Abstract:
This was analytical case control study was conducted in Gezira state during the period from February to April 2016 to investigate the association between GSTT1 Null polymorphism and childhood acute lymphoblastic leukemia. Total of 40 patients diagnosed with ALL attended to the National Cancer Institute, Gezira State and 40 healthy volunteers as control group were enrolled in this study. Three milliliter (ml) of venous blood was collected from each participant in ethylene diamine tetra acetic (EDTA) anticoagulant container.
For molecular analysis DNA is extracted from blood samples by salting out method. The genetic polymorphism analysis for GSTT1 was determined using Allele specific polymerase chain reaction.
The results were analyzed by statistical package for social sciences (SPSS) computer program.
The rate of GSTT1 null polymorphism was 82.5% in ALL patients, while it was 15% in the control group and the difference was statistically significant (O.R=26.71, 95% CI, p.value =0.00).
Mean of blasts percentage was not statistically significantly high (p.value=0.14) in patients with normal genotype (mean ± SD: 75.14 ± 17.68) compared to those with null genotype (mean ± SD: 59.85 ± 25.42).
Mean of platelets counts was not statistically significant low (p.value=0.93) in patients with normal genotype (mean ±SD: 61.00 ± 87.88) compared to those with null genotype (mean ± SD: 64.06± 51.82).
Mean of TWBCs counts was not statistically significantly low (p.value=0.71) in patients with normal genotype (mean ±SD: 44.94 ± 33.44) compared to those with null genotype (mean ±SD: 58.35 ± 92.00).
Mean of Hb level was significantly low (p.value=0.04) in patients with normal genotype (mean ±SD: 4.89 ± 2.64) compared to those with null genotype (mean ±SD: 7.14 ± 2.52).
Mean of age was not statistically significant high (p.value= 0.64) in patients with normal genotype (mean ±SD: 8.29 ± 3.23) compared to those with null genotype (mean ±SD: 7.27 ± 3.56).
Others results showed that no correlation between GSTT1 null polymorphism and each of gender and family history of ALL (p.value= 0.63 and 0.22 respectively). And also demonstrated that GSTT1 null polymorphism was a risk factor for childhood ALL development.
