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

doi:10.1007/s12185-012-1142-6

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

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

10 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 language	English
Pages (from-to)	327-333
Number of pages	7
Journal	International Journal of Hematology
Volume	96
Issue number	3
DOIs	https://doi.org/10.1007/s12185-012-1142-6
State	Published - 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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title = "Polymorphisms of ERCC1 genotype associated with response to imatinib therapy in chronic phase chronic myeloid leukemia",

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.",

keywords = "Chronic myeloid leukemia, DNA repair pathway, ERCC, Imatinib, Single nucleotide polymorphism",

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

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.",

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doi = "10.1007/s12185-012-1142-6",

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volume = "96",

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AU - Kong, Jee Hyun

AU - Mun, Yeung Chul

AU - Kim, Seonwoo

AU - Choi, Hang Seok

AU - Kim, Yeo Kyeoung

AU - Kim, Hyeoung Joon

AU - Moon, Joon Ho

AU - Sohn, Sang Kyun

AU - Kim, Sung Hyun

AU - Jung, Chul Won

AU - Kim, Dong Hwan Dennis

N1 - 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.

PY - 2012/9

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N2 - 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.

AB - 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.

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KW - DNA repair pathway

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

Abstract

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Keywords

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