SMYD2 Expression: Its Relationship to Cytogenetic and Prognosis in a Newly Diagnosed Childhood B-Acute Lymphoblastic Leukemia.

BACKGROUND: The SMYD2 gene adjusts lysine residues on histones and non-histone proteins such as transcription factors, signaling kinases, and cell cycle regulators affecting the cell fate and other genes' expression. As it acts as an oncogene, SMYD2's expression levels may affect tumor progression. In this prospective study, our main aim was to determine the association of SMYD2 gene expression with the prognostic parameters of childhood B-acute lymphoblastic leukemia (B-ALL) and evaluate its influence on disease prognosis. METHODS: SMYD2 gene expression was measured in the peripheral blood (PB) samples of 116 newly diagnosed B-ALL patients and 23 controls using real-time polymerase chain reaction (RT-PCR). RESULTS: SMYD2 expression was significantly higher in the childhood B-ALL patients compared with the control group, p-value < 0.001. The patients with unfavorable rather than favorable structural chromosomal abnormalities had significantly higher SMYD2 mRNA levels, p < 0.001. SMYD2 expression levels were positively correlated with total leucocytes count (r = 0.206, p-value = 0.027) and peripheral blood blasts (r = 0.225, p-value = 0.015). There was a statistical difference between the B-ALL cases with high versus low SMYD2 levels regarding translocation (t12; 21), p-value = 0.015. Cox regression analysis identified the increased levels of SMYD2 as an independent prognostic factor affecting both OS and DFS. CONCLUSIONS: The SMYD2 gene plays a vital oncogenic role in childhood B-ALL. The association of high SMYD2 levels with unfavorable cytogenetics in childhood B-ALL may be helpful in understanding the relationship between structural chromosomal abnormalities and epigenetic dysregulation. High SMYD2 levels may be useful in the prediction of prognosis in childhood B-ALL.

Prognostic Value of a CYP2B6 Gene Polymorphism in Patients with Acute Myeloid Leukemia.

BACKGROUND: The objectives of this study aimed to detect a CYP2B6 polymorphism in de novo cases of acute myeloid leukemia patients and identify any role in disease progression and outcome. MATERIALS AND METHODS: DNA was isolated from peripheral blood of 82 newly diagnosed acute myeloid leukemia cases and the CYP2B6 G15631T gene polymorphism was assayed by PCR restriction fragment length polymorphism (PCR-RFLP). RESULTS: The frequency of the GG genotype (wild type) was 48 (58.5%) and that of the mutant type T allele was 34 (41.9%). GT genotype heterozygous variants were found in 28 (34%), and TT genotype homozygous variants in 6 (7.3%) cases. We found no significant association between the CYP2B6 G15631T polymorphism and complete response (CR) (p-value=0.768), FAB classification (p-value=0.51), cytogenetic analysis (p-value=0.673), and overall survival (p-value=0.325). Also, there were no significant links with early toxic death (p-value=0.92) or progression- free survival (PFS) (p-value=0.245). CONCLUSIONS: Our results suggest that the CYP2B6 polymorphism has no role in disease progression, therapeutic outcome, patient free survival, early toxic death and overall survival in acute myeloid leukemia patients.