You are in:Home/Publications/Polymorphism of CYP1A1 gene and susceptibility to childhood acute lymphoblastic leukemia in Egypt

Prof. Eman Ramadan Abdel Gawad Khater :: Publications:

Title:
Polymorphism of CYP1A1 gene and susceptibility to childhood acute lymphoblastic leukemia in Egypt
Authors: Adel Agha, Howyda Shabaan, Eman Abdel-Gawad & Doaa El-Ghannam
Year: 2013
Keywords: Not Available
Journal: Not Available
Volume: Not Available
Issue: Not Available
Pages: Not Available
Publisher: Not Available
Local/International: International
Paper Link:
Full paper Eman Ramadan Abdel Gawad Khater_01 Polymorphism of CYP1A1 gene.pdf
Supplementary materials Not Available
Abstract:

The origin of acute lymphoblastic leukemia (ALL) may be explained by a combination of genetic susceptibility and environmental exposure. We aimed to study the frequency of CYP1A1 allelic variants in Egyptian patients with ALL, to evaluate their role in the development of ALL and to correlate these allelic variants with clinical and biological characteristics of the patients. Polymorphism of CYP1A1 * 2A , * 2B and * 4 alleles was examined in 186 Egyptian children with ALL and 200 normal individuals using polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP). A higher prevalence of the CYP1A1 * 4 allele was found in patients with ALL than in the normal population (19.4%vs. 10.0%, odds ratio [OR]  2.160, 95% confidence interval [CI]  1.200 – 3.89, p  0.01), especially in the homozygous variant (OR  6.6, 95% CI  2.23 – 19.58, p  0.001) and in male patients ( p  0.005), particularly those aged 2 – 10 years (OR  5.214, 95% CI  1.535 – 17.706, p  0.008). CYP1A1 * 2A showed a significant difference between age groups ( p  0.046), with a higher incidence in the 10 – 17-year-old group (21.1%). Multivariate analysis showed that only the CYP1A1 * 4 allele remained as a probable independent risk factor for ALL development (OR  2.250, 95% CI  1.244 – 4.069; p  0.007). Our results suggest that polymorphic variants in the CYP1A1 * 4 gene may increase the risk of childhood ALL, particularly in male patients aged 2 – 10 years.

Google ScholarAcdemia.eduResearch GateLinkedinFacebookTwitterGoogle PlusYoutubeWordpressInstagramMendeleyZoteroEvernoteORCIDScopus