ArticlePharmacogenetics and genomics2011
Chemotherapeutic-induced apoptosis: a phenotype for pharmacogenomics studies.
Article in Pharmacogenetics and genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Pooled it
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- Silibinin Triggers Mitochondrial Apoptosis and Declines Clonogenic Potential in Detroit 562 Human Pharyngeal Carcinoma Cells.Medicina (Kaunas, Lithuania) · 2025Article
- Integration of genetic and functional genomics data to uncover chemotherapeutic induced cytotoxicity.The pharmacogenomics journal · 2019Article
- Open source machine-learning algorithms for the prediction of optimal cancer drug therapies.PloS one · 2017Article
- CXCL12 Mediates Aberrant Costimulation of B Lymphocytes in Warts, Hypogammaglobulinemia, Infections, Myelokathexis Immunodeficiency.Frontiers in immunology · 2017Article
- Genetic variation is the major determinant of individual differences in leukocyte endothelial adhesion.PloS one · 2014Article
- The AKT1/NF-kappaB/Notch1/PTEN axis has an important role in chemoresistance of gastric cancer cells.Cell death & disease · 2013Article
- Understanding human variation in infectious disease susceptibility through clinical and cellular GWAS.PLoS pathogens · 2013Review
- Article
- Relating human genetic variation to variation in drug responses.Trends in genetics : TIG · 2012Review
- Functional consequences of PRPF39 on distant genes and cisplatin sensitivity.Human molecular genetics · 2012Article
- Genetic variation that predicts platinum sensitivity reveals the role of miR-193b* in chemotherapeutic susceptibility.Molecular cancer therapeutics · 2012Article
- Regulatory polymorphisms in β-tubulin IIa are associated with paclitaxel-induced peripheral neuropathy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Whole-genome studies identify solute carrier transporters in cellular susceptibility to paclitaxel.Pharmacogenetics and genomics · 2012Article
- Mixed effects modeling of proliferation rates in cell-based models: consequence for pharmacogenomics and cancer.PLoS genetics · 2012Article
- Lymphoblastoid cell lines in pharmacogenomic discovery and clinical translation.Pharmacogenomics · 2012Review
- Pharmacogenomics of chemotherapeutic susceptibility and toxicity.Genome medicine · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
aimTo determine whether cellular apoptosis is a suitable phenotypic trait for pharmacogenomics studies by evaluating caspase 3/7-mediated activity in lymphoblastoid cell lines after treatment with six chemotherapeutic agents: 5'-deoxyfluorouridine, pemetrexed, cytarabine, paclitaxel, carboplatin, and cisplatin. MATERIALS AND
methodsUsing monozygotic twin pair and sibling pair lymphoblastoid cell lines, we identified conditions for measurement of caspase 3/7 activity in lymphoblastoid cell lines. Genome-wide association studies were performed with over 2 million single nucleotide polymorphisms (SNPs) and cisplatin-induced apoptosis in HapMap CEU cell lines (n=77).
resultsAlthough treatment with 5'-deoxyfluorouridine and pemetrexed for up to 24 h resulted in low levels of apoptosis or interindividual variation in caspase-dependent cell death; paclitaxel, cisplatin, carboplatin, and cytarabine treatment for 24 h resulted in 9.4-fold, 9.1-fold, 7.0-fold, and 6.0-fold increases in apoptosis relative to control, respectively. There was a weak correlation between caspase activity and cytotoxicity (r(2)=0.03-0.29) demonstrating that cytotoxicity and apoptosis are two distinct phenotypes that may produce independent genetic associations. Estimated heritability (h(2)) for apoptosis was 0.57 and 0.29 for cytarabine (5 and 40 μmol/l, respectively), 0.22 for paclitaxel (12.5 nmol/l), and 0.34 for cisplatin (5 μmol/l). In the genome-wide association study using the HapMap CEU panel, we identified a significant enrichment of cisplatin-induced cytotoxicity SNPs within the significant cisplatin-induced apoptosis SNPs and an enrichment of expression quantitative trait loci (eQTL). Among these eQTLs, we identified several eQTLs with known function related to apoptosis and/or cytotoxicity.
conclusionOur study identifies apoptosis as a phenotype for pharmacogenomic studies in lymphoblastoid cell lines after treatment with paclitaxel, cisplatin, carboplatin, and cytarabine that may have utility for discovering biomarkers to predict response to certain chemotherapeutics.
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