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Updated: Jun 29, 2026

Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity
Published on: March 16, 2018
Genetic variants associated with cisplatin-induced ototoxicity
Jan Oldenburg1, Sophie D Fosså, Tone Ikdahl
1Department of Clinical Cancer Research, The Norwegian Radium Hospital, Rikshospitalet, Montebello, 0310 Oslo, Norway. janolde@ulrik.uio.no
Cisplatin chemotherapy causes hearing loss (ototoxicity) that varies greatly between patients due to genetic factors. Identifying these genetic predictors is key for personalized cisplatin treatment strategies.
Area of Science:
- Pharmacogenomics
- Ototoxicity Research
- Cancer Therapeutics
Background:
- Cisplatin is a widely used chemotherapy agent.
- Cisplatin-induced ototoxicity presents significant interindividual variability.
- Genetic factors are implicated as a major contributor to this variability.
Purpose of the Study:
- To review the prevalence, pathophysiology, and quantification of cisplatin-induced ototoxicity.
- To explore the association between genetic variants and cisplatin ototoxicity.
- To highlight recent advancements in phenotyping and genotyping for this field.
Main Methods:
- Literature review focusing on cisplatin ototoxicity and pharmacogenomics.
- Analysis of studies investigating genetic associations with cisplatin-induced hearing loss.
- Discussion of current phenotyping and genotyping methodologies.
Main Results:
- Ototoxicity is a common and severe side effect of cisplatin treatment.
- Significant genetic variations influence cisplatin-induced ototoxicity risk and severity.
- Limited but growing evidence links specific genetic variants to ototoxicity.
Conclusions:
- Understanding genetic predispositions is crucial for mitigating cisplatin ototoxicity.
- Personalized cisplatin treatment strategies can be developed by identifying predictive genetic markers.
- Further research is needed to fully elucidate the genetic landscape of cisplatin-induced ototoxicity.
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Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase
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