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Background and Aim : Myeloproliferative neoplasms are clonal and heterogeneous disorders of hematopoietic stem cells lead to increase of one or more cell lines in the blood. Recently, the acquired mutation JAK2 V617F has been described in the majority of patients with myeloproliferative neoplasms (MPNs).This mutation is characterized by a G to T transverse at nucleotide 1849 in exon 12 of the JAK2 gene, located on the chromosome 9p, leading to a substitution of valine to phenylalanine at amino acid position 617 in the JAK2 protein. The aim of this study was to assess the prevalence of JAK2 mutation in MPN patients.

Materials and Methods: In this experimental study we evaluated JAK2 mutation in 58 patients with MPNs by simple randomized sampling. The mutation was detected by ARMS-PCR in patients.

Results: The JAK2 V617F mutation was detected in 86.6% (26/30) of patients with polycythemia Vera, 46.6% (7/15) of patients with essential thrombocythemia and 61.5% (8/13) of patients with idiopathic myelofibrosis. Polycythemia Vera patients carrying the mutation displayed a higher levels of WBC (p=0.03) and 61.5% (16/26) of these patients were females. The differences in other groups were not significant. The mutation was confirmed by sequencing.

Conclusions: Our Results show similarity with other studies. Thus, ARMS-PCR can be applied as differential diagnosis test for detection of JAK2 mutation in suspected patients with MPNs.

Background and Aim: Tumor dissemination via blood to distant organs is the main cause of death. Therefore, there is a critical need to set up sensitive methods for the early detection of circulating tumor cells(CTCs) and disseminated tumor cells(DTCs) in peripheral blood (PB) and bone marrow(BM) specimens of breast cancer patients. The aim of this research is to study the detection of micrometastasis using MUC2 in such patients.

Materials and Methods: In this study, PB and BM samples were collected from 50 breast cancer patients after operation and before adjuvant therapy. Mucin 2 (MUC2) was used as a tumor marker and its transcript level in the sample patients was analyzed using gene specific, quantitative real-time PCR reaction with SYBR Green technology. Samples from 20 healthy individuals were used as negative controls. HPRT was used as a reference gene.

Results: MUC2 mRNA was detected in 8 (16%) of PB and BM samples. MUC2 mRNA was not detected in PB samples of healthy individuals. The relapse rate among MUC2-positive patients was higher than MUC2-negative patients and it was statistically significant in BM (P<0.05).

Conclusion: This study shows that MUC2 can be a suitable marker for the detection of micrometastasis in breast cancer patients at early stages of cancer and that it may provide the basis for identifying women at risk of relapse.

 Background and Aim: A goal of modern cancer research is to reach targeted therapies with drugs having fewer side effects. AZD1152 is a highly specific inhibitor of Aurora Kinase B, which leads to the programmed cell death by different mechanisms. The aim of this study was to evaluate the effects of AZD1152 on viability and metabolic activity of NB4 cells (APL derived cell line).

 Materials and Methods: The cells were treated with various concentrations of AZD1152. After 24, 48 and 72h treatments, the metabolic activity and viability of inhibitor-treated NB4 cells were assessed using MTT and trypan blue dye exclusion assays, respectively. Data were analyzed by applying student’s t-test (Microsoft Excel).

 Results: A t 25, 50 and 100 nM, AZD1152 reduced the metabolic activity by 9.2, 15.5 and 56.2% (after 24h), 10.3, 19.5 and 59.9% (after 48h), and 17.1, 28.4 and 64.8% (after 72h), respectively. Meanwhile, the percentage of viability was decreased to about 51, 45 and 40% (after 24h), 39, 36 and 30% (after 48h), and 34, 32 and 28% (after 72h), respectively.

 Conclusion : According to the results, AZD1152 has substantial efficacy on APL cell line and may be applied in some cases, e. g., for patients who have relapse or who become refractory to the conventional chemotherapy. Further studies are needed to show the molecular mechanisms regulating effects of this anti-cancer agent.

Background and Aim: Acute promyelocytic leukemia (APL) is a distinct type of leukemia which is caused due to a blockage in myeloid cells normal maturation. The most important therapeutic strategies include the use of ATRA and Arsenic trioxide. Although ATRA is generally well tolerated, some patients develop Retinoic acid syndrome. Some of the symptoms of this syndrome are directly or indirectly related to elevated WBC counts. This study aims to determine the effect of ATRA and BIBR1532 combination on WBC count as a factor leading to the formation of ATRA syndrome.

Materials and Methods: To investigate the effect of BIBR1532 and ATRA combination, NB4 cells were cultured in the presence of 30μ M and 1 μM densities of the drugs. To study the effect of drugs on living cells count, proliferation activity, and metabolic activity of the cells, Trypan blue, Brdu and MTT tests were used, respectively.

Results: The results of Trypan blue, MTT and Brdu suggest that the combination of ATRA and BIBR1532 is more effective than ATRA alone on the reduction of viable cell count, metabolic activity and proliferation of leukemic cells in the first five days of treatment.

Conclusion: The results suggest that the combination of ATRA and BIBR1532 is probably more effective in the treatment of APL patients. It seems that such improvement in results is more obvious especially among the patients who are at a higher risk of ATRA syndrome.