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The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia

PURPOSE: A growing body of evidence shows an association between DNA repair protein genotypes and susceptibility to various cancers. However, few studies have assessed the contribution of the genotype of XRCC3, a homologous repair gene, to the occurrence or prognosis of childhood acute lymphoblastic...

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Autores principales: Pei, Jen-Sheng, Chang, Wen-Shin, Hsu, Pei-Chen, Chen, Chao-Chun, Cheng, Shun-Ping, Wang, Yun-Chi, Tsai, Chia-Wen, Shen, Te-Chun, Bau, Da-Tian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6245352/
https://www.ncbi.nlm.nih.gov/pubmed/30532590
http://dx.doi.org/10.2147/CMAR.S178411
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author Pei, Jen-Sheng
Chang, Wen-Shin
Hsu, Pei-Chen
Chen, Chao-Chun
Cheng, Shun-Ping
Wang, Yun-Chi
Tsai, Chia-Wen
Shen, Te-Chun
Bau, Da-Tian
author_facet Pei, Jen-Sheng
Chang, Wen-Shin
Hsu, Pei-Chen
Chen, Chao-Chun
Cheng, Shun-Ping
Wang, Yun-Chi
Tsai, Chia-Wen
Shen, Te-Chun
Bau, Da-Tian
author_sort Pei, Jen-Sheng
collection PubMed
description PURPOSE: A growing body of evidence shows an association between DNA repair protein genotypes and susceptibility to various cancers. However, few studies have assessed the contribution of the genotype of XRCC3, a homologous repair gene, to the occurrence or prognosis of childhood acute lymphoblastic leukemia (ALL). In this study, we investigated the contribution of seven XRCC3 polymorphisms to childhood ALL. PATIENTS AND METHODS: We recruited 266 patients with childhood ALL and 266 healthy controls. Genomic DNA was isolated from peripheral blood samples. The XRCC3 rs1799794, rs45603942, rs1799796, rs861530, rs28903081, rs861539, and rs3212057 polymorphic genotypes of each subject were determined through conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. RESULTS: Genotypes with the rs861539 polymorphism were significantly associated with the risk of childhood ALL. The allelic distribution analyses suggested a significant association between the T allele at rs861539 with an increased risk of childhood ALL in the Taiwanese population. Polymorphic variants of XRCC3 at rs3212057 or rs28903081 did not exist in the study population. XRCC3 rs1799794, rs45603942, rs1799796, and rs861530 were not significantly associated with the risk of childhood ALL in the Taiwanese population. CONCLUSION: Our findings suggest that XRCC3 genotypes with polymorphisms at rs861539 may play a role in determining individual susceptibility to childhood ALL in this Taiwanese population. The polymorphism may be a potential detector and predictor of childhood ALL.
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spelling pubmed-62453522018-12-07 The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia Pei, Jen-Sheng Chang, Wen-Shin Hsu, Pei-Chen Chen, Chao-Chun Cheng, Shun-Ping Wang, Yun-Chi Tsai, Chia-Wen Shen, Te-Chun Bau, Da-Tian Cancer Manag Res Original Research PURPOSE: A growing body of evidence shows an association between DNA repair protein genotypes and susceptibility to various cancers. However, few studies have assessed the contribution of the genotype of XRCC3, a homologous repair gene, to the occurrence or prognosis of childhood acute lymphoblastic leukemia (ALL). In this study, we investigated the contribution of seven XRCC3 polymorphisms to childhood ALL. PATIENTS AND METHODS: We recruited 266 patients with childhood ALL and 266 healthy controls. Genomic DNA was isolated from peripheral blood samples. The XRCC3 rs1799794, rs45603942, rs1799796, rs861530, rs28903081, rs861539, and rs3212057 polymorphic genotypes of each subject were determined through conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. RESULTS: Genotypes with the rs861539 polymorphism were significantly associated with the risk of childhood ALL. The allelic distribution analyses suggested a significant association between the T allele at rs861539 with an increased risk of childhood ALL in the Taiwanese population. Polymorphic variants of XRCC3 at rs3212057 or rs28903081 did not exist in the study population. XRCC3 rs1799794, rs45603942, rs1799796, and rs861530 were not significantly associated with the risk of childhood ALL in the Taiwanese population. CONCLUSION: Our findings suggest that XRCC3 genotypes with polymorphisms at rs861539 may play a role in determining individual susceptibility to childhood ALL in this Taiwanese population. The polymorphism may be a potential detector and predictor of childhood ALL. Dove Medical Press 2018-11-15 /pmc/articles/PMC6245352/ /pubmed/30532590 http://dx.doi.org/10.2147/CMAR.S178411 Text en © 2018 Pei et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Pei, Jen-Sheng
Chang, Wen-Shin
Hsu, Pei-Chen
Chen, Chao-Chun
Cheng, Shun-Ping
Wang, Yun-Chi
Tsai, Chia-Wen
Shen, Te-Chun
Bau, Da-Tian
The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title_full The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title_fullStr The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title_full_unstemmed The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title_short The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia
title_sort contribution of xrcc3 genotypes to childhood acute lymphoblastic leukemia
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6245352/
https://www.ncbi.nlm.nih.gov/pubmed/30532590
http://dx.doi.org/10.2147/CMAR.S178411
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