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American Cancer Society

NonprofitAtlanta, Georgia, United States
About: American Cancer Society is a nonprofit organization based out in Atlanta, Georgia, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 1339 authors who have published 3700 publications receiving 688166 citations. The organization is also known as: American Cancer Society, ACS & American Society for the Control of Cancer.


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Journal ArticleDOI
TL;DR: Results indicated that, with the exception of colon-rectal cancer and smoking-related cancers, the difference in risk of fatal cancer between SDA and non-SDA was substantially reduced when SDA were compared with a more socioeconomically similar population.
Abstract: In previous reports concerning cancer among Seventh-Day Adventists (SDA), comparisons were made only with the general population. This report compared California SDA to a sample of non-SDA who were demographically similar to SDA. The study consisted of 17 years of follow-up (1960--76) on 22,940 white California SDA and 13 years of follow-up (1960--72) on 112,725 white California non-SDA. Both groups completed the same base-line questionnaire in 1960. Deaths were ascertained by annual contacts with each study member and by computer-assisted record linkage with the California State death certificate file. Results indicated that, with the exception of colon-rectal cancer and smoking-related cancers, the difference in risk of fatal cancer between SDA and non-SDA was substantially reduced when SDA were compared with a more socioeconomically similar population. The persistence of the low risk for colon-rectal cancer can probably be attributed to some aspect of the diet or life-style of the SDA.

180 citations

Journal ArticleDOI
TL;DR: The increased risk of colorectal cancer associated with a high BMI might be largely restricted to tumors that display the more common MS-stable phenotype, suggesting further that coloreCTal cancer etiology differs by tumor MSI status.
Abstract: status. Methods The study included 1794 case subjects with incident colorectal cancer who were identified through populationbased cancer registries and 2684 of their unaffected sex-matched siblings as control subjects. Recent body mass index (BMI), BMI at age 20 years, and adult weight change were derived from self-reports of height and weight. Tumor MSI status, assessed at as many as 10 markers, was obtained for 69.7% of the case subjects and classified as microsatellite (MS)-stable (0% of markers unstable; n = 913), MSI-low (>0% but <30% of markers unstable; n = 149), or MSI-high (≥30% of markers unstable; n = 188). Multivariable conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). All statistical tests were two-sided. Results Recent BMI, modeled in 5 kg/m 2 increments, was positively associated with risk of colorectal cancer for men and women combined (OR = 1.24; 95% CI = 1.15 to 1.34), for women only (OR = 1.20; 95% CI = 1.10 to 1.32), and for men only (OR = 1.30; 95% CI = 1.15 to 1.47). There was no interaction with sex (P = .22). Recent BMI, per 5 kg/m 2 , was positively associated with the risk of MS-stable (OR = 1.38; 95% CI = 1.24 to 1.54) and MSI-low (OR = 1.33; 95% CI = 1.04 to 1.72) colorectal tumors, but not with the risk of MSI-high tumors (OR = 1.05; 95% CI = 0.84 to 1.31). Conclusion The increased risk of colorectal cancer associated with a high BMI might be largely restricted to tumors that display the more common MS-stable phenotype, suggesting further that colorectal cancer etiology differs by tumor MSI status.

179 citations

Journal ArticleDOI
TL;DR: In this paper, the authors measured temporal trends in mortality across three time periods (1959-1965, 1982-1988, and 2000-2010), comparing absolute and relative risks according to sex and selfreported smoking status in two historical cohort studies and in five pooled contemporary cohort studies, among participants who became 55 years of age or older during follow-up.
Abstract: Background The disease risks from cigarette smoking increased in the United States over most of the 20th century, first among male smokers and later among female smokers. Whether these risks have continued to increase during the past 20 years is unclear. Methods We measured temporal trends in mortality across three time periods (1959-1965, 1982-1988, and 2000-2010), comparing absolute and relative risks according to sex and self-reported smoking status in two historical cohort studies and in five pooled contemporary cohort studies, among participants who became 55 years of age or older during follow-up. Results For women who were current smokers, as compared with women who had never smoked, the relative risks of death from lung cancer were 2.73, 12.65, and 25.66 in the 1960s, 1980s, and contemporary cohorts, respectively; corresponding relative risks for male current smokers, as compared with men who had never smoked, were 12.22, 23.81, and 24.97. In the contemporary cohorts, male and female current smokers also had similar relative risks for death from chronic obstructive pulmonary disease (COPD) (25.61 for men and 22.35 for women), ischemic heart disease (2.50 for men and 2.86 for women), any type of stroke (1.92 for men and 2.10 for women), and all causes combined (2.80 for men and 2.76 for women). Mortality from COPD among male smokers continued to increase in the contemporary cohorts in nearly all the age groups represented in the study and within each stratum of duration and intensity of smoking. Among men 55 to 74 years of age and women 60 to 74 years of age, all-cause mortality was at least three times as high among current smokers as among those who had never smoked. Smoking cessation at any age dramatically reduced death rates. Conclusions The risk of death from cigarette smoking continues to increase among women and the increased risks are now nearly identical for men and women, as compared with persons who have never smoked. Among men, the risks associated with smoking have plateaued at the high levels seen in the 1980s, except for a continuing, unexplained increase in mortality from COPD.

179 citations

Journal ArticleDOI
TL;DR: Long-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure, according to a cross-sectional nationwide study using zero-inflated negative binomial models.
Abstract: Background The novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 600,000 lives worldwide, causing tremendous public health, social, and economic damages. Although the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010–2016) county-level exposures to NO2, PM2.5, and O3 and county-level COVID-19 case-fatality and mortality rates in the United States. We used both single- and multi-pollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level health care capacity, phase of epidemic, population mobility, population density, sociodemographics, socioeconomic status, race and ethnicity, behavioral risk factors, and meteorology. Results From January 22, 2020, to July 17, 2020, 3,659,828 COVID-19 cases and 138,552 deaths were reported in 3,076 US counties, with an overall observed case-fatality rate of 3.8%. County-level average NO2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models. When adjusted for co-pollutants, per interquartile-range (IQR) increase in NO2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 11.3% (95% CI 4.9%–18.2%) and 16.2% (95% CI 8.7%–24.0%), respectively. We did not observe significant associations between COVID-19 case-fatality rate and long-term exposure to PM2.5 or O3, although per IQR increase in PM2.5 (2.6 μg/m3) was marginally associated, with a 14.9% (95% CI 0.0%–31.9%) increase in COVID-19 mortality rate when adjusted for co-pollutants. Discussion Long-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO2 levels. Continuation of current efforts to lower traffic emissions and ambient air pollution may be an important component of reducing population-level risk of COVID-19 case fatality and mortality.

179 citations

Journal ArticleDOI
Afshan Siddiq1, Fergus J. Couch, Gary K. Chen, Sara Lindström, Diana Eccles2, Robert C. Millikan3, Kyriaki Michailidou, Daniel O. Stram, Lars Beckmann, Suhn K. Rhie, Christine B. Ambrosone4, Kristiina Aittomäki, Pilar Amiano, Carmel Apicella5, Laura Baglietto6, Laura Baglietto5, Elisa V. Bandera, Matthias W. Beckmann7, Christine D. Berg, Leslie Bernstein8, Carl Blomqvist9, Hiltrud Brauch10, Louise A. Brinton, Quang M. Bui5, Julie E. Buring11, Saundra S. Buys12, Daniele Campa, Jane Carpenter13, Daniel I. Chasman11, Jenny Chang-Claude14, Constance Chen, Françoise Clavel-Chapelon15, Angela Cox, Simon S. Cross16, Kamila Czene17, Sandra L. Deming18, Robert B. Diasio19, W. Ryan Diver20, Alison M. Dunning21, Lorraine Durcan2, Arif B. Ekici7, Peter A. Fasching7, Peter A. Fasching22, Heather Spencer Feigelson23, Laura Fejerman24, Jonine D. Figueroa, Olivia Fletcher25, Dieter Flesch-Janys26, Mia M. Gaudet20, S Gerty2, Jorge L. Rodriguez-Gil27, Graham G. Giles5, Graham G. Giles6, Carla H. van Gils28, Andrew K. Godwin29, Nikki Graham2, Dario Greco9, Per Hall17, Susan E. Hankinson11, Arndt Hartmann, Rebecca Hein14, Judith Heinz26, Robert N. Hoover, John L. Hopper5, Jennifer J. Hu27, Scott Huntsman23, Sue A. Ingles, Astrid Irwanto30, Claudine Isaacs31, Kevin B. Jacobs32, Esther M. John33, Esther M. John34, Christina Justenhoven10, Rudolf Kaaks14, Laurence N. Kolonel35, Gerhard A. Coetzee36, Mark Lathrop37, Loic Le Marchand35, Adam M. Lee19, I-Min Lee11, Timothy G. Lesnick, Peter Lichtner, Jianjun Liu30, Eiliv Lund38, Enes Makalic5, Nicholas G. Martin39, Catriona McLean40, Hanne Meijers-Heijboer41, Alfons Meindl42, Penelope Miron43, Kristine R. Monroe, Grant W. Montgomery39, Bertram Müller-Myhsok44, Stefan Nickels14, Sarah J. Nyante, Curtis Olswold, Kim Overvad45, Domenico Palli46, Daniel J. Park5, Julie R. Palmer47, Harsh B. Pathak29, Julian Peto48, Paul D.P. Pharoah21, Nazneen Rahman, Fernando Rivadeneira49, Daniel F. Schmidt5, Rita K. Schmutzler50, Susan L. Slager, Melissa C. Southey5, Kristen N. Stevens, Hans-Peter Sinn51, Michael F. Press36, Eric A. Ross, Elio Riboli, Paul M. Ridker11, Fredrick R. Schumacher, Gianluca Severi5, Gianluca Severi6, Isabel dos Santos Silva48, Jennifer Stone5, Malin Sund52, William J. Tapper2, Michael J. Thun20, Ruth C. Travis53, Clare Turnbull, André G. Uitterlinden49, Quinten Waisfisz41, Xianshu Wang, Zhaoming Wang32, JoEllen Weaver54, Rüdiger Schulz-Wendtland7, Lynne R. Wilkens35, David Van Den Berg, Wei Zheng18, Regina G. Ziegler, Elad Ziv24, Heli Nevanlinna9, Douglas F. Easton21, David J. Hunter43, Brian E. Henderson, Stephen J. Chanock, Montserrat Garcia-Closas55, Peter Kraft, Christopher A. Haiman, Celine M. Vachon 
Imperial College London1, University of Southampton2, University of North Carolina at Chapel Hill3, Roswell Park Cancer Institute4, University of Melbourne5, Cancer Council Victoria6, University of Erlangen-Nuremberg7, Beckman Research Institute8, Helsinki University Central Hospital9, Bosch10, Brigham and Women's Hospital11, Huntsman Cancer Institute12, Millennium Institute13, German Cancer Research Center14, French Institute of Health and Medical Research15, University of Sheffield16, Karolinska Institutet17, Vanderbilt University18, Mayo Clinic19, American Cancer Society20, University of Cambridge21, University of California, Los Angeles22, Kaiser Permanente23, University of California, San Francisco24, The Breast Cancer Research Foundation25, University of Hamburg26, University of Miami27, Utrecht University28, University of Kansas29, Genome Institute of Singapore30, Georgetown University31, Science Applications International Corporation32, Stanford University33, Cancer Prevention Institute of California34, University of Hawaii35, University of Southern California36, Council on Education for Public Health37, University of Tromsø38, QIMR Berghofer Medical Research Institute39, Alfred Hospital40, VU University Medical Center41, Technische Universität München42, Harvard University43, Max Planck Society44, Aarhus University Hospital45, Prevention Institute46, Boston University47, University of London48, Erasmus University Rotterdam49, University of Cologne50, University Hospital Heidelberg51, Umeå University52, Cancer Epidemiology Unit53, Fox Chase Cancer Center54, Institute of Cancer Research55
TL;DR: The largest meta-analysis of ER-negative disease to date, comprising 4754 ER- negative cases and 31 663 controls from three GWAS, identified two novel loci for breast cancer at 20q11 and 6q14 and confirmed three known loci associated with ER- Negative, triple negative and ER-positive breast cancer.
Abstract: Genome-wide association studies (GWAS) of breast cancer defined by hormone receptor status have revealed loci contributing to susceptibility of estrogen receptor (ER)-negative subtypes. To identify additional genetic variants for ER-negative breast cancer, we conducted the largest meta-analysis of ER-negative disease to date, comprising 4754 ER-negative cases and 31 663 controls from three GWAS: NCI Breast and Prostate Cancer Cohort Consortium (BPC3) (2188 ER-negative cases; 25 519 controls of European ancestry), Triple Negative Breast Cancer Consortium (TNBCC) (1562 triple negative cases; 3399 controls of European ancestry) and African American Breast Cancer Consortium (AABC) (1004 ER-negative cases; 2745 controls). We performed in silico replication of 86 SNPs at P 1 10(-5) in an additional 11 209 breast cancer cases (946 with ER-negative disease) and 16 057 controls of Japanese, Latino and European ancestry. We identified two novel loci for breast cancer at 20q11 and 6q14. SNP rs2284378 at 20q11 was associated with ER-negative breast cancer (combined two-stage OR 1.16; P 1.1 10(8)) but showed a weaker association with overall breast cancer (OR 1.08, P 1.3 10(6)) based on 17 869 cases and 43 745 controls and no association with ER-positive disease (OR 1.01, P 0.67) based on 9965 cases and 22 902 controls. Similarly, rs17530068 at 6q14 was associated with breast cancer (OR 1.12; P 1.1 10(9)), and with both ER-positive (OR 1.09; P 1.5 10(5)) and ER-negative (OR 1.16, P 2.5 10(7)) disease. We also confirmed three known loci associated with ER-negative (19p13) and both ER-negative and ER-positive breast cancer (6q25 and 12p11). Our results highlight the value of large-scale collaborative studies to identify novel breast cancer risk loci.

179 citations


Authors

Showing all 1345 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Meir J. Stampfer2771414283776
Frank B. Hu2501675253464
David J. Hunter2131836207050
Edward Giovannucci2061671179875
Irving L. Weissman2011141172504
Bernard Rosner1901162147661
Susan E. Hankinson15178988297
Paolo Boffetta148145593876
Jeffrey A. Bluestone14351577080
Richard D. Smith140118079758
Garth D. Illingworth13750561793
Brian E. Henderson13771269921
Ahmedin Jemal132500380474
Michael J. Thun12939279051
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202312
20228
2021202
2020239
2019222
2018194