ReviewCancer metastasis reviews2025
Influence of genetic polymorphisms on gefitinib pharmacokinetics and adverse drug reactions in non-small cell lung cancer patients.
Review in Cancer metastasis reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib is a first-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) used in the treatment of non-small cell lung cancer (NSCLC). It is metabolized extensively in the liver by enzymes encoded by CYP3A4, CYP2D6, and CYP3A5 and is the substrate of membrane transporters including ABCB1 and ABCG2. Evidence shows that single-nucleotide polymorphisms (SNPs) in these metabolizing and transporting genes contribute to the inter-individual variability in gefitinib response and development of gefitinib-induced adverse drug reactions (ADRs). This narrative review identifies the existing literature exploring the impact of SNPs on plasma gefitinib concentration and ADRs in patients with NSCLC receiving gefitinib therapy. SNPs were identified in drug-metabolizing enzyme coding genes, including CYP3A4, CYP2D6, CYP3A5, and other CYP homologs, drug transporters including ABCB1, ABCG2, SLCO1B1 and other genes, including UGT1A7 and FOXO3. Current research has not identified any genetic association between specific SNPs in ABCB1, OATP1B1, and UGT1A7 and the pharmacokinetics of gefitinib. Additionally, most of these studies focused on individual SNP associations; however, it may be more important to consider them in combination to better understand their collective impact on gefitinib ADR. Hence, further comprehensive research is essential to examine these genetic variants across different ethnic groups, monitor the drug-drug interactions, and study the phenoconversion to draw definitive conclusions about the pharmacokinetics of gefitinib. This could lead to the development and implementation of a genotyping-based approach for gefitinib dosage optimization in clinical settings.
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