Introduction: Breast cancer remains the prominent cause of mortality in women. Several biomarkers are used to evaluation the response and targeting to therapy. Tumor suppressor candidate 1 (TUSC1) gene was newly identified as a probable tumor suppressor in human cancers. Nevertheless, the expression and potential function of TUSC1 in breast cancer stay undecided. Therefore, this study aimed the evaluation of TUSC1 gene expression in breast tumor samples.Methods: In this case-control study, 40 formalin-fixed paraffin embedded (FFPE) tumoral of breast cancer and 40 healthy tissues were enrolled. Followed were informed consent and completing clinical information for all samples. Total RNA was extracted and complementary DNA (cDNA) was synthesized. The relative gene expression was determined using quantitative real-time RT PCR (qRT-PCR) and evaluated by 2-DDct method.Results: The expression of TUSC1 gene was lower in tumor tissue compared to the healthy tissue adjacent and it was statistically significant (P=0.0003). Also, in metastatic state gene expression significantly decreased (P=0.027).Conclusion: Our study revealed that the expression of TUSC1 is lower in breast cancer. Subsequently, using considering all the data about the expression of TUSC1 gene from some cancers (e.g. Lung, Hepatocellular and gastric), it could be suggested that the TUSC1 gene might act as a tumor suppressor in breast cancer and influenced in metastasis. Therefore, supplementary studies should be done to elucidate the exact mechanism of action of the gene in tumor-genesis.

Background: Due to homeostatic and regulatory potentials of nitric oxide (NO) in vascular physiology, regulatory systems that determine NO bio-synthesis and bioavailability have been the subject of extensive research in molecular medicine. In the field of vascular system pathophysiology, endothelial nitric oxide synthase (eNOS) which is the major producer and regulator of NO in vascular tissues has received the most attention. Impairment of NO bioavailability (NO quenching) is a common feature in poorly controlled diabetics due to increased catabolism and decreased production of NO. Such impairment in severe forms could end to vasodilation breakdown in peripheral tissues (mainly in skeletal muscles) and defective regional blood flow, that in turn disturb insulin-dependent glucose uptake ensuing insulin resistance state. Methods: The phenotypic impact of an eNOS gene polymorphism at position 786*C/T (that its functionality has been revealed already) on genetic propensity to diabetic retinopathy is evaluated in a British-Caucasian population with type 1 diabetes (T1DM). Results: In contrast to genotypes, there was a significant difference in distribution of allele frequencies between T1DM patients (n= 249) and healthy controls (n= 104) (p= 0/036), that may imply eNOS and/or NO involvement in development of T1DM. Most notably a significant difference also was evident in allele frequency between retinopaths (n= 134) and healthy controls (p= 0/02). No significant difference was detected when the genotype/allele frequencies were compared between retinopaths (n= 134) and non-retinopaths diabetics (n= 115) (p=NS). Conclusion: Our data is compatible with previous studies which demonstrated that allele C of eNOS 786*C/T polymorphism is associated with increased HbA1c levels. By emphasizing the phenotypic and prognostic value of the abovementioned polymorphism, our data calls for further investigations to find out whether this polymorphism can be employed as a genetic marker in clinical medicine to recognize high-risk diabetics at the time of diabetes onset/diagnosis.

Background: IFN-g is one of the most essential and fundamental player in initiation and development of T1DM. This mediator belongs to T Helper-1(Th1) class of cytokines and exerts stimulation and differentiation of naïve T cells towards Th1 cells and meanwhile inhibits differentiation and proliferation of Th2 cells. These effects are highly important in induction and progression of cell mediated immune responses that are aberrantly operative in development of T1DM. Due to such outstanding role, numerous studies including genetic manipulation have focused on the role of this pro-inflammatory cytokine in T1DM.Methods: In a genetic association study the influence of IFN-g gene variation in position +874*T/A on development of T1DM was analysed in 248 British Caucasian T1DM patients in comparison with 119 healthy matched controls. ARMS-PCR procedure was designed for detection of the variants at allele/genotype level.Results: No significant association between IFN-g gene polymorphism and T1DM was apparent (P³0.05). The distribution of these polymorphic variants was in Hardy-Weinberg equilibrium.Conclusion: While some studies have shown an association between the examined polymorphism of IFN-g and T1DM, our data do not support that. According to present study the selected polymorphic marker (+874*T/A) is not among the polymorphisms that governs in part genetic susceptibility to T1DM. That irreproducibility or controversial results is a common observation in genetic studies of complex traits such as T1DM, reflecting a fragile correlation between genotype and phenotype. This study also underlines the importance of replication of association studies to confirm the previous results/interpretations.

Background: The alteration of IGF-I systemic level in diabetes is typically characterized by depletion of free IGF-I plasma level and its decreased bioavailability. With regard to protective and advantageous effects of IGF-I on tissue healing and cellular regeneration such depletion could facilitate or accelerate tissue damages and complications.  By contrast, the local concentration of IGF-I is reportedly increased in particular tissues during some occasions, which has also clinical implications as IGF-I could function in an autocrine and paracrine manner.The present study was conducted to assess that whether the differential outcome of diabetic subjects relative to diabetic retinopathy (DR) is linked to some extent to the structural variations of IGF-I gene.Methods: Two polymorphisms of the IGF-I gene at positions –383*C/T and -1089*C/T were employed for genotyping analysis by ARMS-PCR assay and the data of genotype/allele distribution was compared between two subgroups of 248 British Caucasian type 1 diabetic subjects, 135 cases with DR and 113 controls (DR-).Results: The distribution of these polymorphisms did not associate significantly with presence or absence of DR (P≥ 0.05).Conclusion: Since the involvement of IGF-I in development of DR is fairly rational, our results firstly may reflect some reservations about the functionality of the employed polymorphic markers and secondly may indicate that all regulators of IGF-I functionality or its local concentration level including IGFBPs and IGFRs should be taken into account, so their genes could be the subject of new study to accomplish current investigation.

Aims: One of the most important areas in medical research is the identification of disease-causing genes, which helps the identification of mechanisms underlying disease and as a result helps the early diagnosis of disease and the better treatment. In recent years, microarray technology has assisted biologists to gain a better understanding of cellular processes. To this end, the application of efficient methods in microarray data analysis is very important. The aim of this study was the introduction of GRAP Gene as Alzheimer’ s disease candidate gene using microarray data analysis. Materials & Methods: In the present bioinformatic study, which was conducted on an Alzheimer's microarray data set containing 12990 genes, 15 patients, and 16 healthy subjects, by combining Fisher, Significance Analysis of Microarray (SAM), and Particle Swarm Optimization (PSO) methods as well as Classification and Regression Tree (CART), a new method was presented for analyzing microarray gene expression data to identify genes involved in Alzheimer's incidence. Findings: The accuracy level of the proposed method was 90. 32% and the interpretation of the results from a biological point of view indicated that the proposed method has worked well; finally, the proposed method introduced 4 genes, of which, until now, 3 genes (75%) have been reported in biological studies as genes that cause Alzheimer’ s disease. Conclusion: In addition to proposing a new feature selection method for the analysis of microarray data, this study has introduced a new gene (GRAP) as a candidate gene related to Alzheimer’ s disease.

Background and Objective: Human embryonic stem cells (hESCs) can differentiate in vitro into spontaneously contracting cardiomyocytes and produce a model to investigate the early developmental stages of this system. After removing of cells from their feeder layer, hESCs create embryoid bodies (EB). Plating of EB results in developing areas of beating cells. In the present study, cardiomyocyte gene expression time-points during heart development was investigated.Materials and Methods: After stem cell culture, cardiomyocyte’s mRNA was extracted in different time-points after differentiation. The expression pattern of candidate genes CD-34, OCT-4, Brachyury, Alpha-cardiac actin, FLK1 (Vegfr- 2/KDR), ANF, MLC-2a, and MLC-2v was analyzed in human EB (hEB) by RT-PCR. Results: There was an enhanced expression of CD-34 from day 21 in EB in suspension. The OCT-4 gene expression was in 5-day-old EB and Brachyury expression was significantly increased by day 21. There was an enhanced expression of as Alpha-cardiac actin from day 10 in EB in suspension. The FLK1 (Vegfr-2/KDR) gene expression was first specified in 4-day-old EB and was significantly increased by day 14. There was an enhanced expression of MLC-2a and MLC-2v from day 20 and ANF by day 45 in EB in suspension.Conclusion: hESCs might be useful as an effective model system for understanding the developmental processes and functioning of the human heart.