Chronic myelogenous leukemia (CML) is a kind of blood cancer, which produces abnormal white blood cells uncontrollably. Modeling of this type of disease can help for treatment of it to physicians. In this paper we proposed an efficient method for CML treatment. In this method, a nonlinear multivariable system is considered as the plant of the CML treatment. Then an efficient centralized multi-input multi-output proportional and integral (CMIMOPI) controller is proposed for this system. Results show that proposed CMIMOPI controller can control CML disease well, by using low dosage of drugs. Although the real plant is nonlinear, however the controller has good robustness and can stabilize the system for various conditions. Simulation results show that the steady state population of cancer cells at the end of treatment period is highly reduced and the rate of cancer improvement is independent from reproduction of cancer cells.

Global cancer statistics will continue to grow in the coming years. Leukemia is the fifth leading cause of death in the world and the second one in Iran; therefore, it is very important to study the affected areas, including the cardiovascular system in this disease. In heart cancer, tumors whose primary origin is the heart are called primary tumors, which are very rare. Tumors that originate in other parts of the body and spread to the heart are called secondary tumors. Although heart cancer is still rare, most cancers found in the heart come from other parts of the body and are considered as secondary tumors. The symptoms of metastatic heart cancer vary and depend on the location and extent of the lesion. Cancer can also affect the heart in other ways. One of these ways is the effect of the treatments used, which is reported among acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia due to the use of tyrosine kinase inhibitors as the main drug in reducing mortality among these patients. Pericardial involvement is reported to be the most common cardiovascular complication of drug use among different kinds of leukemias. In this article, we try to collect cardiovascular evidence related to acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia, separately.

Objective: One of the most mechanisms in developing of cancer is epigenetic changes which include promoter DNA hypermethylation of tumor suppressor genes and the post-translationalmodifications that occur on histones. A variety of proteins are identified to play an important role in the regulation of these epigenetic changes. For example, Polycomb group proteins (PcG) have emerged as on of those chromatin regulatory factors. PcG proteins were first identified as regulator of homeotic genes in drosophila melangaster. During every cell cycle transition, these proteins maintain cell identity through regulation of chromatin structure. Suz12 is a component of Polycomb group proteins which its overexpression has been reported to be associated with many cancers. Moreover, its loss of expression leads to the amplified activity of progenitor and hematopoietic stem cells (HSC). For the reason that chronic myeloid leukaemia originates from HSC as a consequent of t (9, 22) translocation the purpose of this study was to examine the expression of suz12 in CML patients in comparison with normal people.Materials and Methods: RNA extracted from14 patients and 15 normal peoples, reverse transcribed and amplified by RT-PCR technique.Results: Our study shows that the expression levels of suz12 in patients are lower than normal peoples.Conclusion: These finding are compatible with the fact that loss of SUZ12 function enhances hematopoietic stem cell activity and the role of epigenetic mechanism in developing cancer.

Chronic Myeloid Leukemia (CML) is a hematopoietic malignancy characterized by the presence of Philadelphia (Ph1) chromosome that results from balanced reciprocal translocation between chromosomes 9 and 22 leading in the formation of bcr/abl fusion gene. The present study was conducted to evaluate cytogenetic and molecular abnormalities in CML patients at presentation and during the course of therapy. Cytogenetic analysis was carried out in bone marrow samples of 165 suspected patients of CML using standard protocols. Sequential cytogenetic analysis was also done in 55 CML patients (50 on IFN-α 2b therapy and 5 on Hydroxyurea) up to variable period of 3 years. Fluorescence In Situ Hybridization (FISH) using specific probes for bcr and abl genes was carried out in cases where conventional cytogenetics was not informative, in cases that were Ph-negative at presentation and in cases with complete or major cytogenetic response (<34% Ph+cells). Of the 165 CML patients, 157 patients (95%) were Ph-positive while 8 patients (5%) were Ph-negative. Cytogenetic abnormalities other than the standard Ph1 translocation were observed in 2 Ph+ patients and 2 Ph-negative patients. Sequential cytogenetic analysis revealed varied degrees of cytogenetic response in 35 patients on IFN-α 2b therapy. Complete cytogenetic response was observed in 8 patients (16%) on IFN-α 2b therapy. However, FISH analysis could detect bcr/abl fusion gene in some of these cases. This finding highlights the sensitivity of this technique in detecting residual disease even in patients with complete cytogenetic remission. The other patients in complete cytogenetic remission did not have evidence of bcr/abl fusion. FISH analysis also revealed bcr/abl fusion signals in Ph-negative cases (with no cytogenetic abnormality) indicating a masked translocation or a sub-microscopic rearrangement. Thus, the results of the present study show that analysis of cancer patients on therapy at the molecular level has tremendous importance for management of CML patients. Further, with the use of highly sensitive FISH technique, results can be obtained within 24 hours thereby, aiding rapid diagnosis and management of these patients. This efficient and highly sensitive molecular cytogenetic technique can also be done on interphase cells and poorly spread metaphases thereby, overcoming the difficulty of conventional chromosomal analysis especially in patients on therapy

Chronic Myelogenic Leukemia (CML) is a rare malignant disorder after solid organ transplantation, especially in renal transplant recipients. Imatinib Mesylate is currently approved as first line treatment of CML. Most reports on CML are from kidney recipients who received azathioprine in combination with cyclosporine and prednisolone as immunosuppressive therapy. We report a case with CML who was treated with Mycophenolate Mofetil.

Background: This study evaluated and compared the quantitative expression of multidrug resistance-associated protein 1 (MRP1 ) and ATP-binding cassette subfamily G member 2 (ABCG2 ), two Multidrug Resistance (MDR) related genes, in 30 CML patients and 27 normal subjects. Methods: Total RNA was isolated from peripheral blood mononuclear cells (MNCs) using the Trizol reagent. Then cDNAs were synthesized. Gene expression was quantified using Real-Time PCR System. The relative expression of target genes was calculated using the 2-Δ Δ Ct method. Results: High expression of MRP1 and ABCG2 mRNAs were detected in the patient group. Intra-group comparisons also revealed increased expression of ABCG2 in Accelerated Phase (AP)-Blastic Crisis (BC) patients compared to Chronic Phase (CP) patients. At the same time, the increased expression of MRP1 in AP-BC patients was not statistically significant. Conclusion: Considering the broad spectrum of ATP Binding Cassette (ABC) transporter superfamily substrates, they can play an essential role in cell fate determination. High expression of MRP1 and ABCG2 genes can result in the efflux of therapeutic agents and subsequent reduction in their intracellular concentration. This mechanism finally protects cells from the therapeutic effects of medications. On the other hand, these transporters can export growth factors out of the cell. Such exported molecules may have a growth-inducing effect on adjacent cells. These are the possible mechanisms for the participation of MRP1 and ABCG2 genes in conferring drug resistance to CML cells.