Matrix metalloproteinases (MMPs) constitute a large family of enzymes that degrade extracellular matrix proteins (ECM). MMPs are implicated in different pathological conditions such as cancer. Bcl-2 and P53 are key controllers of programmed cell death (PCD) or apoptosis. The aim of the present study was to determine the MMP-9, P53 and Bcl-2 levels in Egyptian patients with Mycobacterium tuberculosis (MTB) (Group I) compared with healthy control individuals (Group II). The concentrations of serum MMP-9 were determined quantitatively using enzyme immunoassay (EIA). P53 and Bcl-2 levels were assayed by flow cytometric analysis using specific monoclones. MMP-9 level was significantly higher in MTB patients compared with healthy control. Similarly, P53 and Bcl-2 levels were increased in MTB patients compared with healthy ones. These data reflect the alteration of MMP-9 level during the course of MTB infection, accompanied with apparent dysregulation of cellular apoptosis as indicated by P53 and Bcl-2 over-expression.
17522 Background: Occurrence and biological characteristics of tumors are related not only to over-proliferation of carcinoma cells but also to decrease of apoptosis. Investigation of apoptosis helps to disclose the biological characteristics of tumors, and seeks new methods of diagnosis and treatment for tumors. In this study, we analyzed the level of some antioxidant enzymes in various leukemic patients including SOD. Methods: To investigate the involvement of apoptosis regulating proteins in acute leukemias, immunocytochemical examination of Mcl-1 and Bax proteins expression was investigated in two groups of patients, one with acute lymphoblastic leukemia (ALL) and the other with acute myeloid leukemia(AML). Moreover, the free radicals utilizing enzymes were sought including superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT), in addition to malonaldhyde (MDH), nitric oxide (NO), and glutathione content (GSH). Results: The obtained results showed a significant difference of SOD, GSH-PX, CAT, MDH, NO, and GSH levels in the leukemia patients (AML, ALL) compared to control group (P<0.001 for each comparison). On the other hand, there was a significant difference of SOD, GSH-PX, MDH, NO, and GSH levels in the AML group compared to ALL patients (P<0.001 for each comparison). In AML patients, a significant positive correlation was existed between SOD and GSH-PX (r=0.684, P<0.001) and a negative correlation was existed between catalase and MDH (r=-0.419, P<0.019). Mcl-1 expression was found positive in ten ALL patients out of 31(32.3%) versus 17 out of 31 (54.8%) in AML patients. Concerning Bax reactivity, only seven cases (22.6%) were positive in ALL patients versus 11 cases (35.5%) in AML patients. In ALL patients, a positive correlation was found between Mcl-1 and Bax expressions (r=0.453, P=0.011). Conclusions: Our results collectively reflect remarkable differences between AML and ALL suggesting different mechanisms underlying their formation and their progression. Mcl-1 and Bax expressions relating to the programmed cell death (PCD) or apoptosis in addition to the anti-oxidant status are deregulated mechanisms that contribute in the pathobiology of ALL differently from AML. No significant financial relationships to disclose.
7053 Background: Glutathione S-transferases (GSTs) are enzymes that detoxify potentially mutagenic and carcinogenic xenobiotics. The genes encoding isoenzymes M1 and T1 are polymorphic in humans and the phenotypic absence of enzyme activity is caused by a homozygous inherited deletion of the gene. The null genotype has been associated with incidence of several types of solid tumors. In addition, GSTM1 and GSTT1 polymorphisms have been considered as risk factors for developing acute leukemia in a number of studies; however the overall results of these previous reports are inconsistent and even controversial. Methods: The present study was undertaken to determine the frequencies of allelic variants in the GST genes in Egyptians and to explore the possibleinfluence of GSTT1, M1 genetic polymorphisms on the risk of acuteleukemia (myeloid and lymphoid). Results: The prevalence of the GSTM1 and GSTT1 homozygous deletions in 53 Egyptian patients with leukemia (21 ALL and 32 AML) and 87 racially,geographically, age and sex matched healthy control individuals was determined using a multiplex polymerase chain reaction (PCR)-based method. Thegenotype frequencies in the leukemia patients and normal controls were compared using Fisher's exact test. A significantly increased incidence of the GSTT1 null genotype was found in the group of patients compared to the controls (34% versus 15% P = 0.03, OR = 2.98, 95% CI 1.6–7.6). GSTM1 null genotype frequencies in cases were slightly but non-significantly higher than controls (68 % versus 49 %, respectively, P=0.07). Conclusions: In conclusion, this study has shown an increased risk of acute leukemia in adult Egyptian patients associated with the GSTT1 null genotype, as well as the combined GSTM1/T1 null genotype, particularly in AML cases. Study will be further extended to examine the relation between the GSTT1 and GSTM1 null genotypes and the patient's response to chemotherapy. No significant financial relationships to disclose.
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