Clinically Significant Dysregulation of and Expression in Patients with Surgically Resected Non-Small Cell Lung Cancer.

Background: The cyclin E2 (CYCE2) is an important regulator in the progression and development of NSCLC, and its ectopic expression promoted the proliferation, invasion, and migration in several tumors, including Non-Small Cell Lung Cancer (NSCLC). However, the upregulation of CYCE2 in NSCLC cells suggested that it has a key role in tumorigenicity. In addition, the RAS family proteins as oncoproteins were activated in many major tumor types and its suitability as the therapeutic target in NSCLC was proposed.

Inhibitory Effects of Arsenic Trioxide and Thalidomide on Angiogenesis and Vascular Endothelial Growth Factor Expression in Leukemia Cells.

Acute myeloid leukemia (AML) is a blood disorder characterized by uncontrolled proliferation of myeloid progenitors and decrease in the apoptosis rate. The vascular endothelial growth factor (VEGF) promotes blood vessel regeneration which might play important roles in development and progression of neoplasia. Our previous studies focused on cytotoxicity and anticancer effects of arsenic trioxide (ATO) and thalidomide (THAL) as an anti-VEGF compound in the AML cell model.

Exogenous Expression of Nt-3 and TrkC Genes in Bone Marrow Stromal Cells Elevated the Survival Rate of the Cells in the Course of Neural Differentiation.

Bone marrow stromal cells (BMSCs) are attractive cellular sources for cell therapy of many diseases, specifically neurodegenerative ones. The potential capability of BMSCs could be further augmented by enhancing their neuroprotective property, differentiation potential, and survival rate subsequent to transplantation. Therefore, a concurrent upregulation of neurotrophin-3 (NT-3) and its high affinity receptor, tyrosin kinase C (TrkC), was utilized in our study.

Up-regulation of MSH2, XRCC1 and ATM genes in patients with type 2 diabetes and coronary artery disease.

Aims: Coronary artery disease (CAD) is a major problem in some patients with type 2 diabetes mellitus (T2DM). CAD has been suggested to be the main result of reduced efficacy of DNA repair systems. Analysis of the DNA repair system in patients with diabetes can potentially uncover the molecular basis of their susceptibility to the CAD.

Transplanting p75-suppressed bone marrow stromal cells promotes functional behavior in a rat model of spinal cord injury.

Background: Bone marrow stromal cells (BMSC) have been successfully employed for movement deficit recovery in spinal cord injury (SCI) rat models. One of the unsettled problems in cell transplantation is the relative high proportion of cell death, specifically after neural differentiation. According to our previous studies, p75 receptor, known as the death receptor, is only expressed in BMSC in a time window of 6-12 hours following neural induction.

A plausible anti-apoptotic role of up-regulated OCT4B1 in bladder tumors.

Purpose: To investigate and compare the expression of OCT4B1 between tumor and non-tumor bladder tissues.

Materials And Methods: We investigated the expression of OCT4B1 in 30 tumor and non-tumor surgical specimens of the bladder, using the TaqMan real-time polymerase chain reaction approach and by carefully designing primers and probes specific for the amplification of the variant.

Results: Most tumor and non-tumor samples of the bladder showed OCT4B1 expression, but its expression level was significantly higher in the tumors (P < .

p75NTR suppression in rat bone marrow stromal stem cells significantly reduced their rate of apoptosis during neural differentiation.

Most of the transplanted cells within central nervous system (CNS) undergo extensive cell death. Preventing the death of stem cell-derived neuron-like cells within adult CNS would enhance the efficiency of transplantation in clinics. We have employed an interfering RNA (RNAi) approach to elevate the survival rate of neurally differentiated bone marrow stromal stem cells (BMSCs), by means of suppressing p75NTR expression.

Overexpression of transforming growth factor (TGF)-beta1 and TGF-beta3 genes in lung of toxic-inhaled patients.

Iraq frequently used toxic inhalants during the war with Iran, exposing over 100,000 people to chemical reagents. Bronchiolitis obliterans (BO) is a major pulmonary disease caused by exposure to harmful gases. Recently defect in clearance of apoptotic cells (efferocytosis) has been suggested as a mechanism that leads to several lung diseases.

Gene expression alterations of neurotrophins, their receptors and prohormone convertases in a rat model of spinal cord contusion.

We have used a semi-quantitative RT-PCR approach to investigate the alterations in the expression of the main regulators of neuronal survival and death, neurotrophins (NTs), NT receptors, and prohormone convertases (PC), in a rat model of spinal cord contusion. Our results revealed that the expression of the members of NT family (Nerve-Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF), and Neurotrophin-3 (NT-3)) is significantly declined in the injured spinal cord, as early as 6h after the induction of the contusion. The expression was recovered afterward to that of the control levels.

Proprotein convertases 1 and 2 (PC1 and PC2) are expressed in neurally differentiated rat bone marrow stromal stem cells (BMSCs).

Neural-like cells derived from bone marrow stromal stem cells (BMSCs) have potential usefulness in cell therapy of degenerative or traumatic diseases of the central nervous system (CNS). The functional recovery mediated by these cells, however, depends on the secretion of neurotrophins (NTs) and their cognate receptors, as the main regulators of neural survival and death. The function of NTs is further modulated by proprotein convertase (PC) enzymes which function in converting proproteins (including proNTs) into their functional end products.