TY - JOUR
T1 - Glioma risk associated with extent of estimated European genetic ancestry in African Americans and Hispanics
AU - Ostrom, Quinn T.
AU - Egan, Kathleen M.
AU - Nabors, L. Burt
AU - Gerke, Travis
AU - Thompson, Reid C.
AU - Olson, Jeffrey J.
AU - LaRocca, Renato
AU - Chowdhary, Sajeel
AU - Eckel-Passow, Jeanette E.
AU - Armstrong, Georgina
AU - Wiencke, John K.
AU - Bernstein, Jonine L.
AU - Claus, Elizabeth B.
AU - Il'yasova, Dora
AU - Johansen, Christoffer
AU - Lachance, Daniel H.
AU - Lai, Rose K.
AU - Merrell, Ryan T.
AU - Olson, Sara H.
AU - Sadetzki, Siegal
AU - Schildkraut, Joellen M.
AU - Shete, Sanjay
AU - Houlston, Richard S.
AU - Jenkins, Robert B.
AU - Wrensch, Margaret R.
AU - Melin, Beatrice
AU - Amos, Christopher I.
AU - Huse, Jason T.
AU - Barnholtz-Sloan, Jill S.
AU - Bondy, Melissa L.
N1 - Funding Information:
This work was previously presented at the Society for Neuro-Oncology 2017 Annual Meeting, the American Association for Cancer Research 2018 Annual Meeting, and the Brain Tumor Epidemiology Consortium 2018 Annual Meeting. This work was supported by grants from the National Institutes of Health (grants R01CA116174, R01CA207972, R01CA139020, R01CA52689, P50CA097257, P30CA008748 and P30CA 125123). Additional support was provided by the McNair Medical Institute at Baylor College of Medicine (Houston, Texas) and the Population Sciences Biorepository at Baylor College of Medicine. The University of Alabama at Birmingham Comprehensive Cancer Center Neuro-oncology Research Acceleration Fund contributed to genotyping for the GliomaSE consortium. In Sweden, work was additionally supported by Acta Onco-logica through the Royal Swedish Academy of Science (BM salary) and The Swedish Research Council and Swedish Cancer Foundation. QTO is supported by a Research Training Grant from the Cancer Prevention and Research Institute of Texas (CPRIT; RP160097T). We are grateful to all the patients and individuals for their participation and we would also like to thank the clinicians and other hospital staff, cancer registries and study staff in respective centers who contributed to the blood sample and data collection.
Funding Information:
Key words: glioma, genetic epidemiology, genetic ancestry, genome-wide association study Abbreviations: AFR: African superpopulation; AFR≥0.4: ≥40% African ancestry; AMR: American superpopulation; AMR≥0.15: ≥15% Native American ancestry; CEU: Utah Residents with Northern and Western European Ancestry; CHB: Han Chinese in Beijing China; EA: European ancestry; EAS: East Asian superpopulation; EUR: European superpopulation; GA: global ancestry; GBM: glioblastoma; GICC: Glioma International Case–Control Study; GliomaSE: Glioma Southeast Case–Control Study; GWAS: genome-wide association study; JPT: Japanese in Tokyo Japan; LA: local ancestry; LD: linkage disequilibrium; MAF: minor allele frequency; PEL: Peruvians from Lima Peru; SNP: single nucleotide polymorphism; US: United States; YRI: Yoruba in Ibadan Nigeria Additional Supporting Information may be found in the online version of this article. J.S.B.-S. and M.L.B. have jointly supervised this work and shared joint senior authorship Grant sponsor: Cancer Prevention and Research Institute of Texas (CPRIT); Grant number: RP160097T; Grant sponsor: McNair Medical Institute at Baylor College of Medicine; Grant sponsor: National Cancer Institute; Grant numbers: P30CA008748, P30CA125123, P50CA097257, R01CA116174, R01CA139020, R01CA207972, R01CA52689; Grant sponsor: Population Sciences Biorepository at Baylor College of Medicine; Grant sponsor: University of Alabama at Birmingham Comprehensive Cancer Center Neuro-oncology Research Acceleration Fund; Grant sponsor: Swedish Cancer Foundation; Grant sponsor: Swedish Research Council; Grant sponsor: Royal Swedish Academy of Science DOI: 10.1002/ijc.32318 History: Received 27 Aug 2018; Accepted 14 Feb 2019; Online 9 Apr 2019. Correspondence to: Melissa Bondy, PhD, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA, Tel.: +1-713-798-2953, E-mail: mbondy@bcm.edu; or Jill S. Barnholtz-Sloan, PhD, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, 2-526 Wolstein Research Building, 2103 Cornell Road, Cleveland, OH 44106, USA, Tel.: +1-216-368-1506, E-mail: jsb42@case.edu
Funding Information:
This work was previously presented at the Society for Neuro-Oncology 2017 Annual Meeting, the American Association for Cancer Research 2018 Annual Meeting, and the Brain Tumor Epidemiology Consortium 2018 Annual Meeting. This work was supported by grants from the National Institutes of Health (grants R01CA116174, R01CA207972, R01CA139020, R01CA52689, P50CA097257, P30CA008748 and P30CA125123). Additional support was provided by the McNair Medical Institute at Baylor College of Medicine (Houston, Texas) and the Population Sciences Biorepository at Baylor College of Medicine. The University of Alabama at Birmingham Comprehensive Cancer Center Neuro-oncology Research Acceleration Fund contributed to genotyping for the GliomaSE consortium. In Sweden, work was additionally supported by Acta Oncologica through the Royal Swedish Academy of Science (BM salary) and The Swedish Research Council and Swedish Cancer Foundation. QTO is supported by a Research Training Grant from the Cancer Prevention and Research Institute of Texas (CPRIT; RP160097T). We are grateful to all the patients and individuals for their participation and we would also like to thank the clinicians and other hospital staff, cancer registries and study staff in respective centers who contributed to the blood sample and data collection.
Publisher Copyright:
© 2019 UICC
PY - 2020/2/1
Y1 - 2020/2/1
N2 - Glioma incidence is highest in non-Hispanic Whites, and to date, glioma genome-wide association studies (GWAS) to date have only included European ancestry (EA) populations. African Americans and Hispanics in the US have varying proportions of EA, African (AA) and Native American ancestries (NAA). It is unknown if identified GWAS loci or increased EA is associated with increased glioma risk. We assessed whether EA was associated with glioma in African Americans and Hispanics. Data were obtained for 832 cases and 675 controls from the Glioma International Case–Control Study and GliomaSE Case–Control Study previously estimated to have <80% EA, or self-identify as non-White. We estimated global and local ancestry using fastStructure and RFMix, respectively, using 1,000 genomes project reference populations. Within groups with ≥40% AA (AFR≥0.4), and ≥15% NAA (AMR≥0.15), genome-wide association between local EA and glioma was evaluated using logistic regression conditioned on global EA for all gliomas. We identified two regions (7q21.11, p = 6.36 × 10−4; 11p11.12, p = 7.0 × 10−4) associated with increased EA, and one associated with decreased EA (20p12.13, p = 0.0026) in AFR≥0.4. In addition, we identified a peak at rs1620291 (p = 4.36 × 10−6) in 7q21.3. Among AMR≥0.15, we found an association between increased EA in one region (12q24.21, p = 8.38 × 10−4), and decreased EA in two regions (8q24.21, p = 0. 0010; 20q13.33, p = 6.36 × 10−4). No other significant associations were identified. This analysis identified an association between glioma and two regions previously identified in EA populations (8q24.21, 20q13.33) and four novel regions (7q21.11, 11p11.12, 12q24.21 and 20p12.13). The identifications of novel association with EA suggest regions to target for future genetic association studies.
AB - Glioma incidence is highest in non-Hispanic Whites, and to date, glioma genome-wide association studies (GWAS) to date have only included European ancestry (EA) populations. African Americans and Hispanics in the US have varying proportions of EA, African (AA) and Native American ancestries (NAA). It is unknown if identified GWAS loci or increased EA is associated with increased glioma risk. We assessed whether EA was associated with glioma in African Americans and Hispanics. Data were obtained for 832 cases and 675 controls from the Glioma International Case–Control Study and GliomaSE Case–Control Study previously estimated to have <80% EA, or self-identify as non-White. We estimated global and local ancestry using fastStructure and RFMix, respectively, using 1,000 genomes project reference populations. Within groups with ≥40% AA (AFR≥0.4), and ≥15% NAA (AMR≥0.15), genome-wide association between local EA and glioma was evaluated using logistic regression conditioned on global EA for all gliomas. We identified two regions (7q21.11, p = 6.36 × 10−4; 11p11.12, p = 7.0 × 10−4) associated with increased EA, and one associated with decreased EA (20p12.13, p = 0.0026) in AFR≥0.4. In addition, we identified a peak at rs1620291 (p = 4.36 × 10−6) in 7q21.3. Among AMR≥0.15, we found an association between increased EA in one region (12q24.21, p = 8.38 × 10−4), and decreased EA in two regions (8q24.21, p = 0. 0010; 20q13.33, p = 6.36 × 10−4). No other significant associations were identified. This analysis identified an association between glioma and two regions previously identified in EA populations (8q24.21, 20q13.33) and four novel regions (7q21.11, 11p11.12, 12q24.21 and 20p12.13). The identifications of novel association with EA suggest regions to target for future genetic association studies.
KW - genetic ancestry
KW - genetic epidemiology
KW - genome-wide association study
KW - glioma
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U2 - 10.1002/ijc.32318
DO - 10.1002/ijc.32318
M3 - Article
C2 - 30963577
AN - SCOPUS:85064651435
SN - 0020-7136
VL - 146
SP - 739
EP - 748
JO - International Journal of Cancer
JF - International Journal of Cancer
IS - 3
ER -