Affiliations 

  • 1 Department of Public Health Sciences, University of California Davis, Davis, California
  • 2 Genome Center, University of California Davis, Davis, California
  • 3 Division of General Internal Medicine, Department of Medicine, University of California San Francisco, San Francisco, California
  • 4 Instituto Nacional de Enfermedades Neoplasicas, Lima, Peru
  • 5 Departamento Académico de Medicina Preventiva y Salud Pública, Universidad Nacional Mayor de San Marcos, Lima, Peru
  • 6 Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
  • 7 Grupo de Citogenética, Filogenia y Evolución de Poblaciones, Facultades de Ciencias y Facultad de Ciencias de la Salud, Universidad del Tolima, Ibagué, Colombia
  • 8 Dinamica IPS, Medellín, Colombia
  • 9 Sura, Medellín, Colombia
  • 10 UIM en Enfermedades Infecciosas, UMAE Pediatria, CMN SXXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico
  • 11 UIM en Bioquimica, UMAE especialidades, CMN SXXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico
  • 12 School of Mathematical Sciences, Faculty of Science and Engineering, University of Nottingham Malaysia, Selangor, Malaysia
  • 13 Cancer Research Malaysia, Selangor, Malaysia
  • 14 Department of Epidemiology and Population Health, Stanford University School of Medicine, Stanford, California
  • 15 Department of Population and Public Health Science, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, California
  • 16 Center for Population Health Research, National Institute of Public Health (INSP), Cuernavaca, Mexico
  • 17 Division of Research, Kaiser Permanente Northern California, Oakland, California
  • 18 Department of Population Sciences, Beckman Research Institute of City of Hope, Duarte, California
Cancer Epidemiol Biomarkers Prev, 2025 Feb 06;34(2):234-245.
PMID: 39625644 DOI: 10.1158/1055-9965.EPI-24-1247

Abstract

BACKGROUND: A substantial portion of the genetic predisposition for breast cancer is explained by multiple common genetic variants of relatively small effect. A subset of these variants, which have been identified mostly in individuals of European (EUR) and Asian ancestries, have been combined to construct a polygenic risk score (PRS) to predict breast cancer risk, but the prediction accuracy of existing PRSs in Hispanic/Latinx individuals (H/L) remain relatively low. We assessed the performance of several existing PRS panels with and without addition of H/L-specific variants among self-reported H/L women.

METHODS: PRS performance was evaluated using multivariable logistic regression and the area under the ROC curve.

RESULTS: Both EUR and Asian PRSs performed worse in H/L samples compared with original reports. The best EUR PRS performed better than the best Asian PRS in pooled H/L samples. EUR PRSs had decreased performance with increasing Indigenous American (IA) ancestry, while Asian PRSs had increased performance with increasing IA ancestry. The addition of two H/L SNPs increased performance for all PRSs, most notably in the samples with high IA ancestry, and did not impact the performance of PRSs in individuals with lower IA ancestry.

CONCLUSIONS: A single PRS that incorporates risk variants relevant to the multiple ancestral components of individuals from Latin America, instead of a set of ancestry-specific panels, could be used in clinical practice.

IMPACT: The results highlight the importance of population-specific discovery and suggest a straightforward approach to integrate ancestry-specific variants into PRSs for clinical application.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.