ArticleHPB : the official journal of the International Hepato Pancreato Biliary Association2013
An experimental study to identify the potential role of pharmacogenomics in determining the occurrence of oxaliplatin-induced liver injury.
Article in HPB : the official journal of the International Hepato Pancreato Biliary Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- CanFrontiers in pharmacology · 2026Article
- Predictive Model of Oxaliplatin-induced Liver Injury Based on Artificial Neural Network and Logistic Regression.Journal of clinical and translational hepatology · 2023Article
- Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury.International journal of molecular sciences · 2022Review
- Article
- Global Proteome Changes in Liver Tissue 6 Weeks after FOLFOX Treatment of Colorectal Cancer Liver Metastases.Proteomes · 2016Article
- Effects of oxaliplatin-based chemotherapy on liver function--an analysis of impact and functional recovery using the LiMAx test.Langenbeck's archives of surgery · 2016Observational
- Noninvasive diagnosis of chemotherapy induced liver injury by LiMAx test--two case reports and a review of the literature.BMC research notes · 2015Review
- Sinusoidal obstruction syndrome (hepatic veno-occlusive disease).Journal of clinical and experimental hepatology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOxaliplatin-based chemotherapy has been linked to the development of sinusoidal obstruction syndrome (SOS), which is detrimental to outcome after liver resection for colorectal liver metastases (CLM). The aim of this study was to determine how the expression of genes involved in the transport and metabolism of FOLFOX chemotherapy impacts on tissue injury in a murine model of CLM.
methodsExperimental CLM was established in C57/B16 mice and treated with FOLFOX chemotherapy. After 3 weeks, the animals were killed and RNA extracted from liver, spleen and tumour tissue. DNA damage was assessed by immunohistochemistry for γH2AX. Gene expression was determined by reverse transcriptase polymerase chain reaction.
resultsFOLFOX treatment was associated with an increase in the number of γH2AX-positive cells in both the spleen (P < 0.01) and tumour tissue (P < 0.01), but not the liver. Tissue resistance to injury following FOLFOX was associated with high expression of the copper transporter ATP7B. Differences in the expression of genes related to 5-fluorouracil metabolism or DNA repair did not correlate with the severity of tissue injury.
conclusionsHigh levels of expression of ATP7B are associated with resistance to tissue injury following FOLFOX chemotherapy. Polymorphisms in the ATP7B gene may explain varying susceptibility to SOS among patients following oxaliplatin-based chemotherapy.
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