ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2013
Genome-wide discovery of genetic variants affecting tamoxifen sensitivity and their clinical and functional validation.
Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.
- Genetic Variation and Hot Flashes: A Systematic Review.The Journal of clinical endocrinology and metabolism · 2020Pooled it
- Pharmacogenetics of Toxicities Related to Endocrine Treatment in Breast Cancer: A Systematic Review and Meta-analysis.Cancer genomics & proteomicsPooled it
- No evidence for genotype-treatment interactions with breast cancer endocrine therapy adverse effects in UK Biobank.NPJ breast cancer · 2026Article
- The crosstalk between ubiquitination and endocrine therapy.Journal of molecular medicine (Berlin, Germany) · 2023Review
- The Roles of Common Variation and Somatic Mutation in Cancer Pharmacogenomics.Oncology and therapy · 2019Review
- MicroRNA biogenesis and cellular proliferation.Translational research : the journal of laboratory and clinical medicine · 2015Article
- Article
- Feature selection and classifier performance on diverse bio- logical datasets.BMC bioinformatics · 2014Article
- The safety and efficacy of clomiphene citrate in hypoandrogenic and subfertile men.International journal of impotence researchArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundBeyond estrogen receptor (ER), there are no validated predictors for tamoxifen (TAM) efficacy and toxicity. We utilized a genome-wide cell-based model to comprehensively evaluate genetic variants for their contribution to cellular sensitivity to TAM.
designOur discovery model incorporates multidimensional datasets, including genome-wide genotype, gene expression, and endoxifen-induced cellular growth inhibition in the International HapMap lymphoblastoid cell lines (LCLs). Genome-wide findings were further evaluated in NCI60 cancer cell lines. Gene knock-down experiments were performed in four breast cancer cell lines. Genetic variants identified in the cell-based model were examined in 245 Caucasian breast cancer patients who underwent TAM treatment.
resultsWe identified seven novel single-nucleotide polymorphisms (SNPs) associated with endoxifen sensitivity through the expression of 10 genes using the genome-wide integrative analysis. All 10 genes identified in LCLs were associated with TAM sensitivity in NCI60 cancer cell lines, including USP7. USP7 knock-down resulted in increasing resistance to TAM in four breast cancer cell lines tested, which is consistent with the finding in LCLs and in the NCI60 cells. Furthermore, we identified SNPs that were associated with TAM-induced toxicities in breast cancer patients, after adjusting for other clinical factors.
conclusionOur work demonstrates the utility of a cell-based model in genome-wide identification of pharmacogenomic markers.
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