[Relationship between RAD51-G135C/XRCC3-C241T polymorphisms and development of acute myeloid leukemia with recurrent chromosome translocation].
Zhonghua Xue Ye Xue Za Zhi
; 32(5): 299-303, 2011 May.
Article
in Zh
| MEDLINE
| ID: mdl-21729596
ABSTRACT
OBJECTIVE:
To investigate the relationship between DNA homologous recombination (HR) repair genes RAD51-G135C/XRCC3-C241T polymorphisms and development of acute myeloid leukemia (AML) with recurrent chromosome translocation.METHODS:
Genomic DNA was extracted from bone marrow cells of 625 de novo AML patients and peripheral blood cells of 806 patient family members and 704 unrelated volunteers. Genotypes of RAD51-G135C and XRCC3-C241T were analyzed by PCR-RFLP. Cell lines with genotypes differed from XRCC3-C241T were selected and irradiated in vitro. The CBFß-MYH11 fusion gene was detected by TaqMan real-time PCR.RESULTS:
The XRCC3-C241T variant (C/T + T/T) showed 6.22-fold and 6.99-fold increase in the risk of developing the AML with inv(16)/t(16;16)/CBFß-MYH11 as compared with the volunteer and family member controls respectively; the RAD51-G135C homozygote-type (C/C) variant showed 0.87-fold (P = 0.010) and 1.15-fold (P = 0.001) respectively increase in the risk of this subtype AML. In the irradiated group, the CBFß-MYH11 mRNA level in HL-60 cells was 59.49 times increased than that in KG1a cells. However, the RAD51-G135C and XRCC3-C241T variants had no correlations with the risk of development of t(15;17)/PML-RARα(+)AML, t(8;21)/AML1-ETO(+) AML and 11q23 AML subtypes.CONCLUSION:
The XRCC3-C241T variant and the RAD51-G135C homozygote-type significantly increase the risk of the development of AML with inv(16)/t(16;16)/CBFß-MYH11.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Leukemia, Myeloid, Acute
/
DNA-Binding Proteins
/
Rad51 Recombinase
Type of study:
Etiology_studies
/
Observational_studies
/
Risk_factors_studies
Limits:
Adolescent
/
Adult
/
Aged
/
Aged80
/
Child
/
Child, preschool
/
Female
/
Humans
/
Male
/
Middle aged
Language:
Zh
Journal:
Zhonghua Xue Ye Xue Za Zhi
Year:
2011
Document type:
Article
Affiliation country:
China