Association Between TP53 Gene Codon 72 Polymorphism and Acute Myeloid Leukemia Susceptibility: Evidence Based on a Meta-Analysis.

BACKGROUND: Many studies have reported that the p53 codon 72 polymorphism is associated with acute myeloid leukemia (AML) susceptibility; however, the conclusions are inconsistent. Therefore, we performed this meta-analysis to obtain a more precise result. MATERIAL AND METHODS: We searched PubMed to identify relevant studies, and 6 published case-control studies were retrieved, including 924 AML patients and 3832 controls. Odds ratio (OR) with corresponding 95% confidence interval (95%CI) was applied to assess the association between p53 codon 72 polymorphism and AML susceptibility. The meta-analysis was performed with Comprehensive Meta-Analysis software, version 2.2. RESULTS: Overall, no significant association between p53 codon 72 polymorphism and AML susceptibility was found in this meta-analysis (Pro vs. Arg: OR=0.94, 95%CI=0.81-1.10; Pro/Pro vs. Arg/Arg: OR=0.93, 95%CI=0.71-1.22; Arg/Pro vs. Arg/Arg: OR=0.79, 95%CI=0.55-1.13; (Pro/Pro + Arg/Pro) vs. Arg/Arg: OR=0.84, 95%CI=0.62-1.13; Pro/Pro vs. (Arg/Arg + Arg/Pro): OR=1.06, 95%CI=0.83-1.35). Similar results were also found in stratified analysis according to ethnicity and source of controls. CONCLUSIONS: Our meta-analysis demonstrates that p53 codon 72 polymorphism may not be a risk factor for AML, which should be verified in future studies.

The Role of TP53 Gene Codon 72 Polymorphism in Leukemia: A PRISMA-Compliant Systematic Review and Meta-Analysis.

The purpose of this meta-analysis was aimed to evaluate the association of tumor protein p53 (TP53) gene codon 72 polymorphism with leukemia susceptibility. We searched PubMed to identify relevant studies, and 16 case-control studies from 14 published articles were identified as eligible studies, including 2062 leukemia patients and 5826 controls. After extracting data, odds ratio (OR) with the corresponding 95% confidence interval (95%CI) was applied to assess the association between TP53 codon 72 polymorphism and leukemia susceptibility. The meta-analysis was performed with the Comprehensive Meta-Analysis software, version 2.2. Overall, no significant association between TP53 codon 72 polymorphism and leukemia susceptibility was found in this meta-analysis (Pro vs Arg: OR = 1.05, 95%CI = 0.90-1.21; Pro/Pro vs Arg/Arg: OR = 1.13, 95%CI = 0.84-1.52; Arg/Pro vs Arg/Arg: OR = 0.94, 95%CI = 0.76-1.15; [Pro/Pro + Arg/Pro] vs Arg/Arg: OR = 0.99, 95%CI = 0.80-1.21; Pro/Pro vs [Arg/Arg + Arg/Pro]: OR = 1.19, 95%CI = 0.93-1.51). Similar results were also found in subgroup analysis by ethnicity, source of controls, and types of leukemia (either acute myeloid leukemia or acute lymphocytic leukemia). Our meta-analysis demonstrates that TP53 codon 72 polymorphism may not be a risk factor for acute leukemia; however, due to the limitations of this study, it should be verified in future studies.

[Expression of costimulatory molecules on peripheral blood lymphocytes of patients with idiopathic thrombocytopenic purpura].

OBJECTIVE: To investigate the expressions of costimulators on peripheral T and B lymphocytes in patients with idiopathic thrombocytopenic purpura (ITP). METHODS: The expression of B7-CD(28) and CD(40) of peripheral lymphocytes was measured by flow cytometry in 21 ITP patients and 9 normal subjects. The expression of PAIgG was measured by ELISA method. RESULTS: The expression of CD(4)(+)CD(28)(+) was lower in ITP patients than in normal controls, but the expression of CD(86)(+) and CD(86)(+)CD(19)(+) was higher in ITP patients than in normal controls, while the expression of CD(80)(+), CD(40)(+), CD(28)(+), CD(19)(+)CD(86)(+), CD(19)(+)CD(40)(+), CD(4)(+)CD(28)(+)/CD(4)(+), CD(19)(+)CD(80)(+)/CD(19)(+) and CD(19)(+)CD(40)(+)/CD(19)(+) in ITP patients was normal. The PAIgG level was higher in 16 patients with a mean of (184.62 +/- 38.00) ng/10(7) plt. A positive correlation was found between PAIgG and CD(19)(+)CD(86)(+)/CD(19)(+) expression. CONCLUSION: There is no deficiency in expression of CD(28) on CD(4)(+) T lymphocytes in ITP patients. The change of CD(86) expression on B lymphocytes is possibly involved in pathophysiology of ITP, which may provide a theoretical instruction for ITP patients immunological therapy.