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Relationship between clinical toxicities and ERCC1 rs3212986 and XRCC3 rs861539 polymorphisms in cervical cancer patients

Relationship between clinical toxicities and ERCC1 rs3212986 and XRCC3 rs861539 polymorphisms in cervical cancer patients

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Article Type: ORIGINAL RESEARCH ARTICLE

DOI:10.5301/ijbm.5000279

Authors

Sílvia Soares, Augusto Nogueira, Ana Coelho, Joana Assis, Deolinda Pereira, Isabel Bravo, Rui Medeiros

Abstract

Background

Several studies have suggested that there are single nucleotide polymorphisms (SNPs) that can be considered potential biomarkers in the prognosis and therapeutic response of cancer patients. The present study investigated the association between ERCC1 rs3212986 and XRCC3 rs861539 polymorphisms and clinical toxicities induced by chemoradiotherapy (CRT) in cervical cancer.

Methods

This hospital-based retrospective cohort study included 260 patients with cervical cancer, FIGO stages Ib2-IVa, who underwent CRT (cisplatin). Genetic polymorphisms analysis was performed by allelic discrimination with real-time polymerase chain reaction (RT-PCR).

Results

Our results indicated a link between ERCC1 rs3212986 and the onset of late gastrointestinal toxicity (p = 0.038). Furthermore, using a recessive model (AA vs. CC/CA), we found that patients carrying AA homozygous genotype presented a fourfold increased risk of developing late gastrointestinal toxicity when compared with patients with the C allele (odds ratio = 3.727, 95% confidence interval, 1.199-11.588; p = 0.017). No association was found regarding the XRCC3 rs861539 polymorphism and any clinical toxicity event.

Conclusions

This is the first study evaluating the relationship between these polymorphisms and clinical toxicities in cervical cancer patients submitted to CRT with cisplatin. These results may contribute toward a better understanding of the influence of genetic polymorphisms in genes associated with DNA repair in the clinical response to CRT of patients with cervical cancer.

Article History

Disclosures

Financial support: This work was supported in part by the Research Center of the Portuguese Institute of Oncology of Porto, Portugal (project no. CI-IPOP-22-2015). The authors also thank the Liga Portuguesa Contra o Cancro – Centro Regional do Norte (Portuguese League Against Cancer) for the financial support.
Conflicts of interest: The authors declare they have no conflicts of interest.

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Authors

Affiliations

  •  Molecular Oncology and Viral Pathology Group – Research Center, Portuguese Institute of Oncology, Porto - Portugal
  •  FMUP, Faculty of Medicine of Porto University, Porto - Portugal
  •  Research Department, Portuguese League Against Cancer (NRNorte), Porto - Portugal
  •  Oncology Department, Portuguese Institute of Oncology, Porto - Portugal
  •  Medical Physics, Radiobiology and Radioprotection Group – Research Center, Portuguese Institute of Oncology, Porto - Portugal
  •  CEBIMED, Faculty of Health Sciences of Fernando Pessoa University, Porto - Portugal
  • Sílvia Soares and Augusto Nogueira have contributed equally to this work.

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