Cisplatin ototoxicity in children: risk factors and its relationship with polymorphisms of DNA repair genes ERCC1, ERCC2, and XRCC1

Basit Öğe Kaydı
dc.contributor.authorTuran C.
dc.contributor.authorKantar M.
dc.contributor.authorAktan Ç.
dc.contributor.authorKosova B.
dc.contributor.authorOrman M.
dc.contributor.authorBilgen C.
dc.contributor.authorKirazlı T.
dc.date.accessioned2024-03-13T10:01:08Z
dc.date.available2024-03-13T10:01:08Z
dc.date.issued2019
dc.departmentİstanbul Beykent Üniversitesien_US
dc.description.abstractPurpose: We aimed to investigate the cisplatin-related hearing toxicity and its possible relationship with polymorphic variants in DNA repair genes, ERCC1, ERCC2, and XRCC1. Methods: Fifty patients treated with cisplatin in the past were included in the study. There were 29 females and 21 males; mean age 13.4 ± 6.0 years). The polymorphism in DNA repair genes was studied using primer and probes in Light Cycler device after DNA isolation was carried out with PCR technique. The polymorphisms and clinical risk factors were evaluated using Chi square test and logistic regression modelling. Results: The patients had hearing loss in 44%. For ERCC1 gene, the patients with hearing loss had 50% of GG (wild type), 40.9% of AG and 9.1% of AA genotypes, while the patients without hearing loss had 28.6% of GG, 53.5% of AG, and 17.9% of AA genotypes. For ERCC2 gene, the patients with hearing loss had 18.2% of GG (wild type), 40.9% of TG, and 40.9% of TT genotypes, while the patients without hearing loss had 10.7% of GG 39.3% of TG, and 50% of TT genotypes. For XRCC1 gene, the patients with hearing loss had 18.2% of CC (wild type), 59.1% of CT, and 22.7% of TT genotypes, while the patients without hearing loss had 35.7% of CC, 50% of CT, and 14.3% of TT genotypes. There was no statistically significant association among the groups (p = 0.24). Conclusion: We did not find a relationship between DNA repair gene polymorphisms and hearing toxicity of cisplatin. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.en_US
dc.identifier.doi10.1007/s00280-019-03968-2
dc.identifier.endpage1338en_US
dc.identifier.issn0344-5704
dc.identifier.issue6en_US
dc.identifier.pmid31586226en_US
dc.identifier.scopus2-s2.0-85073948572en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1333en_US
dc.identifier.urihttps://doi.org/10.1007/s00280-019-03968-2
dc.identifier.urihttps://hdl.handle.net/20.500.12662/3009
dc.identifier.volume84en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer Verlagen_US
dc.relation.ispartofCancer Chemotherapy and Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectChildrenen_US
dc.subjectCisplatinen_US
dc.subjectDNA repair genesen_US
dc.subjectOtotoxicityen_US
dc.subjectPolymorphismen_US
dc.titleCisplatin ototoxicity in children: risk factors and its relationship with polymorphisms of DNA repair genes ERCC1, ERCC2, and XRCC1en_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

Scopus İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu