum cotinine concentrations were measured in one laboratory on 5364 lung cancer cases and 5364 individually matched controls. We used conditional logistic regression to evaluate the association between circulating cotinine and lung cancer, and assessed if cotinine provided additional risk-discriminative information compared with self-reported smoking (smoking status, smoking intensity, smoking duration), using receiver-operating characteristic (ROC) curve analysis.

    Results: We observed a strong positive association between cotinine and lung cancer risk for current smokers [odds ratio (OR ) per 500 nmol/L increase in cotinine (OR500): 1.39, 95% confidence interval (CI): 1.32–1.47]. Cotinine concentrations consistent with active smoking (≥115 nmol/L) were common in former smokers (cases: 14.6%; controls: 9.2%) and rare in never smokers (cases: 2.7%; controls: 0.8%). Former and never smokers with cotinine concentrations indicative of active smoking (≥115 nmol/L) also showed increased lung cancer risk. For current smokers, the risk-discriminative performance of cotinine combined with self-reported smoking (AUCintegrated: 0.69, 95% CI: 0.68–0.71) yielded a small improvement over self-reported smoking alone (AUCsmoke: 0.66, 95% CI: 0.64–0.68) (P = 1.5x10–9).

    Conclusions: Circulating cotinine concentrations are consistently associated with lung cancer risk for current smokers and provide additional risk-discriminative information compared with self-report smoking alone.

  • 7. Schoemaker, Minouk J.
    et al.
    Nichols, Hazel B.
    Wright, Lauren B.
    Brook, Mark N.
    Jones, Michael E.
    O'Brien, Katie M.
    Adami, Hans-Olov
    Baglietto, Laura
    Bernstein, Leslie
    Bertrand, Kimberly A.
    Boutron-Ruault, Marie-Christine
    Braaten, Tonje
    Chen, Yu
    Connor, Avonne E.
    Dorronsoro, Miren
    Dossus, Laure
    Eliassen, A. Heather
    Giles, Graham G.
    Hankinson, Susan E.
    Kaaks, Rudolf
    Key, Timothy J.
    Kirsh, Victoria A.
    Kitahara, Cari M.
    Koh, Woon-Puay
    Larsson, Susanna C.
    Linet, Martha S.
    Ma, Huiyan
    Masala, Giovanna
    Merritt, Melissa A.
    Milne, Roger L.
    Overvad, Kim
    Ozasa, Kotaro
    Palmer, Julie R.
    Peeters, Petra H.
    Riboli, Elio
    Rohan, Thomas E.
    Sadakane, Atsuko
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Tamirni, Rulla M.
    Trichopoulou, Antonia
    Ursin, Giske
    Vatten, Lars
    Visvanathan, Kala
    Weiderpass, Elisabete
    Willett, Walter C.
    Wolk, Alicja
    Yuan, Jian-Min
    Zeleniuch-Jacquotte, Anne
    Sandler, Dale P.
    Swerdlow, Anthony J.
    Association of body mass index and age With subsequent breast cancer risk in premenopausal women2018In: JAMA Oncology, ISSN 2374-2437, E-ISSN 2374-2445, Vol. 4, no 11, article id e181771Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE The association between increasing body mass index (BMI; calculated as wei ght in kilograms divided by height in meters squared) and risk of breast cancer is unique in cancer epidemiology in that a crossover effect exists, with risk reduction before and risk increase after menopause. The inverse association with premenopausal breast cancer risk is poorly characterized but might be important in the understanding of breast cancer causation.

    OBJECTIVE To investigate the association of BMI with premenopausal breast cancer risk, in particular by age at BMI, attained age, risk factors for breast cancer, and tumor characteristics.

    DESIGN, SETTING, AND PARTICIPANTS This multicenter analysis used pooled individual-level data from 758 592 premenopausal women from 19 prospective cohorts to estimate hazard ratios (HRs) of premenopausal breast cancer in association with BMI from ages 18 through 54 years using Cox proportional hazards regression analysis. Median follow-up was 9.3 years (interquartile range, 4.9-13.5 years) per participant, with 13 082 incident cases of breast cancer. Participants were recruited from January 1,1963, through December 31, 2013, and data were analyzed from September 1.2013, through December 31, 2017.

    EXPOSURES Body mass index at ages 18 to 24, 25 to 34,35 to 44, and 45 to 54 years.

    MAIN OUTCOMES AND MEASURES Invasive or in situ premenopausal breast cancer.

    RESULTS Among the 758 592 premenopausal women (median age, 40.6 years; interquartile range, 35.2-45.5 years) included in the analysis, inverse linear associations of BMI with breast cancer risk were found that were stronger for BMI at ages 18 to 24 years (HR per 5 kg/m(2) [5.0-U] difference, 0.77; 95% CI, 0.73-0.80) than for BMI at ages 45 to 54 years (HR per 5.0-U difference, 0.88; 95% CI, 0.86-0.91). The inverse associations were observed even among nonoverweight women. There was a 4.2-fold risk gradient between the highest and lowest BMI categories (BMI >= 35.0 vs <17.0) at ages 18 to 24 years (HR, 0.24; 95% CI, 0.14-0.40). Hazard ratios did not appreciably vary by attained age or between strata of other breast cancer risk factors. Associations were stronger for estrogen receptor-positive and/or progesterone receptor-positive than for hormone receptor-negative breast cancer for BMI at every age group (eg, for BMI at age 18 to 24 years: HR per 5.0-U difference for estrogen receptor-positive and progesterone receptor-positive tumors, 0.76 [95% CI, 0.70-0.81] vs hormone receptor-negative tumors, 0.85 [95% CI: 0.76-0.95]); BMI at ages 25 to 54 years was not consistently associated with triple-negative or hormone receptor-negative breast cancer overall.

    CONCLUSIONS AND RELEVANCE The results of this study suggest that increased adiposity is associated with a reduced risk of premenopausal breast cancer at a greater magnitude than previously shown and across the entire distribution of BMI. The strongest associations of risk were observed for BMI in early adulthood. Understanding the biological mechanisms underlying these associations could have important preventive potential.

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