144 results on '"Marchand, Loïc Le"'
Search Results
2. Differences in the association of diet quality with body fat distribution between men and women
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Maskarinec, Gertraud, Namatame, Lisa A., Kang, Minji, Buchthal, Steven D., Ernst, Thomas, Monroe, Kristine R., Shepherd, John A., Wilkens, Lynne R., Boushey, Carol J., Marchand, Loïc Le, and Lim, Unhee
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- 2020
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3. Sex differences in sociodemographic and lifestyle factors associated with diet quality in a multiethnic population
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Kang, Minji, Park, Song-Yi, Shvetsov, Yurii B., Wilkens, Lynne R., Marchand, Loïc Le, Boushey, Carol J., and Paik, Hee-Young
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- 2019
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4. Association of Endocrine Disrupting Chemicals With the Metabolic Syndrome Among Women in the Multiethnic Cohort Study.
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Ihenacho, Ugonna, Guillermo, Cherie, Wilkens, Lynne R, Franke, Adrian A, Tseng, Chiuchen, Li, Yuqing, Sangaramoorthy, Meera, Derouen, Mindy C, Haiman, Christopher A, Stram, Daniel O, Marchand, Loïc Le, Cheng, Iona, and Wu, Anna H
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ENDOCRINE disruptors ,METABOLIC syndrome ,CARDIOVASCULAR diseases ,HDL cholesterol ,AFRICAN American women ,COHORT analysis - Abstract
Metabolic syndrome (MetS) is associated with a high risk of cardiovascular disease, a leading cause of death among women. MetS is a diagnosis of at least 3 of the following: high blood pressure, high fasting glucose, high triglycerides, high waist circumference, and low high-density lipoprotein cholesterol. Epidemiological studies suggest that endocrine disrupting chemical (EDC) exposure is positively associated with individual components of MetS, but evidence of an association between EDCs and MetS remains inconsistent. In a cross-sectional analysis within the Multiethnic Cohort Study, we evaluated the association between 4 classes of urinary EDCs (bisphenol A [BPA], triclosan, parabens, and phthalates) and MetS among 1728 women. Multivariable logistic regression was used to estimate odds ratios and 95% CI for the association between tertiles of each EDC and MetS adjusting for age, body mass index (BMI), racial and ethnic group, and breast cancer status. Stratified analyses by race and ethnicity and BMI were conducted. MetS was identified in 519 (30.0%) women. We did not detect statistically significant associations of MetS with BPA, triclosan, or phthalate metabolite excretion. MetS was inversely associated with total parabens (P
trend =.002). Although there were suggestive inverse associations between EDCs and MetS among Latino and African American women, and women with BMI < 30 kg/m2 , there was no statistically significant heterogeneity in associations by race and ethnicity or BMI. These findings suggest an inverse association between parabens and MetS in larger multiethnic studies. Prospective analyses to investigate suggested differences in associations by race, ethnicity, and BMI are warranted. [ABSTRACT FROM AUTHOR]- Published
- 2023
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5. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Yarmolinsky, James, Robinson, Jamie W, Mariosa, Daniela, Karhunen, Ville, Huang, Jian, Dimou, Niki, Murphy, Neil, Burrows, Kimberley, Bouras, Emmanouil, Smith-Byrne, Karl, Lewis, Sarah J, Galesloot, Tessel E, Kiemeney, Lambertus A, Vermeulen, Sita, Martin, Paul, Albanes, Demetrius, Hou, Lifang, Newcomb, Polly A, White, Emily, Wolk, Alicja, Wu, Anna H, Marchand, Loïc Le, Phipps, Amanda I, Buchanan, Daniel D, Zhao, Sizheng Steven, Gill, Dipender, Chanock, Stephen J, Purdue, Mark P, Smith, George Davey, Brennan, Paul, Herzig, Karl-Heinz, Jarvelin, Marjo-Riitta, Dehghan, Abbas, Johansson, Mattias, Gunter, Marc J, Tsilidis, Kostas K, and Martin, Richard M
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Article - Abstract
BACKGROUND: Tumour-promoting inflammation is a “hallmark” of cancer and conventional epidemiological studies have reported links between various inflammatory markers and cancer risk. The causal nature of these relationships and, thus, the suitability of these markers as intervention targets for cancer prevention is unclear. METHODS: We meta-analysed 6 genome-wide association studies of circulating inflammatory markers comprising 59,969 participants of European ancestry. We then used combined cis -Mendelian randomization and colocalisation analysis to evaluate the causal role of 66 circulating inflammatory markers in risk of 30 adult cancers in 338,162 cancer cases and up to 824,556 controls. Genetic instruments for inflammatory markers were constructed using genome-wide significant ( P < 5.0 x 10 (-8) ) cis -acting SNPs (i.e. in or ±250 kb from the gene encoding the relevant protein) in weak linkage disequilibrium (LD, r (2) < 0.10). Effect estimates were generated using inverse-variance weighted random-effects models and standard errors were inflated to account for weak LD between variants with reference to the 1000 Genomes Phase 3 CEU panel. A false discovery rate (FDR)-corrected P -value (“ q -value”) < 0.05 was used as a threshold to define “strong evidence” to support associations and 0.05 ≤ q -value < 0.20 to define “suggestive evidence”. A colocalisation posterior probability (PPH (4) ) > 70% was employed to indicate support for shared causal variants across inflammatory markers and cancer outcomes. RESULTS: We found strong evidence to support an association of genetically-proxied circulating pro-adrenomedullin concentrations with increased breast cancer risk (OR 1.19, 95% CI 1.10-1.29, q -value=0.033, PPH (4) =84.3%) and suggestive evidence to support associations of interleukin-23 receptor concentrations with increased pancreatic cancer risk (OR 1.42, 95% CI 1.20-1.69, q -value=0.055, PPH (4) =73.9%), prothrombin concentrations with decreased basal cell carcinoma risk (OR 0.66, 95% CI 0.53-0.81, q -value=0.067, PPH (4) =81.8%), macrophage migration inhibitory factor concentrations with increased bladder cancer risk (OR 1.14, 95% CI 1.05-1.23, q -value=0.072, PPH (4) =76.1%), and interleukin-1 receptor-like 1 concentrations with decreased triple-negative breast cancer risk (OR 0.92, 95% CI 0.88-0.97, q -value=0.15), PPH (4) =85.6%). For 22 of 30 cancer outcomes examined, there was little evidence ( q -value ≥ 0.20) that any of the 66 circulating inflammatory markers examined were associated with cancer risk. CONCLUSION: Our comprehensive joint Mendelian randomization and colocalisation analysis of the role of circulating inflammatory markers in cancer risk identified potential roles for 5 circulating inflammatory markers in risk of 5 site-specific cancers. Contrary to reports from some prior conventional epidemiological studies, we found little evidence of association of circulating inflammatory markers with the majority of site-specific cancers evaluated.
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- 2023
6. Association of Hypothyroidism With Nonmelanoma Skin Cancer in the Multiethnic Cohort Population-Based Study
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Ahadiat, Omeed, Setiawan, Veronica W., Higgins, Shauna, Porcel, Jacqueline, Haiman, Christopher, Marchand, Loïc Le, Wilkens, Lynne, and Wysong, Ashley
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- 2019
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7. Diet Quality and Pancreatic Cancer Incidence in the Multiethnic Cohort.
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Steel, Heather, Song-Yi Park, Lim, Tiffany, Stram, Daniel O., Boushey, Carol J., Hébert, James R., Marchand, Loïc Le, Wu, Anna H., and Setiawan, Veronica Wendy
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Background: Data on diet quality and pancreatic cancer are limited. We examined the relationship between diet quality, assessed by the Healthy Eating Index-2015 (HEI-2015), the Alternative Healthy Eating Index-2010 (AHEI-2010), the alternate Mediterranean Diet (aMED) score, the Dietary Approaches to Stop Hypertension (DASH) score and the energy-adjusted Dietary Inflammatory Index (E-DII), and pancreatic cancer incidence in the Multiethnic Cohort Study. Methods: Diet quality scores were calculated from a validated food frequency questionnaire administered at baseline. Cox models were used to calculate HR and 95% confidence intervals (CI) adjusted for age, sex, race/ethnicity, education, diabetes, family history of pancreatic cancer, physical activity, smoking variables, total energy intake, body mass index (BMI), and alcohol consumption. Stratified analyses by sex, race/ethnicity, smoking status, and BMI were conducted. Results: Over an average follow-up of 19.3 years, 1,779 incident pancreatic cancer cases were identified among 177,313 participants (average age of 60.2 years at baseline, 1993-1996). Overall, we did not observe associations between the dietary pattern scores and pancreatic cancer (aMED: 0.98; 95% CI, 0.83-1.16; HEI-2015: 1.03; 95% CI, 0.88-1.21; AHEI-2010: 1.03; 95% CI, 0.88-1.20; DASH: 0.92; 95% CI, 0.79-1.08; E-DII: 1.05; 95% CI, 0.89-1.23). An inverse association was observed with DASH for ever smokers (HR, 0.75; 0.61-0.93), but not for nonsmokers (HR, 1.05; 0.83-1.32). Conclusions: The DASH diet showed an inverse association with pancreatic cancer among ever smokers, but does not show a protective association overall. Impact: Modifiable measures are needed to reduce pancreatic cancer burden in these high-risk populations; our study adds to the discussion of the benefit of dietary changes. [ABSTRACT FROM AUTHOR]
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- 2023
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8. Association of Prostate-Specific Antigen Levels with Prostate Cancer Risk in a Multiethnic Population: Stability Over Time and Comparison with Polygenic Risk Score.
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Chou, Alisha, Darst, Burcu F., Wilkens, Lynne R., Marchand, Loïc Le, Lilja, Hans, Conti, David V., and Haiman, Christopher A.
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Background: Studies in men of European ancestry suggest prostate-specific antigen (PSA) as a marker of early prostate cancer development that may help to risk-stratify men earlier in life. Methods: We examined PSA levels in men measured up to 10+ years before a prostate cancer diagnosis in association with prostate cancer risk in 2,245 cases and 2,203 controls of African American, Latino, Japanese, Native Hawaiian, and White men in the Multiethnic Cohort. We also compared the discriminative ability of PSA to polygenic risk score (PRS) for prostate cancer. Results: Excluding cases diagnosed within 2 and 10 years of blood draw, men with PSA above the median had a prostate cancer OR (95% CIs) of 9.12 (7.66-10.92) and 3.52 (2.50-5.03), respectively, compared with men with PSA below the median. A PSA level above the median identified 90% and 75% of cases diagnosed more than 2 and 10 years after blood draw, respectively. The associations were significantly greater for Gleason =7 versus 8+ disease. At 10+ years, the association of prostate cancer with PSA was comparable with that with the PRS [OR per SD increase: 1.88 (1.45-2.46) and 2.12 (1.55-2.93), respectively]. Conclusions: We found PSA to be an informative marker of prostate cancer risk at least a decade before diagnosis across multiethnic populations. This association was diminished with increasing time, greater for low grade tumors, and comparable with a PRS when measured 10+ years before diagnosis. Impact: Our multiethnic investigation suggests broad clinical implications on the utility of PSA and PRS for risk stratification in prostate cancer screening practices. [ABSTRACT FROM AUTHOR]
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- 2022
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9. Cancer Mortality Patterns by Birthplace and Generation Status of Mexican Latinos: The Multiethnic Cohort.
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Chen, Hongjie, Wu, Anna H, Wang, Songren, Bookstein, Arthur, Marchand, Loïc Le, Wilkens, Lynne R, Haiman, Christopher A, Cheng, Iona, Monroe, Kristine R, Setiawan, Veronica Wendy, and Le Marchand, Loïc
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Background: Latinos are the largest minority group in the United States. We assessed cancer mortality by birthplace and generation status of Mexican Latinos in the Multiethnic Cohort.Methods: We included 26 751 Latinos of Mexican origin and 6093 non-Latino Whites aged 45-74 years at cohort entry (1993-1996) from the California Multiethnic Cohort component. The Mexican Latinos comprised 42% first-generation Mexico-born immigrants, 42% second-generation (28% US-born with both parents Mexico-born and 14% US-born with 1 parent US-born and 1 parent Mexico-born), and 16% third-generation or more who were US-born with both parents US-born. Multivariable Cox models were used to calculate covariate adjusted hazard ratios and 95% confidence intervals for overall and site-specific cancer mortality by birthplace and generation status. All statistical tests were 2-sided.Results: Cancer death rate was highest among the US-born with 1 parent US-born and 1 parent Mexico-born (age-adjusted rate = 471.0 per 100 000 person-years) and US-born with both parents US-born (age-adjusted rate = 469.0 per 100 000 person-years) groups. The US-born with both parents Mexico-born group had a 30% (hazard ratio = 1.30, 95% confidence interval = 1.18 to 1.44) higher risk of cancer death than the first-generation Mexico-born immigrants group, showing US birthplace was associated with an elevated cancer mortality. For cancer-specific mortality, US birthplace was positively associated with colorectal, liver and lung, and ovarian cancer (P values ranged from .04 to .005). Among US-born Mexican Latinos, generation status was not statistically significantly associated with overall cancer or site-specific cancer mortality.Conclusions: Our findings suggest that US birthplace is a risk factor for cancer death in Mexican Americans. Identification of the contributing factors is important to curtail patterns of increasing cancer mortality in US-born Mexican Latinos. [ABSTRACT FROM AUTHOR]- Published
- 2022
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10. Body Fat Distribution, Glucose Metabolism, and Diabetes Status Among Older Adults: The Multiethnic Cohort Adiposity Phenotype Study.
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Maskarinec, Gertraud, Raquinio, Phyllis, Kristal, Bruce S., Franke, Adrian A., Buchthal, Steven D., Ernst, Thomas M., Monroe, Kristine R., Shepherd, John A., Shvetsov, Yurii B., Marchand, Loïc Le, and Lim, Unhee
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- 2022
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11. Racial and Ethnic Disparities in Lung Cancer Screening by the 2021 USPSTF Guidelines Versus Risk-Based Criteria: The Multiethnic Cohort Study.
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Aredo, Jacqueline V, Choi, Eunji, Ding, Victoria Y, Tammemägi, Martin C, Haaf, Kevin ten, Luo, Sophia J, Freedman, Neal D, Wilkens, Lynne R, Marchand, Loïc Le, Wakelee, Heather A, Meza, Rafael, Park, Sung-Shim Lani, Cheng, Iona, and Han, Summer S
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LUNG cancer ,COHORT analysis - Abstract
Background In 2021, the US Preventive Services Task Force (USPSTF) revised its lung cancer screening guidelines to expand screening eligibility. We evaluated screening sensitivities and racial and ethnic disparities under the 2021 USPSTF criteria vs alternative risk-based criteria in a racially and ethnically diverse population. Methods In the Multiethnic Cohort, we evaluated the proportion of ever-smoking lung cancer cases eligible for screening (ie, screening sensitivity) under the 2021 USPSTF criteria and under risk-based criteria through the PLCO
m2012 model (6-year risk ≥1.51%). We also calculated the screening disparity (ie, absolute sensitivity difference) for each of 4 racial or ethnic groups (African American, Japanese American, Latino, Native Hawaiian) vs White cases. Results Among 5900 lung cancer cases, 43.3% were screen eligible under the 2021 USPSTF criteria. Screening sensitivities varied by race and ethnicity, with Native Hawaiian (56.7%) and White (49.6%) cases attaining the highest sensitivities and Latino (37.3%), African American (38.4%), and Japanese American (40.0%) cases attaining the lowest. Latino cases had the greatest screening disparity vs White cases at 12.4%, followed by African American (11.2%) and Japanese American (9.6%) cases. Under risk-based screening, the overall screening sensitivity increased to 75.7%, and all racial and ethnic groups had increased sensitivities (54.5%-91.9%). Whereas the screening disparity decreased to 5.1% for African American cases, it increased to 28.6% for Latino cases and 12.8% for Japanese American cases. Conclusions In the Multiethnic Cohort, racial and ethnic disparities decreased but persisted under the 2021 USPSTF lung cancer screening guidelines. Risk-based screening through PLCOm2012 may increase screening sensitivities and help to reduce disparities in some, but not all, racial and ethnic groups. Further optimization of risk-based screening strategies across diverse populations is needed. [ABSTRACT FROM AUTHOR]- Published
- 2022
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12. Neighborhood Obesogenic Environment and Risk of Prostate Cancer: The Multiethnic Cohort.
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DeRouen, Mindy C., Li Tao, Shariff-Marco, Salma, Juan Yang, Shvetsov, Yurii B., Song-Yi Park, Albright, Cheryl L., Monroe, Kristine R., Marchand, Loïc Le, Wilkens, Lynne R., Gomez, Scarlett Lin, and Iona Cheng
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Background: Obesity is associated with risk of aggressive prostate cancer. It is not known whether neighborhood obesogenic factors are independently associated with prostate cancer risk. Methods: Neighborhood socioeconomic status (nSES) and four neighborhood obesogenic environment factors (urbanicity, mixed-land development, unhealthy food environment, and parks) were assessed for associations with prostate cancer risk among 41,563 African American, Japanese American, Latino, and White males in the Multiethnic Cohort (MEC) Study, California site. Multivariable Cox proportional hazards regression was used to estimate HRs and 95% confidence intervals (CI) for nonaggressive and aggressive prostate cancer, adjusting for individual-level sociodemographic, behavioral, and prostate cancer risk factors. Analyses were stratified by race, ethnicity, and, among Latino males, nativity. Results: Males residing in low-SES, compared with high-SES, neighborhoods had lower risk of nonaggressive prostate cancer [lowest vs. highest quintile HR = 0.81; 95% confidence interval (CI) = 0.68-0.95, P
trend 0.024], driven by a similar trend among foreign-born Latino males. Foreign-born Latino males in neighborhoods with low mixed-land development had increased risk of non-aggressive disease (lowest vs. highest quintile HR = 1.49; 95% CI = 1.07-2.09). For aggressive disease, the only association noted was between lower mixed-land development and lower risk among White males (Ptrend = 0.040). Conclusions: nSES and obesogenic environment factors were independently associated with prostate cancer risk; associations varied by race, ethnicity, nativity, and disease aggressiveness. Impact: Upstream structural and social determinants of health that contribute to neighborhood obesogenic characteristics likely impact prostate cancer risk differently across groups defined by race, ethnicity, and nativity and by disease aggressiveness. [ABSTRACT FROM AUTHOR]- Published
- 2022
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13. Risk Stratification for Early-Onset Colorectal Cancer Using a Combination of Genetic and Environmental Risk Scores: An International Multi-Center Study.
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Archambault, Alexi N, Jeon, Jihyoun, Lin, Yi, Thomas, Minta, Harrison, Tabitha A, Bishop, D Timothy, Brenner, Hermann, Casey, Graham, Chan, Andrew T, Chang-Claude, Jenny, Figueiredo, Jane C, Gallinger, Steven, Gruber, Stephen B, Gunter, Marc J, Guo, Feng, Hoffmeister, Michael, Jenkins, Mark A, Keku, Temitope O, Marchand, Loïc Le, and Li, Li
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RESEARCH ,RESEARCH methodology ,SOCIAL networks ,EARLY detection of cancer ,MEDICAL screening ,EVALUATION research ,COLORECTAL cancer ,RISK assessment ,COMPARATIVE studies ,PSYCHOLOGICAL tests ,DISEASE susceptibility ,RESEARCH funding - Abstract
Background: The incidence of colorectal cancer (CRC) among individuals aged younger than 50 years has been increasing. As screening guidelines lower the recommended age of screening initiation, concerns including the burden on screening capacity and costs have been recognized, suggesting that an individualized approach may be warranted. We developed risk prediction models for early-onset CRC that incorporate an environmental risk score (ERS), including 16 lifestyle and environmental factors, and a polygenic risk score (PRS) of 141 variants.Methods: Relying on risk score weights for ERS and PRS derived from studies of CRC at all ages, we evaluated risks for early-onset CRC in 3486 cases and 3890 controls aged younger than 50 years. Relative and absolute risks for early-onset CRC were assessed according to values of the ERS and PRS. The discriminatory performance of these scores was estimated using the covariate-adjusted area under the receiver operating characteristic curve.Results: Increasing values of ERS and PRS were associated with increasing relative risks for early-onset CRC (odds ratio per SD of ERS = 1.14, 95% confidence interval [CI] = 1.08 to 1.20; odds ratio per SD of PRS = 1.59, 95% CI = 1.51 to 1.68), both contributing to case-control discrimination (area under the curve = 0.631, 95% CI = 0.615 to 0.647). Based on absolute risks, we can expect 26 excess cases per 10 000 men and 21 per 10 000 women among those scoring at the 90th percentile for both risk scores.Conclusions: Personal risk scores have the potential to identify individuals at differential relative and absolute risk for early-onset CRC. Improved discrimination may aid in targeted CRC screening of younger, high-risk individuals, potentially improving outcomes. [ABSTRACT FROM AUTHOR]- Published
- 2022
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14. The Survival Impact of Second Primary Lung Cancer in Patients With Lung Cancer.
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Choi, Eunji, Luo, Sophia J, Aredo, Jacqueline V, Backhus, Leah M, Wilkens, Lynne R, Su, Chloe C, Neal, Joel W, Marchand, Loïc Le, Cheng, Iona, Wakelee, Heather A, Han, Summer S, and Le Marchand, Loïc
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LUNGS ,LUNG tumors ,TUMOR classification ,SECONDARY primary cancer ,RESEARCH funding ,SMOKING ,LONGITUDINAL method - Abstract
Background: Lung cancer survivors have a high risk of developing second primary lung cancer (SPLC), but little is known about the survival impact of SPLC diagnosis.Methods: We analyzed data from 138 969 patients in the Surveillance, Epidemiology, and End Results (SEER), who were surgically treated for initial primary lung cancer (IPLC) in 1988-2013. Each patient was followed from the date of IPLC diagnosis to SPLC diagnosis (for those with SPLC) and last vital status through 2016. We performed multivariable Cox regression to evaluate the association between overall survival and SPLC diagnosis as a time-varying predictor. To investigate potential effect modification, we tested interaction between SPLC and IPLC stage. Using data from the Multiethnic Cohort Study (MEC) (n = 1540 IPLC patients with surgery), we evaluated the survival impact of SPLC by smoking status. All statistical tests were 2-sided.Results: A total of 12 115 (8.7%) patients developed SPLC in SEER over 700 421 person-years of follow-up. Compared with patients with single primary lung cancer, those with SPLC had statistically significantly reduced overall survival (hazard ratio [HR] = 2.12, 95% confidence interval [CI] = 2.06 to 2.17; P < .001). The effect of SPLC on reduced survival was more pronounced among patients with early stage IPLC vs advanced-stage IPLC (HR = 2.14, 95% CI = 2.08 to 2.20, vs HR = 1.43, 95% CI = 1.21 to 1.70, respectively; Pinteraction < .001). Analysis using MEC data showed that the effect of SPLC on reduced survival was statistically significantly larger among persons who actively smoked at initial diagnosis vs those who formerly or never smoked (HR = 2.31, 95% CI = 1.48 to 3.61, vs HR = 1.41, 95% CI = 0.98 to 2.03, respectively; Pinteraction = .04).Conclusions: SPLC diagnosis is statistically significantly associated with decreased survival in SEER and MEC. Intensive surveillance targeting patients with early stage IPLC and active smoking at IPLC diagnosis may lead to a larger survival benefit. [ABSTRACT FROM AUTHOR]- Published
- 2022
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15. Circulating bilirubin levels and risk of colorectal cancer: serological and Mendelian randomization analyses
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Khoei, Nazlisadat Seyed, Jenab, Mazda, Murphy, Neil, Banbury, Barbara L., Carreras Torres, Robert, Viallon, Vivian, Kühn, Tilman, Bueno de Mesquita, H. Bas, Aleksandrova, Krasimira, Cross, Amanda J., Weiderpass, Elisabete, Stepien, Magdalena, Bulmer, Andrew, Tjønneland, Anne, Boutron-Ruault, Marie-Christine, Severi, Gianluca, Carbonnel, Franck, Katzke, Verena, Boeing, Heiner, Bergmann, Manuela M., Trichopoulou, Antonia, Karakatsani, Anna, Martimianaki, Georgia, Palli, Domenico, Tagliabue, Giovanna, Panico, Salvatore, Tumino, Rosario, Sacerdote, Carlotta, Skeie, Guri, Merino, Susana, Bonet Bonet, Catalina, Rodríguez Barranco, Miguel, Gil, Leire, Chirlaque, María Dolores, Ardanaz, Eva, Myte, Robin, Hultdin, Johan, Pérez Cornago, Aurora, Aune, Dagfinn, Tsilidis, Konstantinos K., Albanes, Demetrius, Baron, John A., Berndt, Sonja I., Bézieau, Stéphane, Brenner, Hermann, Campbell, Peter T., Casey, Graham, Chan, Andrew T., Chang Claude, Jenny, Chanock, Stephen J., Cotterchio, Michelle, Gallinger, Steven, Gruber, Stephen B., Haile, Robert W., Hampe, Jochen, Hoffmeister, Michael, Hopper, John L., Hsu, Li, Huyghe, Jeroen R., Jenkins, Mark A., Joshi, Amit D., Kampman, Ellen, Larsson, Susanna C., Marchand, Loïc Le, Li, Christopher I., Li, Li, Lindblom, Annika, Lindor, Noralane M., Martín Sánchez, Vicente, Moreno Aguado, Víctor, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Parfrey, Patrick S., Pharoah, Paul D. P., Rennert, Gad, Sakoda, Lori C., Schafmayer, Clemens, Schmit, Stephanie L., Schoen, Robert E., Slattery, Martha L., Thibodeau, Stephen N., Ulrich, Cornelia M., van Duijnhoven, Franzel J. B., Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zhang, Xuehong, Ferrari, Pietro, Anton, Gabriele, Peters, Annette, Peters, Ulrike, Gunter, Marc J., Wagner, Karl-Heinz, Freisling, Heinz, Apollo - University of Cambridge Repository, and Pharoah, Paul [0000-0001-8494-732X]
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Adult ,Male ,Nutrition and Disease ,Mendelian randomization analysis ,lcsh:Medicine ,Polymorphism, Single Nucleotide ,Antioxidants ,Càncer colorectal ,Risk Factors ,Voeding en Ziekte ,Humans ,Prospective Studies ,VLAG ,Cancer ,Aged ,lcsh:R ,Bilirubin ,Middle Aged ,Colorectal cancer ,Europe ,Case-Control Studies ,Anti-oxidants ,Female ,Colorectal Neoplasms ,Research Article - Abstract
Background: Bilirubin, a byproduct of hemoglobin breakdown and purported anti-oxidant, is thought to be cancer preventive. We conducted complementary serological and Mendelian randomization (MR) analyses to investigate whether alterations in circulating levels of bilirubin are associated with risk of colorectal cancer (CRC). We decided a priori to perform analyses separately in men and women based on suggestive evidence that associations may differ by sex. Methods: In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC), pre-diagnostic unconjugated bilirubin (UCB, the main component of total bilirubin) concentrations were measured by high-performance liquid chromatography in plasma samples of 1386 CRC cases and their individually matched controls. Additionally, 115 single-nucleotide polymorphisms (SNPs) robustly associated (P < 5 × 10−8) with circulating total bilirubin were instrumented in a 2-sample MR to test for a potential causal effect of bilirubin on CRC risk in 52,775 CRC cases and 45,940 matched controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colon Cancer Family Registry (CCFR), and the Colorectal Transdisciplinary (CORECT) study. Results: The associations between circulating UCB levels and CRC risk differed by sex (Pheterogeneity = 0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04–1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76–0.97)). In the MR analysis of the main UGT1A1 SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02–1.12); P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96–1.06); P = 0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were suggestive of an inverse association with CRC in men, but not in women. These differences by sex did not reach formal statistical significance (Pheterogeneity ≥ 0.2). Conclusions: Additional insight into the relationship between circulating bilirubin and CRC is needed in order to conclude on a potential causal role of bilirubin in CRC development.
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- 2020
16. NAT2, meat consumption and colorectal cancer incidence: an ecological study among 27 countries
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Ognjanovic, Simona, Yamamoto, Jennifer, Maskarinec, Gertraud, and Marchand, Loïc Le
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- 2006
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17. B-vitamin intake, metabolic genes, and colorectal cancer risk (United States)
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Marchand, Loïc Le, Donlon, Timothy, Hankin, Jean H., Kolonel, Laurence N., Wilkens, Lynne R., and Seifried, Ann
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- 2002
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18. Development and Validation of a Risk Prediction Model for Second Primary Lung Cancer.
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Choi, Eunji, Sanyal, Nilotpal, Ding, Victoria Y, Gardner, Rebecca M, Aredo, Jacqueline V, Lee, Justin, Wu, Julie T, Hickey, Thomas P, Barrett, Brian, Riley, Thomas L, Wilkens, Lynne R, Leung, Ann N, Marchand, Loïc Le, Tammemägi, Martin C, Hung, Rayjean J, Amos, Christopher I, Freedman, Neal D, Cheng, Iona, Wakelee, Heather A, and Han, Summer S
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LUNG cancer ,PREDICTION models ,RECEIVER operating characteristic curves ,DECISION making ,EARLY detection of cancer ,LUNGS ,LUNG tumors ,SECONDARY primary cancer ,SMOKING - Abstract
Background: With advancing therapeutics, lung cancer (LC) survivors are rapidly increasing in number. Although mounting evidence suggests LC survivors have high risk of second primary lung cancer (SPLC), there is no validated prediction model available for clinical use to identify high-risk LC survivors for SPLC.Methods: Using data from 6325 ever-smokers in the Multiethnic Cohort (MEC) study diagnosed with initial primary lung cancer (IPLC) in 1993-2017, we developed a prediction model for 10-year SPLC risk after IPLC diagnosis using cause-specific Cox regression. We evaluated the model's clinical utility using decision curve analysis and externally validated it using 2 population-based data-Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) and National Lung Screening Trial (NLST)-that included 2963 and 2844 IPLC (101 and 93 SPLC cases), respectively.Results: Over 14 063 person-years, 145 (2.3%) ever-smoking IPLC patients developed SPLC in MEC. Our prediction model demonstrated a high predictive accuracy (Brier score = 2.9, 95% confidence interval [CI] = 2.4 to 3.3) and discrimination (area under the receiver operating characteristics [AUC] = 81.9%, 95% CI = 78.2% to 85.5%) based on bootstrap validation in MEC. Stratification by the estimated risk quartiles showed that the observed SPLC incidence was statistically significantly higher in the 4th vs 1st quartile (9.5% vs 0.2%; P < .001). Decision curve analysis indicated that in a wide range of 10-year risk thresholds from 1% to 20%, the model yielded a larger net-benefit vs hypothetical all-screening or no-screening scenarios. External validation using PLCO and NLST showed an AUC of 78.8% (95% CI = 74.6% to 82.9%) and 72.7% (95% CI = 67.7% to 77.7%), respectively.Conclusions: We developed and validated a SPLC prediction model based on large population-based cohorts. The proposed prediction model can help identify high-risk LC patients for SPLC and can be incorporated into clinical decision making for SPLC surveillance and screening. [ABSTRACT FROM AUTHOR]- Published
- 2022
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19. Risks of Primary Extracolonic Cancers Following Colorectal Cancer in Lynch Syndrome
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Win, Aung Ko, Lindor, Noralane M., Young, Joanne P., Macrae, Finlay A., Young, Graeme P., Williamson, Elizabeth, Parry, Susan, Goldblatt, Jack, Lipton, Lara, Winship, Ingrid, Leggett, Barbara, Tucker, Katherine M., Giles, Graham G., Buchanan, Daniel D., Clendenning, Mark, Rosty, Christophe, Arnold, Julie, Levine, Joan A., Haile, Robert W., Gallinger, Steven, Marchand, Loïc Le, Newcomb, Polly A., Hopper, John L., and Jenkins, Mark A.
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- 2012
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20. Cancer risks for monoallelic MUTYH mutation carriers with a family history of colorectal cancer
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Win, Aung Ko, Cleary, Sean P., Dowty, James G., Baron, John A., Young, Joanne P., Buchanan, Daniel D., Southey, Melissa C., Burnett, Terrilea, Parfrey, Patrick S., Green, Roger C., Marchand, Loïc Le, Newcomb, Polly A., Haile, Robert W., Lindor, Noralane M., Hopper, John L., Gallinger, Steven, and Jenkins, Mark A.
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- 2011
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21. GENETIC SENSITIVITY TO BITTER TASTE, DIETARY INTAKES, AND COLORECTAL ADENOMA RISK: C-005
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Schembre, Susan M., Cheng, Iona, Wilkens, Lynne, Albright, Cheryl, and Marchand, Loïc Le
- Published
- 2011
22. A pooled analysis of melanocytic nevus phenotype and the risk of cutaneous melanoma at different latitudes
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Chang, Yu-mei, Newton-Bishop, Julia A., Bishop, Timothy D., Armstrong, Bruce K., Bataille, Veronique, Bergman, Wilma, Berwick, Marianne, Bracci, Paige M., Elwood, Mark J., Ernstoff, Marc S., Green, Adèle C., Gruis, Nelleke A., Holly, Elizabeth A., Ingvar, Christian, Kanetsky, Peter A., Karagas, Margaret R., Marchand, Loïc Le, Mackie, Rona M., Olsson, Håkan, sterlind, Anne, Rebbeck, Timothy R., Reich, Kristian, Sasieni, Peter, Siskind, Victor, Swerdlow, Anthony J., Titus-Ernstoff, Linda, Zens, Michael S., Ziegler, Andreas, and Barrett, Jennifer H.
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- 2009
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23. Multiethnic Prediction of Nicotine Biomarkers and Association With Nicotine Dependence.
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Bergen, Andrew W, McMahan, Christopher S, McGee, Stephen, Ervin, Carolyn M, Tindle, Hilary A, Marchand, Loïc Le, Murphy, Sharon E, Stram, Daniel O, Patel, Yesha M, Park, Sungshim L, Baurley, James W, and Le Marchand, Loïc
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NICOTINE addiction ,COTININE ,SMOKING statistics ,NICOTINE ,GENETIC variation ,STATISTICAL learning ,SUBSTANCE abuse ,RESEARCH funding ,TOBACCO products ,SMOKING - Abstract
Introduction: The nicotine metabolite ratio and nicotine equivalents are measures of metabolism rate and intake. Genome-wide prediction of these nicotine biomarkers in multiethnic samples will enable tobacco-related biomarker, behavioral, and exposure research in studies without measured biomarkers.Aims and Methods: We screened genetic variants genome-wide using marginal scans and applied statistical learning algorithms on top-ranked genetic variants, age, ethnicity and sex, and, in additional modeling, cigarettes per day (CPD), (in additional modeling) to build prediction models for the urinary nicotine metabolite ratio (uNMR) and creatinine-standardized total nicotine equivalents (TNE) in 2239 current cigarette smokers in five ethnic groups. We predicted these nicotine biomarkers using model ensembles and evaluated external validity using dependence measures in 1864 treatment-seeking smokers in two ethnic groups.Results: The genomic regions with the most selected and included variants for measured biomarkers were chr19q13.2 (uNMR, without and with CPD) and chr15q25.1 and chr10q25.3 (TNE, without and with CPD). We observed ensemble correlations between measured and predicted biomarker values for the uNMR and TNE without (with CPD) of 0.67 (0.68) and 0.65 (0.72) in the training sample. We observed inconsistency in penalized regression models of TNE (with CPD) with fewer variants at chr15q25.1 selected and included. In treatment-seeking smokers, predicted uNMR (without CPD) was significantly associated with CPD and predicted TNE (without CPD) with CPD, time-to-first-cigarette, and Fagerström total score.Conclusions: Nicotine metabolites, genome-wide data, and statistical learning approaches developed novel robust predictive models for urinary nicotine biomarkers in multiple ethnic groups. Predicted biomarker associations helped define genetically influenced components of nicotine dependence.Implications: We demonstrate development of robust models and multiethnic prediction of the uNMR and TNE using statistical and machine learning approaches. Variants included in trained models for nicotine biomarkers include top-ranked variants in multiethnic genome-wide studies of smoking behavior, nicotine metabolites, and related disease. Association of the two predicted nicotine biomarkers with Fagerström Test for Nicotine Dependence items supports models of nicotine biomarkers as predictors of physical dependence and nicotine exposure. Predicted nicotine biomarkers may facilitate tobacco-related disease and treatment research in samples with genomic data and limited nicotine metabolite or tobacco exposure data. [ABSTRACT FROM AUTHOR]- Published
- 2021
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24. Type 2 Diabetes Among Filipino American Adults in the Multiethnic Cohort.
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H. Raquinio, Phyllis Aira Sheer, Maskarinec, Gertraud, Cruz, Rica Dela, Setiawan, Veronica W., Kristal, Bruce S., Wilkens, Lynne R., Marchand, Loïc Le, Raquinio, Phyllis Aira Sheer H, Dela Cruz, Rica, and Le Marchand, Loïc
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- 2021
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25. Smoking Cessation After Lung Cancer Diagnosis and the Risk of Second Primary Lung Cancer: The Multiethnic Cohort Study.
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Luo, Sophia J, Choi, Eunji, Aredo, Jacqueline V, Wilkens, Lynne R, Tammemägi, Martin C, Marchand, Loïc Le, Cheng, Iona, Wakelee, Heather A, and Han, Summer S
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SMOKING cessation ,LUNG cancer diagnosis - Abstract
Background Smoking cessation reduces lung cancer mortality. However, little is known about whether diagnosis of lung cancer impacts changes in smoking behaviors. Furthermore, the effects of smoking cessation on the risk of second primary lung cancer (SPLC) have not been established yet. This study aims to examine smoking behavior changes after initial primary lung cancer (IPLC) diagnosis and estimate the effect of smoking cessation on SPLC risk following IPLC diagnosis. Methods The study cohort consisted of 986 participants in the Multiethnic Cohort Study who were free of lung cancer and active smokers at baseline (1993-1996), provided 10-year follow-up smoking data (2003-2008), and were diagnosed with IPLC in 1993-2017. The primary outcome was a change in smoking status from "current" at baseline to "former" at 10-year follow-up (ie, smoking cessation), analyzed using logistic regression. The second outcome was SPLC incidence after smoking cessation, estimated using cause-specific Cox regression. All statistical tests were 2-sided. Results Among 986 current smokers at baseline, 51.1% reported smoking cessation at 10-year follow-up. The smoking cessation rate was statistically significantly higher (80.6%) for those diagnosed with IPLC between baseline and 10-year follow-up vs those without IPLC diagnosis (45.4%) during the 10-year period (adjusted odds ratio = 5.12, 95% confidence interval [CI] = 3.38 to 7.98; P < .001). Incidence of SPLC was statistically significantly lower among the 504 participants who reported smoking cessation at follow-up compared with those without smoking cessation (adjusted hazard ratio = 0.31, 95% CI = 0.14 to 0.67; P = .003). Conclusion Lung cancer diagnosis has a statistically significant impact on smoking cessation. Quitting smoking after IPLC diagnosis may reduce the risk of developing a subsequent malignancy in the lungs. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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26. Pooled analysis of the CYP1A1 exon 7 polymorphism and lung cancer (United States)
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Marchand, Loïc Le, Guo, Chuanfa, Benhamou, Simone, Bouchardy, Christine, Cascorbi, Ingolf, Clapper, Margie L., Garte, Seymour, Haugen, Aage, Ingelman-sundberg, Magnus, Kihara, Masahiro, Rannug, Agneta, Ryberg, David, Stücker, Isabelle, Sugimura, Haruhiko, and Taioli, Emanuela
- Published
- 2003
27. Nongenetic Determinants of Risk for Early-Onset Colorectal Cancer.
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Archambault, Alexi N, Lin, Yi, Jeon, Jihyoun, Harrison, Tabitha A, Bishop, D Timothy, Brenner, Hermann, Casey, Graham, Chan, Andrew T, Chang-Claude, Jenny, Figueiredo, Jane C, Gallinger, Steven, Gruber, Stephen B, Gunter, Marc J, Hoffmeister, Michael, Jenkins, Mark A, Keku, Temitope O, Marchand, Loïc Le, Li, Li, Moreno, Victor, and Newcomb, Polly A
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COLORECTAL cancer ,ODDS ratio ,ANTI-inflammatory agents - Abstract
Background Incidence of early-onset (younger than 50 years of age) colorectal cancer (CRC) is increasing in many countries. Thus, elucidating the role of traditional CRC risk factors in early-onset CRC is a high priority. We sought to determine whether risk factors associated with late-onset CRC were also linked to early-onset CRC and whether association patterns differed by anatomic subsite. Methods Using data pooled from 13 population-based studies, we studied 3767 CRC cases and 4049 controls aged younger than 50 years and 23 437 CRC cases and 35 311 controls aged 50 years and older. Using multivariable and multinomial logistic regression, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) to assess the association between risk factors and early-onset CRC and by anatomic subsite. Results Early-onset CRC was associated with not regularly using nonsteroidal anti-inflammatory drugs (OR = 1.43, 95% CI = 1.21 to 1.68), greater red meat intake (OR = 1.10, 95% CI = 1.04 to 1.16), lower educational attainment (OR = 1.10, 95% CI = 1.04 to 1.16), alcohol abstinence (OR = 1.23, 95% CI = 1.08 to 1.39), and heavier alcohol use (OR = 1.25, 95% CI = 1.04 to 1.50). No factors exhibited a greater excess in early-onset compared with late-onset CRC. Evaluating risks by anatomic subsite, we found that lower total fiber intake was linked more strongly to rectal (OR = 1.30, 95% CI = 1.14 to 1.48) than colon cancer (OR = 1.14, 95% CI = 1.02 to 1.27; P = .04). Conclusion In this large study, we identified several nongenetic risk factors associated with early-onset CRC, providing a basis for targeted identification of those most at risk, which is imperative in mitigating the rising burden of this disease. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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28. Assessment of a Polygenic Risk Score for Colorectal Cancer to Predict Risk of Lynch Syndrome Colorectal Cancer.
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Jenkins, Mark A, Buchanan, Daniel D, Lai, John, Makalic, Enes, Dite, Gillian S, Win, Aung K, Clendenning, Mark, Winship, Ingrid M, Hayes, Richard B, Huyghe, Jeroen R, Peters, Ulrike, Gallinger, Steven, Marchand, Loïc Le, Figueiredo, Jane C, Pai, Rish K, Newcomb, Polly A, Church, James M, Casey, Graham, and Hopper, John L
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COLORECTAL cancer ,DNA mismatch repair - Abstract
It was not known whether the polygenic risk scores (PRSs) that predict colorectal cancer could predict colorectal cancer for people with inherited pathogenic variants in DNA mismatch repair genes—people with Lynch syndrome. We tested a PRS comprising 107 established single-nucleotide polymorphisms associated with colorectal cancer in European populations for 826 European-descent carriers of pathogenic variants in DNA mismatch repair genes (293 MLH1 , 314 MSH2 , 126 MSH6 , 71 PMS2 , and 22 EPCAM) from the Colon Cancer Family Registry, of whom 504 had colorectal cancer. There was no evidence of an association between the PRS and colorectal cancer risk, irrespective of which DNA mismatch repair gene was mutated, or sex (all 2-sided P > .05). The hazard ratio per standard deviation of the PRS for colorectal cancer was 0.97 (95% confidence interval = 0.88 to 1.06; 2-sided P = .51). Whereas PRSs are predictive of colorectal cancer in the general population, they do not predict Lynch syndrome colorectal cancer. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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29. Should Smokers Be Given Specific Nutritional Recommendations
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Marchand, Loïc Le
- Published
- 1997
30. Common variants in the obesity-associated genes FTO and MC4R are not associated with risk of colorectal cancer
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Yang, Baiyu, Thrift, Aaron P., Figueiredo, Jane C., Jenkins, Mark A., Schumacher, Fredrick R., Conti, David V., Lin, Yi, Win, Aung Ko, Limburg, Paul J., Berndt, Sonja I., Brenner, Hermann, Chan, Andrew T., Chang-Claude, Jenny, Hoffmeister, Michael, Hudson, Thomas J., Marchand, Loïc Le, Newcomb, Polly A., Slattery, Martha L., White, Emily, Peters, Ulrike, Casey, Graham, and Campbell, Peter T.
- Published
- 2016
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31. Population-specific reference panels are crucial for genetic analyses: an example of the CREBRF locus in Native Hawaiians.
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Lin, Meng, Caberto, Christian, Wan, Peggy, Li, Yuqing, Lum-Jones, Annette, Tiirikainen, Maarit, Pooler, Loreall, Nakamura, Brooke, Sheng, Xin, Porcel, Jacqueline, Lim, Unhee, Setiawan, Veronica Wendy, Marchand, Loïc Le, Wilkens, Lynne R, Haiman, Christopher A, Cheng, Iona, and Chiang, Charleston W K
- Published
- 2020
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32. Smoking-Related Risks of Colorectal Cancer by Anatomical Subsite and Sex.
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Gram, Inger T, Park, Song-Yi, Wilkens, Lynne R, Haiman, Christopher A, and Marchand, Loïc Le
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ADENOCARCINOMA ,CANCER invasiveness ,COLON (Anatomy) ,COLON tumors ,CONFIDENCE intervals ,ETHNIC groups ,LONGITUDINAL method ,MULTIVARIATE analysis ,RECTUM tumors ,SEX distribution ,SMOKING ,PROPORTIONAL hazards models ,DESCRIPTIVE statistics ,DISEASE risk factors - Abstract
The purpose of this study was to examine whether the increased risk of colorectal cancer due to cigarette smoking differed by anatomical subsite or sex. We analyzed data from 188,052 participants aged 45–75 years (45% men) who were enrolled in the Multiethnic Cohort Study in 1993–1996. During a mean follow-up period of 16.7 years, we identified 4,879 incident cases of invasive colorectal adenocarcinoma. In multivariate Cox regression models, as compared with never smokers of the same sex, male ever smokers had a 39% higher risk (hazard ratio (HR) = 1.39, 95% confidence interval (CI): 1.16, 1.67) of cancer of the left (distal or descending) colon but not of the right (proximal or ascending) colon (HR = 1.03, 95% CI: 0.89, 1.18), while female ever smokers had a 20% higher risk (HR = 1.20, 95% CI: 1.06, 1.36) of cancer of the right colon but not of the left colon (HR = 0.96, 95% CI: 0.80, 1.15). Compared with male smokers, female smokers had a greater increase in risk of rectal cancer with number of pack-years of smoking (P for heterogeneity = 0.03). Our results suggest that male smokers are at increased risk of left colon cancer and female smokers are at increased risk of right colon cancer. Our study also suggests that females who smoke may have a higher risk of rectal cancer due to smoking than their male counterparts. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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33. Association Between Outdoor Air Pollution and Risk of Malignant and Benign Brain Tumors: The Multiethnic Cohort Study.
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Wu, Anna H, Wu, Jun, Tseng, Chiuchen, Yang, Juan, Shariff-Marco, Salma, Fruin, Scott, Larson, Timothy, Setiawan, Veronica W, Masri, Shahir, Porcel, Jacqueline, Jain, Jennifer, Chen, Thomas C, Stram, Daniel O, Marchand, Loïc Le, Ritz, Beate, and Cheng, Iona
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AIR pollution ,BRAIN cancer ,BENIGN tumors ,COHORT analysis ,MICROGLIA ,PROPORTIONAL hazards models - Abstract
Background There are increasing concerns about the potential impact of air pollution on chronic brain inflammation and microglia cell activation, but evidence of its carcinogenic effects is limited. Methods We used kriging interpolation and land use regression models to estimate long-term air pollutant exposures of oxides of nitrogen (NO
x , NO2 ), kriging interpolation for ozone (O3 ), carbon monoxide, and particulate matter (PM2.5 , PM10 ), and nearest monitoring station measurements for benzene for 103 308 men and women from the Multiethnic Cohort, residing largely in Los Angeles County from recruitment (1993–1996) through 2013. We used Cox proportional hazards models to examine the associations between time-varying pollutants and risk of malignant brain cancer (94 men, 116 women) and meningioma (130 men, 425 women) with adjustment for sex, race and ethnicity, neighborhood socioeconomic status, smoking, occupation, and other covariates. Stratified analyses were conducted by sex and race and ethnicity. Results Brain cancer risk in men increased in association with exposure to benzene (hazard ratio [HR] = 3.52, 95% confidence interval [CI] = 1.55 to 7.55) and PM10 (HR = 1.80, 95% CI = 1.00 to 3.23). Stronger associations with PM10 (HR = 3.02, 95% CI = 1.26 to 7.23), O3 (HR = 2.93, 95% CI = 1.09 to 7.88), and benzene (HR = 4.06, 95% CI = 1.17 to 18.2) were observed among Latino men. Air pollution was unrelated to risk of meningioma except that O3 exposure was associated with risk in men (HR = 1.77, 95% CI = 1.02 to 3.06). Brain cancer risk in women was unrelated to air pollution exposures. Conclusions Confirmation of these sex differences in air pollution–brain cancer associations and the stronger findings in Latino men in additional diverse populations is warranted. [ABSTRACT FROM AUTHOR]- Published
- 2020
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34. Association between mitochondrial genetic variation and breast cancer risk: The Multiethnic Cohort.
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Li, Yuqing, Giorgi, Elena E., Beckman, Kenneth B., Caberto, Christian, Kazma, Remi, Lum-Jones, Annette, Haiman, Christopher A., Marchand, Loïc Le, Stram, Daniel O., Saxena, Richa, and Cheng, Iona
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NADH dehydrogenase ,BREAST cancer ,CYTOCHROME oxidase ,MITOCHONDRIAL proteins ,OXIDATIVE phosphorylation - Abstract
Background: The mitochondrial genome encodes for thirty-seven proteins, among them thirteen are essential for the oxidative phosphorylation (OXPHOS) system. Inherited variation in mitochondrial genes may influence cancer development through changes in mitochondrial proteins, altering the OXPHOS process and promoting the production of reactive oxidative species. Methods: To investigate the association between mitochondrial genetic variation and breast cancer risk, we tested 314 mitochondrial SNPs (mtSNPs), capturing four complexes of the mitochondrial OXPHOS pathway and mtSNP groupings for rRNA and tRNA, in 2,723 breast cancer cases and 3,260 controls from the Multiethnic Cohort Study. Results: We examined the collective set of 314 mtSNPs as well as subsets of mtSNPs grouped by mitochondrial OXPHOS pathway, complexes, and genes, using the sequence kernel association test and adjusting for age, sex, and principal components of global ancestry. We also tested haplogroup associations using unconditional logistic regression and adjusting for the same covariates. Stratified analyses were conducted by self-reported maternal race/ethnicity. No significant mitochondrial OXPHOS pathway, gene, and haplogroup associations were observed in African Americans, Asian Americans, Latinos, and Native Hawaiians. In European Americans, a global test of all genetic variants of the mitochondrial genome identified an association with breast cancer risk (P = 0.017, q = 0.102). In mtSNP-subset analysis, the gene MT-CO2 (P = 0.001, q = 0.09) in Complex IV (cytochrome c oxidase) and MT-ND2 (P = 0.004, q = 0.19) in Complex I (NADH dehydrogenase (ubiquinone)) were significantly associated with breast cancer risk. Conclusions: In summary, our findings suggest that collective mitochondrial genetic variation and particularly in the MT-CO2 and MT-ND2 may play a role in breast cancer risk among European Americans. Further replication is warranted in larger populations and future studies should evaluate the contribution of mitochondrial proteins encoded by both the nuclear and mitochondrial genomes to breast cancer risk. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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35. Validation of a Quantitative Food Frequency Questionnaire for a Japanese Population in Hawaii.
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Pakseresht, Mohammadreza, Earle, Maj, Kolahdooz, Fariba, Marchand, Loïc Le, and Sharma, Sangita
- Published
- 2019
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36. Smoking and breast cancer risk by race/ethnicity and oestrogen and progesterone receptor status: the Multiethnic Cohort (MEC) study.
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Gram, Inger T, Park, Song-Yi, Maskarinec, Gertraud, Wilkens, Lynne R, Haiman, Christopher A, Marchand, Loïc Le, and Le Marchand, Loïc
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PROGESTERONE receptors ,BREAST cancer ,TOBACCO & cancer ,HYDROXYPROGESTERONE ,ETHNICITY ,ESTROGEN ,BLACK people ,BREAST tumors ,CELL receptors ,REPORTING of diseases ,ETHNIC groups ,LONGITUDINAL method ,PROTEINS ,RESEARCH funding ,SMOKING ,ACQUISITION of data ,PROPORTIONAL hazards models - Abstract
Background: The purpose of this study was to examine if the smoking-related higher breast cancer risk was similar for the five race/ethnicity groups in the Multiethnic Cohort (MEC) study and by oestrogen (ER) and progesterone (PR) receptor status.Methods: From 1993 to 2013, we followed 67 313 women who were enrolled in the MEC study at 45-75 years of age. We identified breast cancer cases and tumour receptor status via linkage to the Hawaii and California Surveillance, Epidemiology and End Results Program cancer registries through December 2013. We used Cox proportional hazards regression to estimate multivariable-adjusted hazard ratios with 95% confidence intervals (CI).Results: During a mean follow-up of 16.7 years, we identified 4230 incident, invasive breast cancer cases. Compared with parous never smokers, parous ever smokers who had smoked more than 5 years before their first live childbirth had a higher risk of breast cancer overall of 31% (95% CI: 1.14-1.51). This higher risk was 51% (95% CI: 1.05-2.16) for African Americans, 66% (95% CI: 1.10-2.50) for Native Hawaiians, 42% (95% CI: 1.13-1.78) for Whites, 37% (95% CI: 1.17-1.61) for ER-positive (ER+) tumours and 33% (95% CI: 1.11-1.59) for PR+ tumours. No difference was suggested by racial/ethnic groups (Pheterogeneity = 0.15) or tumour receptor status (Pheterogeneity = 0.60 by ER status and 0.95 by PR status).Conclusions: We find that the higher breast cancer risk related to smoking is similar across racial/ethnic groups and by ER and PR status, indicating that breast cancer should be considered as a smoking-related cancer. [ABSTRACT FROM AUTHOR]- Published
- 2019
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37. Body mass index, comorbidities, and hormonal factors in relation to meningioma in an ethnically diverse population: the Multiethnic Cohort.
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Muskens, Ivo S, Wu, Anna H, Porcel, Jacqueline, Cheng, Iona, Marchand, Loïc Le, Wiemels, Joseph L, and Setiawan, Veronica Wendy
- Published
- 2019
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38. Pancreatic Cancer Following Incident Diabetes in African Americans and Latinos: The Multiethnic Cohort.
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Setiawan, Veronica Wendy, Stram, Daniel O, Porcel, Jacqueline, Chari, Suresh T, Maskarinec, Gertraud, Marchand, Loïc Le, Wilkens, Lynne R, Haiman, Christopher A, Pandol, Stephen J, Monroe, Kristine R, and Le Marchand, Loïc
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PANCREATIC cancer ,DIABETES ,AFRICAN Americans ,CANCER ,DISEASE risk factors - Abstract
Background: Diabetes has been proposed to be a risk factor for and a consequence of pancreatic cancer (PC). The relationship between recent-onset diabetes and PC is not well understood, and data in minorities are sparse. We examined the relationships between recent-onset diabetes and PC incidence in African Americans and Latinos in the Multiethnic Cohort.Methods: A total of 48 995 African Americans and Latinos without prior diabetes and cancer at baseline (1993-1996) were included in the study. Questionnaires, Medicare data, and California hospital discharge files were used to identify new diabetes diagnoses. Cox regressions were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for cancer associated with diabetes and with diabetes duration.Results: A total of 15 833 (32.3%) participants developed diabetes between baseline and 2013. A total of 408 incident PC cases were identified during follow-up. Diabetes was associated with PC (HRage75 = 2.39, 95% CI = 1.91 to 2.98). Individuals with recent-onset diabetes (within three or fewer years of PC diagnosis) had a greater risk compared with those with long-term diabetes across all ages. The HRage75 for recent-onset diabetes was 4.08 (95% CI = 2.76 to 6.03) in Latinos and 3.38 (95% CI = 2.30 to 4.98) in African Americans.Conclusions: Diabetes was associated with a more than twofold higher risk of PC in African Americans and Latinos, but recent-onset diabetes was associated with a 2.3-fold greater increase in risk of PC than long-standing diabetes. Our findings support the hypothesis that recent-onset diabetes is a manifestation of PC and that long-standing diabetes is a risk factor for this malignancy. [ABSTRACT FROM AUTHOR]- Published
- 2019
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39. Alcohol Intake and Colorectal Cancer Risk in the Multiethnic Cohort Study.
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Park, Song-Yi, Wilkens, Lynne R, Setiawan, Veronica Wendy, Monroe, Kristine R, Haiman, Christopher A, and Marchand, Loïc Le
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RECTUM tumors ,COLON tumors ,ALCOHOLIC beverages ,BLACK people ,CONFIDENCE intervals ,ETHNIC groups ,DIETARY fiber ,FOLIC acid ,HISPANIC Americans ,JAPANESE people ,LONGITUDINAL method ,NONSTEROIDAL anti-inflammatory agents ,RACE ,WHITE people ,WINES ,BODY mass index ,LIFESTYLES ,PROPORTIONAL hazards models ,ODDS ratio ,TUMOR risk factors ,CANCER risk factors - Abstract
To investigate the association of alcohol intake with colorectal cancer risk according to race/ethnicity as well as sex, lifestyle-related factors, alcoholic beverage type, and anatomical subsite, we analyzed data from 190,698 black, Native Hawaiian, Japanese-American, Latino, and white persons in Hawaii and California in the Multiethnic Cohort Study, with 4,923 incident cases during a 16.7-year follow-up period (1993–2013). In multivariate Cox regression models, the hazard ratio was 1.16 (95% confidence interval (CI): 1.01, 1.34) for 15.0–29.9 g/day of alcohol and 1.28 (95% CI: 1.12, 1.45) for ≥30.0 g/day among men, and 1.06 (95% CI: 0.85, 1.32) and 1.15 (95% CI: 0.92, 1.43), respectively, among women, compared with nondrinkers (P for heterogeneity according to sex = 0.74). An increased risk was apparent among Native Hawaiians, Japanese Americans, Latinos, and white persons and among individuals with body mass index <25.0 (calculated as weight (kg)/height (m)
2 ), never-users of nonsteroidal antiinflammatory drugs, and those with lower intake of dietary fiber and folate. Beer and wine, but not liquor, consumption was positively related to colorectal cancer risk. The association was stronger for rectum and left-colon tumors than for right-colon tumors. Our findings suggest that the positive association between alcohol and colorectal cancer varies according to race/ethnicity, lifestyle factors, alcoholic beverage type, and anatomical subsite of tumors. [ABSTRACT FROM AUTHOR]- Published
- 2019
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40. Biomonitoring an albumin adduct of the cooked meat carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in humans.
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Bellamri, Medjda, Wang, Yi, Yonemori, Kim, White, Kami K, Wilkens, Lynne R, Marchand, Loïc Le, and Turesky, Robert J
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PROSTATE cancer ,ALBUMINS - Abstract
2-Amino-1-methyl-6-phenylimidazo[4,5- b ]pyridine (PhIP) is formed in cooked meats and may be linked to dietary-associated colorectal, prostate and mammary cancers. Genotoxic N-oxidized metabolites of PhIP react with the Cys
34 of albumin (Alb) to form a sulfinamide adduct, a biomarker of the biologically effective dose. We examined the kinetics of PhIP-Alb adduct formation in plasma of volunteers on a 4-week semicontrolled diet of cooked meat containing known quantities of PhIP. The adduct was below the limit of detection (LOD) (10 femtograms PhIP/mg Alb) in most subjects before the meat feeding but increased by up to 560-fold at week 4 in subjects who ate meat containing 8.0 to 11.7 μg of PhIP per 150–200 g serving. In contrast, the adduct remained below the LOD in subjects who ingested 1.2 or 3.0 μg PhIP per serving. Correlations were not seen between PhIP-Alb adduct levels and PhIP intake levels (P = 0.76), the amount of PhIP accrued in hair (P = 0.13), the amounts of N-oxidized urinary metabolites of PhIP (P = 0.66) or caffeine CYP1A2 activity (P = 0.55), a key enzyme involved in the bioactivation of PhIP. The half-life of the PhIP-Alb adduct was <2 weeks, signifying that the adduct was not stable. PhIP-Alb adduct formation is direct evidence of bioactivation of PhIP in vivo. However, the PhIP hair biomarker is a longer lived and more sensitive biomarker to assess exposure to this potential human carcinogen. [ABSTRACT FROM AUTHOR]- Published
- 2018
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41. PS-203-Dietary risk factors for non-alcoholic fatty liver disease by cirrhosis status: The US multiethnic cohort
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Noureddin, Mazen, Porcel, Jacqueline, Zelber-Sagi, Shira, Marchand, Loic Le, and Setiawan, VeronicaWendy
- Published
- 2019
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42. Prevalence and Penetrance of Major Genes and Polygenes for Colorectal Cancer.
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Aung Ko Win, Jenkins, Mark A., Dowty, James G., Antoniou, Antonis C., Lee, Andrew, Giles, Graham G., Buchanan, Daniel D., Clendenning, Mark, Rosty, Christophe, Ahnen, Dennis J., Thibodeau, Stephen N., Casey, Graham, Gallinger, Steven, Marchand, Loïc Le, Haile, Robert W., Potter, John D., Yingye Zheng, Lindor, Noralane M., Newcomb, Polly A., and Hopper, John L.
- Abstract
Background: Although high-risk mutations in identified major susceptibility genes (DNA mismatch repair genes and MUTYH) account for some familial aggregation of colorectal cancer, their population prevalence and the causes of the remaining familial aggregation are not known. Methods: We studied the families of 5,744 colorectal cancer cases (probands) recruited from population cancer registries in the United States, Canada, and Australia and screened probands for mutations in mismatch repair genes and MUTYH. We conducted modified segregation analyses using the cancer history of first-degree relatives, conditional on the proband's age at diagnosis. We estimated the prevalence of mutations in the identified genes, the prevalence of HR for unidentified major gene mutations, and the variance of the residual polygenic component. Results: We estimated that 1 in 279 of the population carry mutations in mismatch repair genes (MLH1 = 1 in 1,946, MSH2 = 1 in 2,841, MSH6 = 1 in 758, PMS2 = 1 in 714), 1 in 45 carry mutations in MUTYH, and 1 in 504 carry mutations associated with an average 31-fold increased risk of colorectal cancer in unidentified major genes. The estimated polygenic variance was reduced by 30% to 50% after allowing for unidentified major genes and decreased from 3.3 for age <40 years to 0.5 for age ≥70 years (equivalent to sibling relative risks of 5.1 to 1.3, respectively). Conclusions: Unidentified major genes might explain one third to one half of the missing heritability of colorectal cancer. Impact: Our findings could aid gene discovery and development of better colorectal cancer risk prediction models. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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43. Alcohol Consumption and the Risk of Colorectal Cancer for Mismatch Repair Gene Mutation Carriers.
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Dashti, S. Ghazaleh, Buchanan, Daniel D., Jayasekara, Harindra, Ouakrim, Driss Ait, Clendenning, Mark, Rosty, Christophe, Winship, Ingrid M., Macrae, Finlay A., Giles, Graham G., Parry, Susan, Casey, Graham, Haile, Robert W., Gallinger, Steven, Marchand, Loïc Le, Thibodeau, Stephen N., Lindor, Noralane M., Newcomb, Polly A., Potter, John D., Baron, John A., and Hopper, John L.
- Abstract
Background: People with germline mutation in one of the DNA mismatch repair (MMR) genes have increased colorectal cancer risk. For these high-risk people, study findings of the relationship between alcohol consumption and colorectal cancer risk have been inconclusive. Methods: 1,925 MMR gene mutations carriers recruited into the Colon Cancer Family Registry who had completed a questionnaire on lifestyle factors were included. Weighted Cox proportional hazard regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between alcohol consumption and colorectal cancer. Results: Colorectal cancer was diagnosed in 769 carriers (40%) at a mean (SD) age of 42.6 (10.3) years. Compared with abstention, ethanol consumption from any alcoholic beverage up to 14 g/day and >28 g/day was associated with increased colorectal cancer risk (HR, 1.50; 95% CI, 1.09-2.07 and 1.69; 95% CI, 1.07-2.65, respectively; P
trend = 0.05), and colon cancer risk (HR, 1.78; 95% CI, 1.27-2.49 and 1.94; 95% CI, 1.19-3.18, respectively; Ptrend = 0.02). However, there was no clear evidence for an association with rectal cancer risk. Also, there was no evidence for associations between consumption of individual alcoholic beverage types (beer, wine, spirits) and colorectal, colon, or rectal cancer risk. Conclusions: Our data suggest that alcohol consumption, particularly more than 28 g/day of ethanol (~2 standard drinks of alcohol in the United States), is associated with increased colorectal cancer risk for MMR gene mutation carriers. Impact: Although these data suggested that alcohol consumption in MMR carriers was associated with increased colorectal cancer risk, there was no evidence of a dose-response, and not all types of alcohol consumption were associated with increased risk. [ABSTRACT FROM AUTHOR]- Published
- 2017
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44. Body Shape and Fat Distribution From Whole-Body DXA Accurately Predict Metabolic Syndrome Across Sex and Ethnicity Subgroups
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Ng, Bennett K., Fan, Bo, Lim, Unhee, Marchand, Loic Le, Wilkens, Lynne, and Shepherd, John A.
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- 2016
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45. Agreement between MRI and DXA VAT in Multiethnic Adult Population
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Kazemi, Leila, Fan, Bo, Lim, Unhee, Marchand, Loic Le, Ernst, Thomas, Buchthal, Steven D., and Shepherd, John
- Published
- 2016
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46. Multivitamin, calcium and folic acid supplements and the risk of colorectal cancer in Lynch syndrome.
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Chau, Rowena, Ghazaleh, Seyedeh, Dashti, Ouakrim, Driss Ait, Buchanan, Daniel D., Clendenning, Mark, Rosty, Christophe, Winship, Ingrid M., Young, Joanne P., Giles, Graham G., Macrae, Finlay A., Boussioutas, Alex, Parry, Susan, Figueiredo, Jane C., Levine, A. Joan, Ahnen, Dennis J., Casey, Graham, Haile, Robert W., Gallinger, Steven, and Marchand, Loïc Le
- Subjects
CANCER risk factors ,HEREDITARY nonpolyposis colorectal cancer ,FOLIC acid in human nutrition ,CALCIUM supplements ,DNA repair ,GENETIC mutation ,CALCIUM ,DIETARY supplements ,DNA ,FOLIC acid ,RESEARCH funding ,VITAMINS ,ACQUISITION of data ,PROPORTIONAL hazards models ,GENETIC carriers - Abstract
Background: People with a DNA mismatch repair (MMR) gene mutation have a substantially elevated risk of colorectal cancer (CRC) but the modifiers of this risk are not well established. We investigated the association between dietary supplement intake and CRC risk for carriers.Methods: This study included 1966 (56% female) carriers of an MMR gene mutation (719 MLH1, 931 MSH2, 211 MSH6 and 105 PMS2) who were recruited from the USA, Canada, Australia and New Zealand into the Colon Cancer Family Registry between 1997 and 2012. Information on lifestyle factors including supplement intake was collected at the time of recruitment. Using Cox proportional hazards regression weighted to correct for ascertainment bias, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between self-reported multivitamin, calcium and folic acid supplement intake and CRC risk.Results: Of 744 carriers with CRC, 18%, 6% and 5% reported intake of multivitamin, calcium and folic acid supplements for at least 1 month, respectively, compared with 27%, 11% and 10% of 1222 carriers without CRC. After adjusting for identified confounding variables, a decreased CRC risk was associated with multivitam inintake for at least 3 years (HR 0.47, 95% CI 0.32-0.69) and calcium intake for at least 3 years(HR 0.42, 95% CI 0.23-0.74), compared with never users. There was no evidence of an association between folic acid supplement intake and CRC risk (P = 0.82).Conclusion: Intake of multivitamin and calcium supplements might be associated with a decreased risk of CRC for MMR gene mutation carriers. [ABSTRACT FROM AUTHOR]- Published
- 2016
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47. Association of Genes, Pathways, and Haplogroups of the Mitochondrial Genome with the Risk of Colorectal Cancer: The Multiethnic Cohort.
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Li, Yuqing, Beckman, Kenneth B., Caberto, Christian, Kazma, Remi, Lum-Jones, Annette, Haiman, Christopher A., Marchand, Loïc Le, Stram, Daniel O., Saxena, Richa, and Cheng, Iona
- Subjects
COLON cancer risk factors ,COHORT analysis ,PROTEIN synthesis ,OXIDATIVE phosphorylation ,SINGLE nucleotide polymorphisms ,RIBOSOMAL RNA - Abstract
The mitochondrial genome encodes for the synthesis of 13 proteins that are essential for the oxidative phosphorylation (OXPHOS) system. Inherited variation in mitochondrial genes may influence cancer development through changes in mitochondrial proteins, altering the OXPHOS process, and promoting the production of reactive oxidative species. To investigate the role of the OXPHOS pathway and mitochondrial genes in colorectal cancer (CRC) risk, we tested 185 mitochondrial SNPs (mtSNPs), located in 13 genes that comprise four complexes of the OXPHOS pathway and mtSNP groupings for rRNA and tRNA, in 2,453 colorectal cancer cases and 11,930 controls from the Multiethnic Cohort Study. Using the sequence kernel association test, we examined the collective set of 185 mtSNPs, as well as subsets of mtSNPs grouped by mitochondrial pathways, complexes, and genes, adjusting for age, sex, principal components of global ancestry, and self-reported maternal race/ethnicity. We also tested for haplogroup associations using unconditional logistic regression, adjusting for the same covariates. Stratified analyses were conducted by self-reported maternal race/ethnicity. In European Americans, a global test of all genetic variants of the mitochondrial genome identified an association with CRC risk (P = 0.04). In mtSNP-subset analysis, the NADH dehydrogenase 2 (MT-ND2) gene in Complex I was associated with CRC risk at a P-value of 0.001 (q = 0.015). In addition, haplogroup T was associated with CRC risk (OR = 1.66, 95% CI: 1.19–2.33, P = 0.003). No significant mitochondrial pathway and gene associations were observed in the remaining four racial/ethnic groups—African Americans, Asian Americans, Latinos, and Native Hawaiians. In summary, our findings suggest that variations in the mitochondrial genome and particularly in the MT-ND2 gene may play a role in CRC risk among European Americans, but not in other maternal racial/ethnic groups. Further replication is warranted and future studies should evaluate the contribution of mitochondrial proteins encoded by both the nuclear and mitochondrial genomes to CRC risk. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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48. Association between Body Mass Index and Mortality for Colorectal Cancer Survivors: Overall and by Tumor Molecular Phenotype.
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Campbell, Peter T., Newton, Christina C., Newcomb, Polly A., Phipps, Amanda I., Ahnen, Dennis J., Baron, John A., Buchanan, Daniel D., Casey, Graham, Cleary, Sean P., Cotterchio, Michelle, Farris, Alton B., Figueiredo, Jane C., Gallinger, Steven, Green, Roger C., Haile, Robert W., Hopper, John L., Jenkins, Mark A., Marchand, Loïc Le, Makar, Karen W., and McLaughlin, John R.
- Abstract
Background: Microsatellite instability (MSI) and BRAF mutation status are associated with colorectal cancer survival, whereas the role of body mass index (BMI) is less clear. We evaluated the association between BMI and colorectal cancer survival, overall and by strata of MSI, BRAF mutation, sex, and other factors. Methods: This study included 5,615 men and women diagnosed with invasive colorectal cancer who were followed for mortality (maximum: 14.7 years; mean: 5.9 years). Prediagnosis BMI was derived from self-reported weight approximately one year before diagnosis and height. Tumor MSI and BRAF mutation status were available for 4,131 and 4,414 persons, respectively. Multivariable hazard ratios (HR) and 95% confidence intervals (CI) were estimated from delayed-entry Cox proportional hazards models. Results: In multivariable models, high prediagnosis BMI was associated with higher risk of all-cause mortality in both sexes (per 5-kg/m²; HR, 1.10; 95% CI, 1.06-1.15), with similar associations stratified by sex (P
interaction : 0.41), colon versus rectum (Pinteraction : 0.86), MSI status (Pinteraction : 0.84), and BRAF mutation status (Pinteraction : 0.28). In joint models, with MS-stable/MSI-low and normal BMI as the reference group, risk of death was higher for MS-stable/MSI-low and obese BMI (HR, 1.32; P value: 0.0002), not statistically significantly lower for MSI-high and normal BMI (HR, 0.86; P value: 0.29), and approximately the same for MSIhigh and obese BMI (HR, 1.00; P value: 0.98). Conclusions: High prediagnosis BMI was associated with increased mortality; this association was consistent across participant subgroups, including strata of tumor molecular phenotype. Impact: High BMI may attenuate the survival benefit otherwise observed with MSI-high tumors. [ABSTRACT FROM AUTHOR]- Published
- 2015
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49. Comparison of plasma levels of nutrient-related biomarkers among Japanese populations in Tokyo, Japan, Sã o Paulo, Brazil, and Hawaii, USA.
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Iwasaki, Motoki, Franke, Adrian A., Hamada, Gerson S., Miyajima, Nelson T., Sharma, Sangita, Ishihara, Junko, Takachi, Ribeka, Tsugane, Shoichiro, and Marchand, Loïc Le
- Published
- 2015
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50. Role of tumour molecular and pathology features to estimate colorectal cancer risk for first-degree relatives.
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Win, Aung Ko, Buchanan, Daniel D., Rosty, Christophe, Maclnnis, Robert J., Dowty, James G., Dite, Gillian S., Giles, Graham G., Southey, Melissa C., Young, Joanne P., Clendenning, Mark, Walsh, Michael D., Walters, Rhiannon J., Boussioutas, Alex, Smyrk, Thomas C., Thibodeau, Stephen N., Baron, John A., Potter, John D., Newcomb, Polly A., Marchand, Loïc Le, and Haile, Robert W.
- Subjects
COLON cancer risk factors ,CANCER invasiveness ,HEREDITARY nonpolyposis colorectal cancer ,MOLECULAR pathology ,COLON cancer diagnosis - Abstract
Objective To estimate risk of colorectal cancer (CRC) for first-degree relatives of CRC cases based on CRC molecular subtypes and tumour pathology features. Design We studied a cohort of 33 496 first-degree relatives of 4853 incident invasive CRC cases (probands) who were recruited to the Colon Cancer Family Registry through population cancer registries in the USA, Canada and Australia. We categorised the first-degree relatives into four groups: 28 156 of 4095 mismatch repair (MMR)- proficient probands, 2302 of 301 MMR-deficient non- Lynch syndrome probands, 1799 of 271 suspected Lynch syndrome probands and 1239 of 186 Lynch syndrome probands. We compared CRC risk for first-degree relatives stratified by the absence or presence of specific tumour molecular pathology features in probands across each of these four groups and for all groups combined. Results Compared with first-degree relatives of MMRproficient CRC cases, a higher risk of CRC was estimated for first-degree relatives of CRC cases with suspected Lynch syndrome (HR 2.06, 95% CI 1.59 to 2.67) and with Lynch syndrome (HR 5.37, 95% CI 4.16 to 6.94), but not with MMR-deficient non-Lynch syndrome (HR 1.04, 95% CI 0.82 to 1.31). A greater risk of CRC was estimated for first-degree relatives if CRC cases were diagnosed before age 50 years, had proximal colon cancer or if their tumours had any of the following: expanding tumour margin, peritumoral lymphocytes, tumour-infiltrating lymphocytes or synchronous CRC. Conclusions Molecular pathology features are potentially useful to refine screening recommendations for first-degree relatives of CRC cases and to identify which cases are more likely to be caused by genetic or other familial factors. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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