Chemotherapy-induced peripheral neurotoxicity and ototoxicity: new paradigms for translational genomics.
Level 5 - mechanism / opinion, no new human data
Narrative review and expert commentary proposing research frameworks without primary empirical data
PubMed 24623533 · doi:10.1093/jnci/dju044
What was done
A transdisciplinary team spanning pharmacogenomics, statistical genetics, neurology, audiology, oncology, epidemiology, and survivorship outlined a translational genomics research framework. The commentary describes strategies—including cell-based models—to investigate mechanisms, risk identification, and interventions for chemotherapy-induced peripheral neurotoxicity (CIPN) and ototoxicity, with a primary focus on cisplatin.
What was found
The paper reviews epidemiologic estimates: the 5-year relative cancer survival rate is approximately 66%, yielding over 13.7 million US cancer survivors (increasing ~2% annually). Approximately 20% to 40% of patients treated with neurotoxic chemotherapy develop CIPN, and platinum-based regimens (cisplatin, carboplatin) frequently cause permanent bilateral hearing loss and/or tinnitus. No primary empirical trial results or novel experimental data are reported in the abstract.
Why it matters
CIPN and ototoxicity remain debilitating, irreversible toxicities without established preventive measures or validated predictive biomarkers. Establishing translational genomics paradigms helps guide research to identify at-risk patients and targetable mechanisms.
Limits
As a conceptual commentary and narrative review, this paper presents no new clinical or experimental data, systematic evidence synthesis, or validated predictive genomic variants.
Cited by
- supports Platinum-containing cancer chemotherapy compounds are toxic to the ear, auditory neurons, and neurons throughout the body.