Polymorphisms of ERCC1 genotype associated with response to imatinib therapy in chronic phase chronic myeloid leukemia

Jee Hyun Kong, Yeung Chul Mun, Seonwoo Kim, Hang Seok Choi, Yeo Kyeoung Kim, Hyeoung Joon Kim, Joon Ho Moon, Sang Kyun Sohn, Sung Hyun Kim, Chul Won Jung, Dong Hwan Dennis Kim

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

DNA repair machinery may contribute to the mechanism of the action in imatinib. We examined the association between the single nucleotide polymorphism (SNP) markers involved in the DNA repair enzyme pathway (ERCC1/2/4/5, XRCC1/2/4/5) and the clinical outcomes following an imatinib therapy in chronic phase chronic myeloid leukemia (CML) patients. A total of 169 Korean patients were included. Of the 19 SNPs from these patients, those with the TT genotype of ERCC1 (rs11615) showed a higher probability of achieving major cytogenetic response [P = 0.002, HR 5.14 (95 % CI 1.83-14.43)], complete cytogenetic response [P = 0.012, HR 3.47 (95 % CI 1.31-9.17)], and major molecular response [P = 0.001, HR 5.71 (95 % CI 2.13-15.30)] than those with CC or CT genotypes. This suggests that SNP markers on ERCC1 may predict the response to imatinib therapy, which proposes the potential involvement of the DNA repair machinery in the mechanism of imatinib action in chronic phase CML.

Original languageEnglish
Pages (from-to)327-333
Number of pages7
JournalInternational Journal of Hematology
Volume96
Issue number3
DOIs
StatePublished - Sep 2012

Bibliographical note

Funding Information:
Conflict of interest This study was supported by grants from the Samsung Biomedical Research Institute, #SBRI C-A9-206, the National Research Foundation of Korea (NRF) Grant funded by the Ministry of Education, Science and Technology of the Korean Government (NRF-2010-0010208), and by a research grant from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (A010385). This grant was used for laboratory work and collecting data.

Keywords

  • Chronic myeloid leukemia
  • DNA repair pathway
  • ERCC
  • Imatinib
  • Single nucleotide polymorphism

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