title: IL-10 promoter polymorphisms affect IL-10 production and associate with susceptibility to acute myeloid leukemia.
abstract: We investigated the possible association of Interleukin-10 (IL-10) single nucleotide polymorphisms (SNPs) and susceptibility to acute myeloid leukemia (AML) in 115 AML patients and 137 gender- and age-matched controls. Genetic analysis of IL-10 SNPs at -819 and -592 was carried out by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results revealed that the -819AA genotype frequencies and the -819A allele frequencies of AML group were higher than the controls (59.1% vs 40.9%; 75.6% vs 63.9%, respectively); there were remarkable differences in -819T/C and -592A/C gene distribution (P<0.05) and the TA haploid frequencies were higher in AML group (75.6% vs 63.9%, P<0.05). The IL-10 mRNA expression of AML patients and controls with different genotype was detected by Real-time quantitative Polymerase Chain Reaction (RT-PCR). IL-10 mRNA expression in incipient AML patients increased obviously compared with the non-tumor group and remission group (P<0.05). Further analysis suggested that the IL-10 mRNA expression of TA/TA genotype was the lowest and CC/CC genotype was the highest; the haploid TA and genotype TA/TA may be associated with AML. The research suggested the IL-10 SNPs at -819 and -592 sites were associated with AML and may affect the IL-10 mRNA expression in AML patients in Han people of Hunan province.
authors.affiliation: Department of Hematology, The Third Xiangya Hospital of Central South University, Changsha, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Chenjiao
authors.forename: Fan
authors.initials: F
authors.lastname: Zili
authors.forename: Chen
authors.initials: C
authors.lastname: Haibin
authors.forename: Liu
authors.initials: L
authors.lastname: Ying
authors.forename: Xiao
authors.initials: X
authors.lastname: Sheng
authors.forename: Huang
authors.initials: H
authors.lastname: Lihua
authors.forename: Du
authors.initials: D
authors.lastname: Wei
mesh_terms: D000483:Alleles; D001853:Bone Marrow / Q000378:metabolism; D017931:DNA Primers; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006238:Haploidy; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000235:genetics*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000378:metabolism*; D015810:Linkage Disequilibrium; D016133:Polymerase Chain Reaction; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D016753:Interleukin-10