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Cancer Epidemiology, Biomarkers & Prevention Research Article Genetic Susceptibility Loci for Subtypes of Breast Cancer in an African American Population Julie R. Palmer, Edward A. Ruiz-Narvaez, Charles N. Rotimi, L. Adrienne Cupples, Yvette C. Cozier, Lucile L. Adams-Campbell, and Lynn Rosenberg Julie R. Palmer Abstract Background: Most genome-wide association studies (GWAS) have been carried out in European ancestry populations; no risk variants for breast cancer have been identified solely from African ancestry GWAS data. Few GWAS hits have replicated in African ancestry populations. Methods: In a nested case–control study of breast cancer in the Black Women’s Health Study (1,199 cases/1,948 controls), we evaluated index single-nucleotide polymorphisms (SNP) in 21 loci from GWAS of European or Asian ancestry populations, overall, in subtypes defined by estrogen receptor (ER) and progesterone receptor (PR) status (ER+/PR+, n = 336; ER−/PR−, n = 229), and in triple-negative breast cancer (TNBC, N = 81). To evaluate the contribution of genetic factors to population differences in breast cancer subtype, we also examined global percent African ancestry. Results: Index SNPs in five loci were replicated, including three associated with ER−/PR− breast cancer (TERT rs10069690 in 5p15.33, rs704010 in 10q22.3, and rs8170 in 19p13.11): per allele ORs were 1.29 [95% confidence interval (CI) 1.04–1.59], P = 0.02, 1.52 (95% CI 1.12–2.08), P = 0.01, and 1.30 (95% CI 1.01–1.68), P = 0.04, respectively. Stronger associations were observed for TNBC. Furthermore, cases in the highest quintile of percent African ancestry were three times more likely to have TNBC than ER+/PR+ cancer. Conclusions: These findings provide the first confirmation of the TNBC SNP rs8170 in an African ancestry population, and independent confirmation of the TERT ER− SNP. Furthermore, the risk of developing ER− breast cancer, particularly TNBC, increased with increasing proportion of global African ancestry. Impact: The findings illustrate the importance of genetic factors in the disproportionately high occurrence of TNBC in African American women. Cancer Epidemiol Biomarkers Prev; 22(1); 127– 34. ©2012 AACR. Cancer Epidemiol Biomarkers Prev January 2013 22:127–34; Published OnlineFirst November 7, 2012; doi:10.1158/1055-9965. EPI-12-0769 Research Article Drinking Water Arsenic in Northern Chile: High Cancer Risks 40 Years after Exposure Cessation Craig M. Steinmaus, Catterina Ferreccio, Johanna Acevedo Romo, Yan Yuan, Sandra Cortes, Guillermo Marshall, Lee E. Moore, John R. Balmes, Jane Liaw, Todd Golden, and Allan H. Smith Craig M. Steinmaus Abstract Background: Millions of people worldwide are exposed to arsenic-contaminated water. In the largest city in northern Chile (Antofagasta), more than 250,000 people were exposed to high arsenic drinking water concentrations from 1958 until 1970 when a water treatment plant was installed. Because of its unique geology, limited water sources, and good historical records, lifetime exposure and long-term latency patterns can be assessed in this area with better accuracy than in other arsenic-exposed areas worldwide. Methods: We conducted a population-based case–control study in northern Chile from October 2007 to December 2010 involving 232 bladder and 306 lung cancer cases and 640 age- and gendermatched controls, with detailed information on past exposure and potential confounders, including smoking and occupation. Results: Bladder cancer ORs for quartiles of average arsenic concentrations in water before 1971 (335 μg/L) were 1.00, 1.36 [95% confidence interval (CI), 0.78–2.37], 3.87 (2.25–6.64), and 6.50 (3.69–11.43), respectively. Corresponding lung cancer ORs were 1.00, 1.27 (0.81–1.98), 2.00 (1.24–3.24), and 4.32 (2.60–7.17). Bladder and lung cancer ORs in those highly exposed in Antofagasta during 1958 to 1970 but not thereafter were 6.88 (3.84–12.32) and 4.35 (2.57–7.36), respectively. Conclusions: The lung and bladder cancer risks that we found up to 40 years after high exposures have ended are very high. Impact: Our findings suggest that prevention, treatment, and other mortality reduction efforts in arsenic-exposed countries will be needed for decades after exposure cessation. Cancer Epidemiol Biomarkers Prev; 22(4); 623–30. ©2013 AACR. Cancer Epidemiol Biomarkers Prev April 2013 22:623–30; Published OnlineFirst January 25, 2013; doi:10.1158/1055-9965.EPI-12-1190 6 aacrjournals.org
In collaboration with the Cancer Immunology Research Cancer Immunology Research Cancer Immunology Research July 2013 • Volume 1 • Number 1 • Pages 1–76 Illuminating the Interplay of Cancer and the Immune System www.aacrjournals.org Cancer Research Institute Glenn Dranoff, MD Editor-in-Chief Scope Cancer Immunology Research publishes outstanding original articles reporting major advances in cancer immunology that span the discipline from basic investigations in host-tumor interactions to developmental therapeutics in model systems, early translational studies in patients, and late-stage clinical trials. The journal disseminates knowledge of immunology to the cancer research community, catalyzing crossdisciplinary work that yields a deeper understanding of the host-tumor relationship, more potent cancer treatments, and improved clinical outcomes. Review Article Getting Personal with Neoantigen-Based Therapeutic Cancer Vaccines Nir Hacohen, Edward F. Fritsch, Todd A. Carter, Eric S. Lander, and Catherine J. Wu Abstract Despite years of preclinical efforts and hundreds of clinical studies, therapeutic cancer vaccines with the routine ability to limit or eliminate tumor growth in humans have been elusive. With advances in genome sequencing, it is now possible to identify a new class of tumor-specific antigens derived from mutated proteins that are present only in the tumor. These “neoantigens” should provide highly specific targets for antitumor immunity. Although many challenges Catherine J. Wu remain in producing and testing neoantigen-based vaccines customized for each patient, a neoantigen vaccine offers a promising new approach to induce highly focused antitumor T cells aimed at eradicating cancer cells. Cancer Immunol Res; 1(1); 11–15. 2013 AACR. Cancer Immunol Res July 2013; 1:11–15; Published OnlineFirst April 7, 2013; doi: 10.1158/2326-6066.CIR-13-0022 The Best of the AACR Journals 7
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