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Recent advances in genome research have suggested strong associations between genetic factors and complex human traits, such as an individual’s disease susceptibility, response to drugs and gene expression levels. Most chemotherapeutic drugs exhibit serious toxicity; hence elucidating the genetic variants that alter response to chemotherapy and/or toxicity is an important but challenging project. Challenges include our inability to do family studies evaluating the effects of chemotherapy on individuals without cancer and the multigenic nature of drug response. Our research program focuses on determining the genetic variants responsible for inter-individual and inter-ethnic differences in response to chemotherapy using lymphoblastoid cell lines derived from individuals collected for the International HapMap Project. The long-term goal is to identify patients at risk for non response or toxicity associated with chemotherapy. We have developed several cell-based models that employ EBV-transformed lymphoblastoid cell lines from Caucasians of European descent (CEU); Yorubans of African descent (YRI); Japanese in Tokyo, Japan; Han Chinese in Beijing, China; Chinese in metropolitan Denver, CO, USA; African ancestry in the Southwest USA; and Mexican ancestry in Los Angeles, CA, USA to evaluate chemotherapeutic-induced cytotoxicity and/or apoptosis. Our laboratory was the first to demonstrate that chemotherapeutic induced cytotoxicity is a heritable trait. We systematically evaluated SNPs associated with chemotherapeutic-induced cytotoxicity for various chemotherapeutic agents and found that these pharmacogenomic markers are disproportionately likely to be expression quantitative trait loci (eQTLs, indicating that a SNP genotype is associated with the transcript abundance level of a gene). We developed a “triangle approach” to identify genetic variants associated with chemotherapeutic-induced cytotoxicity that are also associated with gene expression and whose target genes’ baseline expression significantly correlate to drug cytotoxicity. We have numerous clinical trials aimed at testing these SNPs as pharmacogenomic markers for patient response and/or toxicity to chemotherapy.
Recent advances in genome research have suggested strong associations between genetic factors and complex human traits, such as an individual’s disease susceptibility, response to drugs and gene expression levels. Most chemotherapeutic drugs exhibit serious toxicity; hence elucidating the genetic variants that alter response to chemotherapy and/or toxicity is an important but challenging project. Challenges include our inability to do family studies evaluating the effects of chemotherapy on individuals without cancer and the multigenic nature of drug response. Our research program focuses on determining the genetic variants responsible for inter-individual and inter-ethnic differences in response to chemotherapy using lymphoblastoid cell lines derived from individuals collected for the International HapMap Project. The long-term goal is to identify patients at risk for non response or toxicity associated with chemotherapy. We have developed several cell-based models that employ EBV-transformed lymphoblastoid cell lines from Caucasians of European descent (CEU); Yorubans of African descent (YRI); Japanese in Tokyo, Japan; Han Chinese in Beijing, China; Chinese in metropolitan Denver, CO, USA; African ancestry in the Southwest USA; and Mexican ancestry in Los Angeles, CA, USA to evaluate chemotherapeutic-induced cytotoxicity and/or apoptosis. Our laboratory was the first to demonstrate that chemotherapeutic induced cytotoxicity is a heritable trait. We systematically evaluated SNPs associated with chemotherapeutic-induced cytotoxicity for various chemotherapeutic agents and found that these pharmacogenomic markers are disproportionately likely to be expression quantitative trait loci (eQTLs, indicating that a SNP genotype is associated with the transcript abundance level of a gene). We developed a “triangle approach” to identify genetic variants associated with chemotherapeutic-induced cytotoxicity that are also associated with gene expression and whose target genes’ baseline expression significantly correlate to drug cytotoxicity. We have numerous clinical trials aimed at testing these SNPs as pharmacogenomic markers for patient response and/or toxicity to chemotherapy.
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