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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
01 Jan 2018-Gut
TL;DR: Supporting evidence that oral microbiota may play a role in the aetiology of pancreatic cancer is provided, following a large nested case–control study.
Abstract: Objective A history of periodontal disease and the presence of circulating antibodies to selected oral pathogens have been associated with increased risk of pancreatic cancer; however, direct relationships of oral microbes with pancreatic cancer have not been evaluated in prospective studies. We examine the relationship of oral microbiota with subsequent risk of pancreatic cancer in a large nested case–control study. Design We selected 361 incident adenocarcinoma of pancreas and 371 matched controls from two prospective cohort studies, the American Cancer Society Cancer Prevention Study II and the National Cancer Institute Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. From pre-diagnostic oral wash samples, we characterised the composition of the oral microbiota using bacterial 16S ribosomal RNA (16S rRNA) gene sequencing. The associations between oral microbiota and risk of pancreatic cancer, controlling for the random effect of cohorts and other covariates, were examined using traditional and L1-penalised least absolute shrinkage and selection operator logistic regression. Results Carriage of oral pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans , were associated with higher risk of pancreatic cancer (adjusted OR for presence vs absence=1.60 and 95% CI 1.15 to 2.22; OR=2.20 and 95% CI 1.16 to 4.18, respectively). Phylum Fusobacteria and its genus Leptotrichia were associated with decreased pancreatic cancer risk (OR per per cent increase of relative abundance=0.94 and 95% CI 0.89 to 0.99; OR=0.87 and 95% CI 0.79 to 0.95, respectively). Risks related to these phylotypes remained after exclusion of cases that developed within 2 years of sample collection, reducing the likelihood of reverse causation in this prospective study. Conclusions This study provides supportive evidence that oral microbiota may play a role in the aetiology of pancreatic cancer.

484 citations

Journal ArticleDOI
Shahana Ahmed1, Gilles Thomas2, Maya Ghoussaini1, Catherine S. Healey1, Manjeet K. Humphreys1, Radka Platte1, Jonathan J. Morrison1, Melanie Maranian1, Karen A. Pooley1, Robert Luben1, Diana Eccles3, D. Gareth Evans4, Olivia Fletcher, Nichola Johnson, Isabel dos Santos Silva, Julian Peto, Michael R. Stratton5, Nazneen Rahman, Kevin B. Jacobs6, Kevin B. Jacobs2, Ross L. Prentice7, Garnet L. Anderson7, Aleksandar Rajkovic8, J. David Curb9, Regina G. Ziegler2, Christine D. Berg2, Saundra S. Buys10, Catherine A. McCarty11, Heather Spencer Feigelson12, Eugenia E. Calle12, Michael J. Thun12, W. Ryan Diver12, Stig E. Bojesen13, Børge G. Nordestgaard13, Henrik Flyger13, Thilo Dörk14, Peter Schürmann14, Peter Hillemanns14, Johann H. Karstens14, Natalia Bogdanova14, Natalia Antonenkova, Iosif V. Zalutsky, Marina Bermisheva14, S. A. Fedorova15, Elza Khusnutdinova, Daehee Kang16, Keun-Young Yoo16, Dong Young Noh16, Sei Hyun Ahn16, Peter Devilee17, Christi J. van Asperen17, R.A.E.M. Tollenaar17, Caroline Seynaeve18, Montserrat Garcia-Closas2, Jolanta Lissowska19, Louise A. Brinton2, Beata Peplonska20, Heli Nevanlinna21, Tuomas Heikkinen21, Kristiina Aittomäki21, Carl Blomqvist21, John L. Hopper22, Melissa C. Southey22, Letitia D. Smith23, Amanda B. Spurdle23, Marjanka K. Schmidt24, Annegien Broeks24, Richard van Hien24, Sten Cornelissen24, Roger L. Milne25, Gloria Ribas25, Anna González-Neira25, Javier Benitez25, Rita K. Schmutzler26, Barbara Burwinkel27, Barbara Burwinkel28, Claus R. Bartram27, Alfons Meindl29, Hiltrud Brauch30, Hiltrud Brauch31, Christina Justenhoven30, Christina Justenhoven31, Ute Hamann28, Jenny Chang-Claude28, Rebecca Hein28, Shan Wang-Gohrke32, Annika Lindblom33, Sara Margolin33, Arto Mannermaa34, Veli-Matti Kosma34, Vesa Kataja34, Janet E. Olson35, Xianshu Wang35, Zachary S. Fredericksen35, Graham G. Giles36, Graham G. Giles22, Gianluca Severi22, Gianluca Severi36, Laura Baglietto22, Laura Baglietto36, Dallas R. English22, Dallas R. English25, Susan E. Hankinson37, David G. Cox37, Peter Kraft37, Lars J. Vatten38, Kristian Hveem38, Merethe Kumle, Alice J. Sigurdson2, Michele M. Doody2, Parveen Bhatti2, Bruce H. Alexander39, Maartje J. Hooning18, Ans M.W. van den Ouweland18, Rogier A. Oldenburg18, Mieke Schutte18, Per Hall33, Kamila Czene33, Jianjun Liu40, Yuqing Li40, Angela Cox41, Graeme Elliott41, Ian W. Brock41, Malcolm W.R. Reed41, Chen-Yang Shen42, Chen-Yang Shen43, Jyh Cherng Yu44, Giu Cheng Hsu44, Shou Tung Chen, Hoda Anton-Culver45, Argyrios Ziogas45, Irene L. Andrulis46, Julia A. Knight46, Jonathan Beesley23, Ellen L. Goode35, Fergus J. Couch35, Georgia Chenevix-Trench23, Robert N. Hoover2, Bruce A.J. Ponder47, Bruce A.J. Ponder1, David J. Hunter37, Paul D.P. Pharoah1, Alison M. Dunning1, Stephen J. Chanock2, Douglas F. Easton1 
TL;DR: Strong evidence is found for additional susceptibility loci on 3p and 17q and potential causative genes include SLC4A7 and NEK10 on3p and COX11 on 17q.
Abstract: Genome-wide association studies (GWAS) have identified seven breast cancer susceptibility loci, but these explain only a small fraction of the familial risk of the disease. Five of these loci were identified through a two-stage GWAS involving 390 familial cases and 364 controls in the first stage, and 3,990 cases and 3,916 controls in the second stage. To identify additional loci, we tested over 800 promising associations from this GWAS in a further two stages involving 37,012 cases and 40,069 controls from 33 studies in the CGEMS collaboration and Breast Cancer Association Consortium. We found strong evidence for additional susceptibility loci on 3p (rs4973768: per-allele OR = 1.11, 95% CI = 1.08-1.13, P = 4.1 x 10(-23)) and 17q (rs6504950: per-allele OR = 0.95, 95% CI = 0.92-0.97, P = 1.4 x 10(-8)). Potential causative genes include SLC4A7 and NEK10 on 3p and COX11 on 17q.

480 citations

Journal ArticleDOI
TL;DR: Recommendations on the use of prophylactic HPV vaccines, including who should be vaccinated and at what age, as well as a summary of policy and implementation issues, and implications for screening are discussed.
Abstract: The American Cancer Society (ACS) has developed guidelines for the use of the prophylactic human papillomavirus (HPV) vaccine for the prevention of cervical intraepithelial neoplasia and cervical cancer. These recommendations are based on a formal review of the available evidence. They address the use of prophylactic HPV vaccines, including who should be vaccinated and at what age, as well as a summary of policy and implementation issues. Implications for screening are also discussed.

475 citations

Journal ArticleDOI
14 Dec 2005-JAMA
TL;DR: In this large pooled analysis, dietary fiber intake was inversely associated with risk of colorectal cancer in age-adjusted analyses and after accounting for other dietary risk factors, high dietary Fiber intake was not associated with a reduced risk of colon cancer.
Abstract: Context: Inconsistent findings from observational studies have continued the controversy over the effects of dietary fiber on colorectal cancer. Objective: To evaluate the association between dietary fiber intake and risk of colorectal cancer. Design, Setting, and Participants: From 13 prospective cohort studies included in the Pooling Project of Prospective Studies of Diet and Cancer, 725 628 men and women were followed up for 6 to 20 years across studies. Study- and sex-specific relative risks (RRs) were estimated with the Cox proportional hazards model and were subsequently pooled using a random-effects model. Main Outcome Measure: Incident colorectal cancer. Results: During 6 to 20 years of follow-up across studies, 8081 colorectal cancer cases were identified. For comparison of the highest vs lowest study- and sex-specific quintile of dietary fiber intake, a significant inverse association was found in the age-adjusted model (pooled RR=0.84; 95% confidence interval [CI], 0.77-0.92). However, the association was attenuated and no longer statistically significant after adjusting for other risk factors (pooled multivariate RR=0.94; 95% CI, 0.86-1.03). In categorical analyses compared with dietary fiber intake of 10 to <15 g/d, the pooled multivariate RR was 1.18 (95% CI, 1.05-1.31) for less than 10 g/d (11% of the overall study population); and RR, 1.00 (95% CI, 0.85-1.17) for 30 or more g/d. Fiber intake from cereals, fruits, and vegetables was not associated with risk of colorectal cancer. The pooled multivariate RRs comparing the highest vs lowest study- and sex-specific quintile of dietary fiber intake were 1.00 (95% CI, 0.90-1.11) for colon cancer and 0.85 (95% CI, 0.72-1.01) for rectal cancer (P for common effects by tumor site=.07). Conclusions: In this large pooled analysis, dietary fiber intake was inversely associated with risk of colorectal cancer in age-adjusted analyses. However, after accounting for other dietary risk factors, high dietary fiber intake was not associated with a reduced risk of colorectal cancer. ©2005 American Medical Association. All rights reserved.

472 citations

Journal ArticleDOI
TL;DR: A large fraction of lung cancers occurring in never smokers cannot be definitively associated with established environmental risk factors, highlighting the need for additional epidemiologic research in this area.
Abstract: More than 161,000 lung cancer deaths are projected to occur in the United States in 2008. Of these, an estimated 10 to 15% will be caused by factors other than active smoking, corresponding to 16,000 to 24,000 deaths annually. Thus lung cancer in never smokers would rank among the most common causes of cancer mortality in the United States if considered as a separate category. Slightly more than half of the lung cancers caused by factors other than active smoking occur in never smokers. As summarized in the accompanying article, lung cancers that occur in never smokers differ from those that occur in smokers in their molecular profile and response to targeted therapy. These recent laboratory and clinical observations highlight the importance of defining the genetic and environmental factors responsible for the development of lung cancer in never smokers. This article summarizes available data on the clinical epidemiology of lung cancer in never smokers, and several environmental risk factors that population-based research has implicated in the etiology of these cancers. Primary factors closely tied to lung cancer in never smokers include exposure to known and suspected carcinogens including radon, second-hand tobacco smoke, and other indoor air pollutants. Several other exposures have been implicated. However, a large fraction of lung cancers occurring in never smokers cannot be definitively associated with established environmental risk factors, highlighting the need for additional epidemiologic research in this area.

472 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