Institution
American Cancer Society
Nonprofit•Atlanta, 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.
Papers published on a yearly basis
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Harvard University1, American Cancer Society2, University of Southern California3, National Institutes of Health4, University of Cambridge5, University of Oxford6, University of Hawaii at Manoa7, International Agency for Research on Cancer8, Council on Education for Public Health9, National Institute for Health and Welfare10, Washington University in St. Louis11, Columbia University12
TL;DR: Although the gene responsible has yet to be identified, the validation of this marker in this large sample of prostate cancer cases leaves little room for the possibility of a false-positive result.
Abstract: Two recent studies independently identified polymorphisms in the 8q24 region, including a single nucleotide polymorphism (rs1447295), strongly associated with prostate cancer risk. Here, we replicate the overall association in a large nested case-control study from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium using 6,637 prostate cancer cases and 7,361 matched controls. We also examine whether this polymorphism is associated with breast cancer among 2,604 Caucasian breast cancer cases and 3,118 matched controls. The rs1447295 marker was strongly associated with prostate cancer among Caucasians (P = 1.23 × 10−13). When we exclude the Multiethnic Cohort samples, previously reported by Freedman et al., the association remains highly significant (P = 8.64 × 10−13). Compared with wild-type homozygotes, carriers with one copy of the minor allele had an ORAC = 1.34 (99% confidence intervals, 1.19–1.50) and carriers with two copies of the minor allele had an ORAA = 1.86 (99% confidence intervals, 1.30–2.67). Among African Americans, the genotype association was statistically significant in men diagnosed with prostate cancer at an early age (P = 0.011) and nonsignificant for those diagnosed at a later age (P = 0.924). This difference in risk by age at diagnosis was not present among Caucasians. We found no statistically significant difference in risk when tumors were classified by Gleason score, stage, or mortality. We found no association between rs1447295 and breast cancer risk (P = 0.590). Although the gene responsible has yet to be identified, the validation of this marker in this large sample of prostate cancer cases leaves little room for the possibility of a false-positive result. [Cancer Res 2007;67(7):2951–6]
151 citations
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TL;DR: Limited support is provided for the hypothesis that the -2578C and -1154G VEGF alleles are associated with increased risk for invasive but not in situ breast cancer in postmenopausal women.
Abstract: Vascular endothelial growth factor (VEGF) plays a central role in promoting angiogenesis and is over-expressed in breast cancer. At least four polymorphisms in the VEGF gene have been associated with changes in VEGF expression levels: -2578C/A, -1154G/A and -634G/C are all located in the promoter region; and +936C/T is located in the 3'-untranslated region. We examined the association between these four VEGF polymorphisms and risk for breast cancer among postmenopausal women in CPS-II (Cancer Prevention Study II) Nutrition Cohort. This cohort was established in 1992 and participants were invited to provide a blood sample between 1998 and 2001. Included in this analysis were 501 postmenopausal women who provided a blood sample and were diagnosed with breast cancer between 1992 and 2001 (cases). Control individuals were 504 cancer-free postmenopausal women matched to the cases with respect to age, race/ethnicity, and date of blood collection (controls). We found no association between any of the polymorphisms examined and overall breast cancer risk. However, associations were markedly different in separate analyses of invasive cancer (n = 380) and in situ cancer (n = 107). The -2578C and -1154G alleles, which are both hypothesized to increase expression of VEGF, were associated with increased risk for invasive breast cancer (odds ratio [OR] 1.46, 95% confidence interval [CI] 1.00–2.14 for -2578 CC versus AA; OR 1.64, 95% CI 1.02–2.64 for -1154 GG versus AA) but they were not associated with risk for in situ cancer. The +936C allele, which is also hypothesized to increase VEGF expression, was not clearly associated with invasive breast cancer (OR 1.21, 95% CI 0.88–1.67 for +936 CC versus TT/CT), but it was associated with reduced risk for in situ cancer (OR 0.59, 95% CI 0.37–0.93 for CC versus TT/CT). The -634 C/G polymorphism was not associated with either invasive or in situ cancer. Our findings provide limited support for the hypothesis that the -2578C and -1154G VEGF alleles are associated with increased risk for invasive but not in situ breast cancer in postmenopausal women.
151 citations
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University of Southern California1, Fred Hutchinson Cancer Research Center2, University of Hawaii at Manoa3, Third Military Medical University4, University of Michigan5, Clalit Health Services6, National Institutes of Health7, German Cancer Research Center8, Kaiser Permanente9, Harvard University10, University of Washington11, New York University12, Ohio State University13, University of Nantes14, Ontario Institute for Cancer Research15, Phoenix College16, Kyushu University17, American Cancer Society18, Translational Genomics Research Institute19, University of Toronto20, Cancer Council Victoria21, Memorial University of Newfoundland22, Stanford University23, University of Melbourne24, National Cancer Research Institute25, Yonsei University26, Sun Yat-sen University27, Case Western Reserve University28, Mayo Clinic29, Vanderbilt University30, University of Pittsburgh31, University of Utah32, University of Ottawa33
TL;DR: Six new susceptibility loci reaching a genome-wide threshold of P<5.0E-08 are described, providing additional insight into the underlying biological mechanisms of colorectal cancer and demonstrating the scientific value of large consortia-based genetic epidemiology studies.
Abstract: Genetic susceptibility to colorectal cancer is caused by rare pathogenic mutations and common genetic variants that contribute to familial risk. Here we report the results of a two-stage association study with 18,299 cases of colorectal cancer and 19,656 controls, with follow-up of the most statistically significant genetic loci in 4,725 cases and 9,969 controls from two Asian consortia. We describe six new susceptibility loci reaching a genome-wide threshold of P<5.0E-08. These findings provide additional insight into the underlying biological mechanisms of colorectal cancer and demonstrate the scientific value of large consortia-based genetic epidemiology studies.
150 citations
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TL;DR: In an attempt to assess the success in the identification of adolescent and young adult patients 15 to 21 years of age, an analysis of data provided through the Los Angeles County Cancer Surveillance Program was undertaken.
Abstract: Adolescent cancer patients present a unique challenge to health care professionals because of the impact of the disease and its treatment on the successful acquisition of age-appropriate developmental milestones, as well as the psychosocial concerns raised by the illness itself. Understanding normal adolescent development provides a framework for identifying psychosocial concerns, predicting problems, and developing appropriate interventional strategies for adolescents with cancer. A comprehensive support program with specific goals of promoting adjustment to the illness and providing a basis for community reentry by strengthening recognized coping strategies based on identified psychosocial concerns is described as a model. Cancer 1993; 71:3276-80.
150 citations
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TL;DR: The results support an early reduction in mortality from breast cancer with annual mammography screening in women aged 40-49 years and suggest at worst a small amount of overdiagnosis.
Abstract: Summary Background Age-specific effects of mammographic screening, and the timing of such effects, are a matter of debate. The results of the UK Age trial, which compared the effect of invitation to annual mammographic screening from age 40 years with commencement of screening at age 50 years on breast cancer mortality, have been reported at 10 years of follow-up and showed no significant difference in mortality between the trial groups. Here, we report the results of the UK Age trial after 17 years of follow-up. Methods Women aged 39–41 from 23 UK NHS Breast Screening Programme units years were randomly assigned by individual randomisation (1:2) to either an intervention group offered annual screening by mammography up to and including the calendar year of their 48th birthday or to a control group receiving usual medical care (invited for screening at age 50 years and every 3 years thereafter). Both groups were stratified by general practice. We compared breast cancer incidence and mortality by time since randomisation. Analyses included all women randomly assigned who could be traced with the National Health Service Central Register and who had not died or emigrated before entry. The primary outcome measures were mortality from breast cancer (defined as deaths with breast cancer coded as the underlying cause of death) and breast cancer incidence, including in-situ, invasive, and total incidence. Because there is an interest in the timing of the mortality effect, we analysed the results in different follow-up periods. This trial is registered, number ISRCTN24647151. Findings Between Oct 14, 1990, and Sept 25, 1997, 160 921 participants were randomly assigned; 53 883 women in the intervention group and 106 953 assigned to usual medical care were included in this analysis. After a median follow-up of 17 years (IQR 16·8–18·8), the rate ratio (RR) for breast cancer mortality was 0·88 (95% CI 0·74–1·04) from tumours diagnosed during the intervention phase. A significant reduction in breast cancer mortality was noted in the intervention group compared with the control group in the first 10 years after diagnosis (RR 0·75, 0·58–0·97) but not thereafter (RR 1·02, 0·80–1·30) from tumours diagnosed during the intervention phase. The overall breast cancer incidence during 17 year follow-up was similar between the intervention group and the control group (RR 0·98, 0·93–1·04). Interpretation Our results support an early reduction in mortality from breast cancer with annual mammography screening in women aged 40–49 years. Further data are needed to fully understand long-term effects. Cumulative incidence figures suggest at worst a small amount of overdiagnosis. Funding National Institute for Health Research Health Technology Assessment programme and the American Cancer Society. Past funding was received from the Medical Research Council, Cancer Research UK, the UK Department of Health, and the US National Cancer Institute.
150 citations
Authors
Showing all 1345 results
Name | H-index | Papers | Citations |
---|---|---|---|
Walter C. Willett | 334 | 2399 | 413322 |
Meir J. Stampfer | 277 | 1414 | 283776 |
Frank B. Hu | 250 | 1675 | 253464 |
David J. Hunter | 213 | 1836 | 207050 |
Edward Giovannucci | 206 | 1671 | 179875 |
Irving L. Weissman | 201 | 1141 | 172504 |
Bernard Rosner | 190 | 1162 | 147661 |
Susan E. Hankinson | 151 | 789 | 88297 |
Paolo Boffetta | 148 | 1455 | 93876 |
Jeffrey A. Bluestone | 143 | 515 | 77080 |
Richard D. Smith | 140 | 1180 | 79758 |
Garth D. Illingworth | 137 | 505 | 61793 |
Brian E. Henderson | 137 | 712 | 69921 |
Ahmedin Jemal | 132 | 500 | 380474 |
Michael J. Thun | 129 | 392 | 79051 |