ArticleProceedings of the National Academy of Sciences of the United States of America2007
A genome-wide approach to identify genetic variants that contribute to etoposide-induced cytotoxicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
136 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.
- Pooled it
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- Pharmacogenetics in Neuroblastoma: What Can Already Be Clinically Implemented and What Is Coming Next?International journal of molecular sciences · 2021Review
- Systems pharmacogenomics identifies novel targets and clinically actionable therapeutics for medulloblastoma.Genome medicine · 2021Article
- Genetically regulated expression underlies cellular sensitivity to chemotherapy in diverse populations.Human molecular genetics · 2021Article
- Article
- Association of Genetic Variants atFrontiers in cardiovascular medicine · 2020Article
- Expression Changes Confirm Genomic Variants Predicted to Result in Allele-Specific, Alternative mRNA Splicing.Frontiers in genetics · 2020Article
- Integration of genetic and functional genomics data to uncover chemotherapeutic induced cytotoxicity.The pharmacogenomics journal · 2019Article
- Extensive epigenetic and transcriptomic variability between genetically identical human B-lymphoblastoid cells with implications in pharmacogenomics research.Scientific reports · 2019Article
- Differential roles of ERRFI1 in EGFR and AKT pathway regulation affect cancer proliferation.EMBO reports · 2018Article
- Transcriptional signature of lymphoblastoid cell lines ofOncotarget · 2017Article
- Backward genotype-transcript-phenotype association mapping.Methods (San Diego, Calif.) · 2017Article
- Natural variation in a single amino acid substitution underlies physiological responses to topoisomerase II poisons.PLoS genetics · 2017Article
- Genetic variations associated with gemcitabine treatment outcome in pancreatic cancer.Pharmacogenetics and genomics · 2016Article
- Clinical Evaluation of Cisplatin Sensitivity of Germline Polymorphisms in Neoadjuvant Chemotherapy for Urothelial Cancer.Clinical genitourinary cancer · 2016Article
- Computational discovery of transcription factors associated with drug response.The pharmacogenomics journal · 2016Article
- A Cellular GWAS Approach to Define Human Variation in Cellular Pathways Important to Inflammation.Pathogens (Basel, Switzerland) · 2016Review
76 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Large interindividual variance has been observed in sensitivity to drugs. To comprehensively decipher the genetic contribution to these variations in drug susceptibility, we present a genome-wide model using human lymphoblastoid cell lines from the International HapMap consortium, of which extensive genotypic information is available, to identify genetic variants that contribute to chemotherapeutic agent-induced cytotoxicity. Our model integrated genotype, gene expression, and sensitivity of HapMap cell lines to drugs. Cell lines derived from 30 trios of European descent (Center d'Etude du Polymorphisme Humain population) and 30 trios of African descent (Yoruban population) were used. Cell growth inhibition at increasing concentrations of etoposide for 72 h was determined by using alamarBlue assay. Gene expression on 176 HapMap cell lines (87 Center d'Etude du Polymorphisme Humain population and 89 Yoruban population) was determined by using the Affymetrix GeneChip Human Exon 1.0ST Array. We evaluated associations between genotype and cytotoxicity, genotype and gene expression and correlated gene expression of the identified candidates with cytotoxicity. The analysis identified 63 genetic variants that contribute to etoposide-induced toxicity through their effect on gene expression. These include genes that may play a role in cancer (AGPAT2, IL1B, and WNT5B) and genes not yet known to be associated with sensitivity to etoposide. This unbiased method can be used to elucidate genetic variants contributing to a wide range of cellular phenotypes induced by chemotherapeutic agents.
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Registered trials
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