Loic Le Marchand
National Institutes of Health
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Featured researches published by Loic Le Marchand.
American Journal of Epidemiology | 2010
Rachael Z. Stolzenberg-Solomon; Eric J. Jacobs; Alan A. Arslan; Dai Qi; Alpa V. Patel; Kathy J. Helzlsouer; Stephanie J. Weinstein; Marjorie L. McCullough; Mark P. Purdue; Xiao Ou Shu; Kirk Snyder; Jarmo Virtamo; Kai Yu; Anne Zeleniuch-Jacquotte; Wei Zheng; Demetrius Albanes; Qiuyin Cai; Chinonye Harvey; Richard B. Hayes; Sandra Clipp; Ronald L. Horst; Lonn Irish; Karen Koenig; Loic Le Marchand; Laurence N. Kolonel
Results from epidemiologic studies examining pancreatic cancer risk and vitamin D intake or 25-hydroxyvitamin D (25(OH)D) concentrations (the best indicator of vitamin D derived from diet and sun) have been inconsistent. Therefore, the authors conducted a pooled nested case-control study of participants from 8 cohorts within the Cohort Consortium Vitamin D Pooling Project of Rarer Cancers (VDPP) (1974–2006) to evaluate whether prediagnostic circulating 25(OH)D concentrations were associated with the development of pancreatic cancer. In total, 952 incident pancreatic adenocarcinoma cases occurred among participants (median follow-up, 6.5 years). Controls (n = 1,333) were matched to each case by cohort, age, sex, race/ethnicity, date of blood draw, and follow-up time. Conditional logistic regression analysis was used to calculate smoking-, body mass index-, and diabetes-adjusted odds ratios and 95% confidence intervals for pancreatic cancer. Clinically relevant 25(OH)D cutpoints were compared with a referent category of 50–<75 nmol/L. No significant associations were observed for participants with lower 25(OH)D status. However, a high 25(OH)D concentration (≥100 nmol/L) was associated with a statistically significant 2-fold increase in pancreatic cancer risk overall (odds ratio = 2.12, 95% confidence interval: 1.23, 3.64). Given this result, recommendations to increase vitamin D concentrations in healthy persons for the prevention of cancer should be carefully considered.
Nature | 2011
Anjali G. Hinch; Arti Tandon; Nick Patterson; Yunli Song; Nadin Rohland; C. Palmer; Gary K. Chen; Kai Wang; Sarah G. Buxbaum; Ermeg L. Akylbekova; Melinda C. Aldrich; Christine B. Ambrosone; Christopher I. Amos; Elisa V. Bandera; Sonja I. Berndt; Leslie Bernstein; William J. Blot; Cathryn H. Bock; Eric Boerwinkle; Qiuyin Cai; Neil E. Caporaso; Graham Casey; L. Adrienne Cupples; Sandra L. Deming; W. Ryan Diver; Jasmin Divers; Myriam Fornage; Elizabeth M. Gillanders; Joseph T. Glessner; Curtis C. Harris
Recombination, together with mutation, gives rise to genetic variation in populations. Here we leverage the recent mixture of people of African and European ancestry in the Americas to build a genetic map measuring the probability of crossing over at each position in the genome, based on about 2.1 million crossovers in 30,000 unrelated African Americans. At intervals of more than three megabases it is nearly identical to a map built in Europeans. At finer scales it differs significantly, and we identify about 2,500 recombination hotspots that are active in people of West African ancestry but nearly inactive in Europeans. The probability of a crossover at these hotspots is almost fully controlled by the alleles an individual carries at PRDM9 (P value < 10−245). We identify a 17-base-pair DNA sequence motif that is enriched in these hotspots, and is an excellent match to the predicted binding target of PRDM9 alleles common in West Africans and rare in Europeans. Sites of this motif are predicted to be risk loci for disease-causing genomic rearrangements in individuals carrying these alleles. More generally, this map provides a resource for research in human genetic variation and evolution.
Carcinogenesis | 2010
Laure Dossus; Rudolf Kaaks; Federico Canzian; Demetrius Albanes; Sonja I. Berndt; Heiner Boeing; Julie E. Buring; Stephen J. Chanock; Françoise Clavel-Chapelon; Heather Spencer Feigelson; John Michael Gaziano; Edward Giovannucci; Carlos A. González; Christopher A. Haiman; Göran Hallmans; Susan E. Hankinson; Richard B. Hayes; Brian E. Henderson; Robert N. Hoover; David J. Hunter; Kay-Tee Khaw; Laurence N. Kolonel; Peter Kraft; Jing Ma; Loic Le Marchand; Eiliv Lund; Petra H.M. Peeters; Meir J. Stampfer; Daniel O. Stram; Gilles Thomas
Genes involved in the inflammation pathway have been associated with cancer risk. Genetic variants in the interleukin-6 (IL6) and prostaglandin-endoperoxide synthase-2 (PTGS2, encoding for the COX-2 enzyme) genes, in particular, have been related to several cancer types, including breast and prostate cancers. We conducted a study within the Breast and Prostate Cancer Cohort Consortium to examine the association between IL6 and PTGS2 polymorphisms and breast and prostate cancer risk. Twenty-seven polymorphisms, selected by pairwise tagging, were genotyped on 6292 breast cancer cases and 8135 matched controls and 8008 prostate cancer cases and 8604 matched controls. The large sample sizes and comprehensive single nucleotide polymorphism tagging in this study gave us excellent power to detect modest effects for common variants. After adjustment for multiple testing, none of the associations examined remained statistically significant at P = 0.01. In analyses not adjusted for multiple testing, one IL6 polymorphism (rs6949149) was marginally associated with breast cancer risk (TT versus GG, odds ratios (OR): 1.32; 99% confidence intervals (CI): 1.00-1.74, P(trend) = 0.003) and two were marginally associated with prostate cancer risk (rs6969502-AA versus rs6969502-GG, OR: 0.87, 99% CI: 0.75-1.02; P(trend) = 0.002 and rs7805828-AA versus rs7805828-GG, OR: 1.11, 99% CI: 0.99-1.26; P(trend) = 0.007). An increase in breast cancer risk was observed for the PTGS2 polymorphism rs7550380 (TT versus GG, OR: 1.38, 99% CI: 1.04-1.83). No association was observed between PTGS2 polymorphisms and prostate cancer risk. In conclusion, common genetic variation in these two genes might play at best a limited role in breast and prostate cancers.
Journal of the National Cancer Institute | 2015
Li-Shiun Chen; Rayjean J. Hung; Timothy B. Baker; Amy C. Horton; Rob Culverhouse; Nancy L. Saccone; Iona Cheng; Bo Deng; Younghun Han; Helen M. Hansen; Janet Horsman; Claire H. Kim; Sharon M. Lutz; Albert Rosenberger; Katja K. Aben; Angeline S. Andrew; Naomi Breslau; Shen Chih Chang; Aida Karina Dieffenbach; Hendrik Dienemann; Brittni Frederiksen; Jiali Han; Dorothy K. Hatsukami; Eric O. Johnson; Mala Pande; Margaret Wrensch; John McLaughlin; Vidar Skaug; Henricus F. M. van der Heijden; Jason A. Wampfler
BACKGROUND Recent meta-analyses show strong evidence of associations among genetic variants in CHRNA5 on chromosome 15q25, smoking quantity, and lung cancer. This meta-analysis tests whether the CHRNA5 variant rs16969968 predicts age of smoking cessation and age of lung cancer diagnosis. METHODS Meta-analyses examined associations between rs16969968, age of quitting smoking, and age of lung cancer diagnosis in 24 studies of European ancestry (n = 29 072). In each dataset, we used Cox regression models to evaluate the association between rs16969968 and the two primary phenotypes (age of smoking cessation among ever smokers and age of lung cancer diagnosis among lung cancer case patients) and the secondary phenotype of smoking duration. Heterogeneity across studies was assessed with the Cochran Q test. All statistical tests were two-sided. RESULTS The rs16969968 allele (A) was associated with a lower likelihood of smoking cessation (hazard ratio [HR] = 0.95, 95% confidence interval [CI] = 0.91 to 0.98, P = .0042), and the AA genotype was associated with a four-year delay in median age of quitting compared with the GG genotype. Among smokers with lung cancer diagnoses, the rs16969968 genotype (AA) was associated with a four-year earlier median age of diagnosis compared with the low-risk genotype (GG) (HR = 1.08, 95% CI = 1.04 to 1.12, P = 1.1*10(-5)). CONCLUSION These data support the clinical significance of the CHRNA5 variant rs16969968. It predicts delayed smoking cessation and an earlier age of lung cancer diagnosis in this meta-analysis. Given the existing evidence that this CHRNA5 variant predicts favorable response to cessation pharmacotherapy, these findings underscore the potential clinical and public health importance of rs16969968 in CHRNA5 in relation to smoking cessation success and lung cancer risk.
Cancer Epidemiology, Biomarkers & Prevention | 2009
Ruth C. Travis; Fredrick R. Schumacher; Joel N. Hirschhorn; Peter Kraft; Naomi E. Allen; Demetrius Albanes; Göran Berglund; Sonja I. Berndt; Heiner Boeing; H. Bas Bueno-de-Mesquita; Eugenia E. Calle; Stephen J. Chanock; Alison M. Dunning; Richard B. Hayes; Heather Spencer Feigelson; J. Michael Gaziano; Edward Giovannucci; Christopher A. Haiman; Brian E. Henderson; Rudolf Kaaks; Laurence N. Kolonel; Jing Ma; Laudina Rodríguez; Elio Riboli; Meir J. Stampfer; Daniel O. Stram; Michael J. Thun; Anne Tjønneland; Dimitrios Trichopoulos; Paolo Vineis
Sex hormones, particularly the androgens, are important for the growth of the prostate gland and have been implicated in prostate cancer carcinogenesis, yet the determinants of endogenous steroid hormone levels remain poorly understood. Twin studies suggest a heritable component for circulating concentrations of sex hormones, although epidemiologic evidence linking steroid hormone gene variants to prostate cancer is limited. Here we report on findings from a comprehensive study of genetic variation at the CYP19A1 locus in relation to prostate cancer risk and to circulating steroid hormone concentrations in men by the Breast and Prostate Cancer Cohort Consortium (BPC3), a large collaborative prospective study. The BPC3 systematically characterized variation in CYP19A1 by targeted resequencing and dense genotyping; selected haplotype-tagging single nucleotide polymorphisms (htSNP) that efficiently predict common variants in U.S. and European whites, Latinos, Japanese Americans, and Native Hawaiians; and genotyped these htSNPs in 8,166 prostate cancer cases and 9,079 study-, age-, and ethnicity-matched controls. CYP19A1 htSNPs, two common missense variants and common haplotypes were not significantly associated with risk of prostate cancer. However, several htSNPs in linkage disequilibrium blocks 3 and 4 were significantly associated with a 5% to 10% difference in estradiol concentrations in men [association per copy of the two-SNP haplotype rs749292-rs727479 (A-A) versus noncarriers; P = 1 × 10-5], and with inverse, although less marked changes, in free testosterone concentrations. These results suggest that although germline variation in CYP19A1 characterized by the htSNPs produces measurable differences in sex hormone concentrations in men, they do not substantially influence risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2734–44)
Journal of the National Cancer Institute | 2015
Rayjean J. Hung; Cornelia M. Ulrich; Ellen L. Goode; Yonathan Brhane; Kenneth Muir; Andrew T. Chan; Loic Le Marchand; Joellen M. Schildkraut; John S. Witte; Rosalind Eeles; Paolo Boffetta; Margaret R. Spitz; Julia G. Poirier; David N. Rider; Brooke L. Fridley; Zhihua Chen; Christopher A. Haiman; Fredrick R. Schumacher; Douglas F. Easton; Maria Teresa Landi; Paul Brennan; Richard S. Houlston; David C. Christiani; John K. Field; Heike Bickeböller; Angela Risch; Zsofia Kote-Jarai; Fredrik Wiklund; Henrik Grönberg; Stephen K Chanock
BACKGROUND Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted. METHODS We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided. RESULTS We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10(-8), and it showed an association with lung cancer (P = 2.01 x 10(-6)), colorectal cancer (GECCO P = 6.72x10(-6); CORECT P = 3.32x10(-5)), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10(-6)), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003). CONCLUSIONS Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer.
Journal of the National Cancer Institute | 2018
Anouar Fanidi; David C. Muller; Jian-Min Yuan; Victoria L. Stevens; Stephanie J. Weinstein; Demetrius Albanes; Ross Prentice; Cynthia A Thomsen; Mary Pettinger; Qiuyin Cai; William Blot; Jie Wu; Alan A. Arslan; Anne Zeleniuch-Jacquotte; Marjorie L. McCullough; Loic Le Marchand; Lynne R. Wilkens; Christopher A. Haiman; Xuehong Zhang; Jiali Han; Meir J. Stampfer; Stephanie A. Smith-Warner; Edward Giovannucci; Graham G. Giles; Allison Hodge; Gianluca Severi; Mikael Johansson; Kjell Grankvist; Arnulf Langhammer; Steinar Krokstad
Background Circulating concentrations of B vitamins and factors related to one-carbon metabolism have been found to be strongly inversely associated with lung cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The extent to which these associations are present in other study populations is unknown. Methods Within 20 prospective cohorts from the National Cancer Institute Cohort Consortium, a nested case-control study was designed including 5364 incident lung cancer case patients and 5364 control subjects who were individually matched to case patients by age, sex, cohort, and smoking status. Centralized biochemical analyses were performed to measure circulating concentrations of vitamin B6, folate, and methionine, as well as cotinine as an indicator of recent tobacco exposure. The association between these biomarkers and lung cancer risk was evaluated using conditional logistic regression models. Results Participants with higher circulating concentrations of vitamin B6 and folate had a modestly decreased risk of lung cancer risk overall, the odds ratios when comparing the top and bottom fourths (OR 4vs1 ) being 0.88 (95% confidence interval [CI] = 0.78 to 1.00) and 0.86 (95% CI = 0.74 to 0.99), respectively. We found stronger associations among men (vitamin B6: OR 4vs1 = 0.74, 95% CI = 0.62 to 0.89; folate: OR 4vs1 = 0.75, 95% CI = 0.61 to 0.93) and ever smokers (vitamin B6: OR 4vs1 = 0.78, 95% CI = 0.67 to 0.91; folate: OR 4vs1 = 0.87, 95% CI = 0.73 to 1.03). We further noted that the association of folate was restricted to Europe/Australia and Asia, whereas no clear association was observed for the United States. Circulating concentrations of methionine were not associated with lung cancer risk overall or in important subgroups. Conclusions Although confounding by tobacco exposure or reverse causation cannot be ruled out, these study results are compatible with a small decrease in lung cancer risk in ever smokers who avoid low concentrations of circulating folate and vitamin B6.
Archive | 1994
Loic Le Marchand; Jean H. Hankin; Laurence N. Kolonel; Lynne R. Wilkens
The relationship of diet to malignant melanoma has remained rela tively unexplored. However, there is evidence, primarily from labora tory studies, that dietary factors may play a role in the etiology of melanoma [1]. Retinoids appear to inhibit the growth of murine and human melanoma cell lines [2,3], as well as that of transplanted melanocytic tumors in mice [4]. There has also been one report of successful treatment of melanoma with trans-retinoic acid [5].
American Journal of Epidemiology | 2010
Christian C. Abnet; Yu Chen; Wong Ho Chow; Yu-tang Gao; Kathy J. Helzlsouer; Loic Le Marchand; Marjorie L. McCullough; James M. Shikany; Jarmo Virtamo; Stephanie J. Weinstein; Yong Bing Xiang; Kai Yu; Wei Zheng; Demetrius Albanes; Alan A. Arslan; David Campbell; Peter T. Campbell; Richard B. Hayes; Ronald L. Horst; Laurence N. Kolonel; Abraham M. Y. Nomura; Mark P. Purdue; Kirk Snyder; Xiao Ou Shu
Archive | 2016
Sara Lindstrรถm; Akweley Ablorh; Brad Chapman; Alexander Gusev; Gary Chen; Constance Turman; A. Eliassen; Alkes L. Price; Brian E. Henderson; Loic Le Marchand; Oliver Hofmann; C A Haiman; Peter Kraft