Acute myeloid leukemia (AML) is a heterogeneous clonal disease that is considered to originate from hematopoietic stem cells, which are characterized by impaired myelopoiesis and blast proliferation. TET oncogene family member 2 (TET2) mutations are frequent in myeloid malignancies and several studies have assessed the clinical importance of TET2 mutations. However, its frequency ratio has not yet been fully clarified. Method: Hence, our study was aimed to analyze TET2mut in patients with de-novo AML and their association with clinical, molecular characteristics and Nucleophosmin 1 (NPM1), Fms-like tyrosine kinase 3 (FLT3), CCAAT Enhancer Binding Protein Alpha (CEBPA) and Wilms’ tumor protein ( WT1 ) gene expression. Fifty-one Iranian patients were screened by polymerase chain reaction (PCR) and direct sequencing to evaluate TET2 mutations frequency. Results: Out of all patients, 10 mutations in 8 patients (15.6%) were detected and closely associated with higher age and higher hemoglobin levels (p-value <0.05). Although FLT3, NPM1 and CEBPA gene expression did not show any significant correlation with TET2mut, cytogenetically normal acute myeloid leukemia (CN-AML) patients appear to bear TET2mut more frequently with lower platelet counts. Monocyte-lineages leukemia has seemed to be more linked with TET2mut in these patients. Conclusion: Our study suggests the frequency of TET2mut in our study (15.6%) is in line with previous studies and reveals the critical role of TET2 in myeloid transformation, especially in leukemia with monocytic subtypes.

Background and Aims: Detection of overexpression in tumor-inhibiting genes provides valuable information for leukemia diagnosis and prognosis. Chronic myeloid leukemia (CML) is a stem cell disorder determined by a well-defined genetic anomaly involving BCR-ABL translocation in the Philadelphia chromosome. Curcumin is a chemo-preventive agent for the primary cancer targets, such as the breast, prostate, lung, stomach, duodenum, colon cancers, and leukemias. Imatinib (Gleevec®, Glivec®) is a synthetic tyrosine kinase inhibitor that treats CML. This study aimed to investigate Curcumin and Imatinib's effect on K562, a human CML cell line that expresses p210 BCR-ABL. Materials and Methods: In this study, Curcumin nanomicelles and Imatinib's apoptotic effects on the K562 cells and the expression of BCR-ABL were studied. BCR-ABL gene expression was evaluated using real-time polymerase chain reaction. Results: The findings indicated a decrease in the desired gene expression, but the BCR-ABL gene expression of the samples treated with Curcumin nanomicelles did not differ significantly from Imatinib (group control). The amount fold change of the BCR-ABL gene for Imatinib and Curcumin nanomicelle was 0.497 and 0.540, respectively. Conclusions: The present study showed that treating cellular category k562 with Curcumin nanomicelle and Imatinib reduces the BCR-ABL gene expression. Also, data showed that the Curcumin nanomicelle and Imatinib induced the apoptotic process.

Background and Aims: DNA methyltransferase3A (DNMT3A) is necessary for the adjustment of gene expression, and the mutations in the DNMT3A gene are reported in a variety of leukemia cases. DNMT3A mutations are during cancer progression and cause poor prognosis in many leukemias. Thus, this gene can be a target for new treatments. This study aimed to examine the distribution of DNMT3A mutations in Iranian acute leukemia patients. Materials and Methods: In this study, diagnostic samples from 45 patients with de novo acute leukemia, including 22 acute myeloid leukemia (AML) patients, and 23 acute leukemia lymphoblastic (ALL) patients were screened, from April 2017 to March 2018 for the incidence of DNMT3A mutations by polymerase chain reaction and direct sequencing. Results: A total of 2 (9.1%) AML cases and 1 (4.34%) ALL cases were found to have the DNMT3A R882H mutation. It was found that a total of 22.7% and 21.7% of patients with AML and ALL had polymorphism rs368516543, respectively. DNMT3A mutations were considerably associated with higher age in AML patients. Conclusions: The findings suggest that the DNMT3A mutations are probably a new biomarker in the early examination and treatment of acute leukemia, even though further studies are needed.