Abstract
With over 28 million cancer survivors worldwide, there is a heightened awareness of the long-term toxicities resulting from treatment and their impact on quality of life in cancer survivors. Understanding genomic factors contributing to cancer related symptom burden would be highly beneficial to cancer patients. Preclinical studies using HapMap lymphoblastoid cell lines have indicated inter-individual and inter-population differences in cellular sensitivity to chemotherapeutics (as a representation of toxicity). The differences can be explained, to some extent, by variation in: 1) genetics; 2) gene expression and; 3) modified cytosines. Although this preclinical model provides a means to elucidate the genetic, transcriptomic and molecular underpinnings of population differences in sensitivity to chemotherapeutics, lymphoblastoid cell lines do not represent tissues of toxicity (peripheral neurons, kidney, cardiac cells, hair cells). To this end, clinical genome wide association studies (GWAS) of chemotherapeutic toxicity have been conducted. Unfortunately, most patients in these studies have been white subjects of European descent with an under representation of minorities. Since it is known that allele frequencies of polymorphisms within important pharmacogenes differ among different populations, there is a need to perform GWAS in under represented populations. Unfortunately, GWAS in oncology continue to widen the disparity gap because of the lack of knowledge of genetic variants that put minority populations at risk for chemotherapeutic toxicity.
Citation Format: M. Eileen Dolan. Pharmacogenomics of anticancer agent toxicity in different populations. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr IA08.
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