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Breast cancer as the most common cancer worldwide is influenced by genetic and physiological factors. Based on some evidence indicating the role of estrogen receptor 1 gene (ESR1) in breast cancer development, in this study, the association of three common variations in ESR1 gene with breast cancer and density in an Iranian population was evaluated. In a case–control study, 400 blood samples were collected for DNA extraction and genotyping. Breast density was assessed using mammography. ESR1 rs6915267 (G/A), rs2077647 (C/T) and rs1801132 (C/G) were genotyped using ARMS-PCR method. PHASE program was used to estimate the haplotypes frequencies. Our data analysis showed rs6915267 GA genotype in the heterozygous (GA) as well as co-dominant models was associated with lower mammographic density. None of the three variations were associated with the breast cancer risk. Haplotype analysis indicated G-T-C haplotype of rs6915267, rs2077647 and rs1801132 [OR = 0.54, 95% CI (0.31–0.92), p = 0.025] and G-T/G-T diplotype of rs6915267-rs2077647 [OR = 0.38, 95% CI (0.17–0.86), p = 0.019] were associated with a decreased risk of breast cancer. ESR1 may affect density of the breast and its haplotypes may modulate breast cancer risk.

Oxcarbazepine as an anticonvulsant has been suggested as an effective drug in affective disorders. The present study was designed to compare the efficacy of oxcarbazepine and sodium valproate in the treatment of acute mania in the Iranian population. In a double-blind, randomized clinical trial, hospitalized bipolar patients in the acute manic phase who were admitted to Ibn-e-Sina psychiatric hospital in Mashhad city (north-eastern part of Iran) were enrolled. The diagnosis was confirmed using Structured Clinical Interview for DSM-IV-TR. Patients were then randomly allocated into two groups taking oxcarbazepine (900-2400 mg/day) and sodium valproate (about 20 mg/kg/day) for 6 weeks. Young Mania Rating Scale (YMRS), Clinical Global Impression Scale (CGI-S), and adverse effects of drugs were assessed at baseline and after 3 and 6 weeks. Mania symptoms based on mean scores of YMRS and CGI-S significantly decreased from baseline to endpoint in both treatments (P0.01). However, there was no significant difference between the two groups in terms of reduction of symptoms during times (P = 0.715 and P = 0.446, respectively) and adverse events (P0.05). This study confirmed the previous findings that indicate the efficacy of oxcarbazepine as same as sodium valproate. Moreover, its adverse effects resemble sodium valproate in the treatment of acutely manic patients.

Due to the association between substance use abstinence with some psychological syndromes, the use of herbal medicines such as Crocus sativus L. have been considered as a proper approach to controlling withdrawal syndrome. The present study aimed to identify the effect of Krocina™ in reducing withdrawal symptoms, craving, depression, stress, anxiety and durability of treatment in the detoxification period and abstinence phase.In a double-blind randomized parallel clinical trial, 72 opioid users passing the detoxification period who were referred to the Soroush Center during 2020, randomly categorized into the two groups. Motivational interviewing sessions and 15 mg of Krocina™ twice a day were provided for six weeks for the cases. The placebo group received pills with the same coating and motivational interviewing. Withdrawal symptoms, craving, depression, stress and anxiety were assessed at the start of the study and then weekly using the Clinical Opiate Withdrawal Scale, Obsessive-Compulsive Drug Use Scale, and the Depression Anxiety Stress Scales-21, respectively. SPSS-v16 was used for statistical analyses.Drug withdrawal symptoms and craving did not indicate a significant difference by Krocina™ intervention during the time (Our finding rejected the effectiveness of 30 mg/day of Krocina™ for six weeks as an effective substance for decreasing withdrawal symptoms, craving, depression, anxiety and stress at the detoxification period and abstinence phase.

Objective Mutations of TP53 as a tumor suppressor gene are frequently observed in different types of cancer. A codon 72 polymorphism located on exon 4 with two alleles encoding either Proline (CCC) or Arginine (CGC) has been indicated as a common variation in association with cancers. Controversial results have been reported regarding the association of allelic polymorphism of codon 72 of TP53 gene and breast cancer risk in Iranian patients. Therefore, a case-control study was designed. A meta-analysis was also carried out to provide evidence of association between this variation and breast cancer in Iran, based on all available published data. Materials And Methods In this case-control study, blood sample of 622 participants, including 308 breast cancer cases and 314 controls were collected. Genotyping for rs1042522 was conducted by Allele Specific polymerase chain reaction (AS-PCR). In order to set a meta-analysis study, PubMed, Scopus and ISI Web of Knowledge and Persian databases were searched to explore relevant studies, published up to September 2018, containing information on TP53 polymorphism and the risk of breast cancer in Iran. Statistical analysis was performed using SPSS 16.0 and MetaGenyo. Results All retrieved available data as well as the results of our current study were consisted of 1965 breast cancer cases and 1999 healthy controls. No significant difference was observed in allele frequencies between groups (P=0.90) in our study. The cumulative results did not also show any association between rs1042522 and breast cancer risk on the dominant (P=0.61) and recessive (P=0.89) models. Conclusion These findings cannot support contribution of rs1042522 polymorphism to breast cancer risk in an Iranian population. Future larger studies may help confirm this finding with a greater power.

Introduction Single nucleotide polymorphisms account for most genetic predispositions to breast cancer in the general population. Because of the lack of studies concerning the 2 common polymorphisms in caspase 8 (CASP8), namely rs104548 and rs10931936 in Iranian population, we evaluated the association of these 2 polymorphisms and their haplotypes with breast cancer and molecular profile. Materials and Method Blood samples were collected from 287 breast cancer patients and 490 controls. Genotyping of rs1045485 and rs10931936 was conducted using an amplification refractory mutation system and polymerase chain reaction restriction fragment length polymorphism, respectively. PHASE version 2 (Matthew Stephens) was used to estimate the frequencies of haplotypes. Statistical analysis was performed using SPSS 16.0 (SPSS Inc). Results Although hormone receptors and the molecular profile did not indicate any significant association with different genotypes (P > .05), patients with CC genotype of rs1045485 were more likely to have HER2-positive breast cancer than those with GG genotype (odds ratio [OR], 2.93; 95% confidence interval [CI], 1.0 4-8.26). In addition, CC genotype of D302H was associated with a decreased risk of breast cancer to 48% (OR, 0.52; 95% CI, 0.30-0.90) whereas no significant association was found between rs10931936 and breast cancer. Haplotype analysis indicated C-C haplotype is associated with the decreased risk of breast cancer (OR, 0.69; 95% CI, 0.52-0.91). Conclusion Our data showed a protective effect for CC genotype of rs1045485 variant and C-C haplotype of rs10931936-rs104548 in CASP8 in association with the decrease risk of breast cancer whereas rs10931936 showed no significant association. CASP8 rs1045485 polymorphism might be a candidate genetic marker to evaluate risk of breast cancer. However, further larger studies can confirm such findings.

Background Different genetic variants in hormone‐regulating pathways have been identified to influence the risk of breast cancer. This study aimed to evaluate the association of CYP19A1 rs10046 and rs700519 polymorphisms with the risk, clinicopathological factors and prognosis of breast cancer. Methods In a case‐control study, rs10046 and rs700519 polymorphisms were genotyped using ARMS‐PCR and high‐resolution melting (HRM), respectively, in a total of 702 females. Statistical analysis and evaluation of haplotypes and linkage disequilibrium were performed using SPSS v16, PHASE and 2LD. Results Although no association of rs700519 with breast cancer was observed, rs10046 in different genetic models as well as C‐C/C‐T and C‐C/C‐C diplotypes, revealed the association with the risk of breast cancer (p, This study aimed to evaluate the association of CYP19A1 rs10046 and rs700519 polymorphisms with the risk, clinicopathological factors and prognosis of breast cancer. Our findings help to enrich the literature about the genetic basis of breast cancer. rs10046 and rs700519 may have a diagnostic and prognostic role, respectively. ​

Breast Cancer is the most frequent neoplasm diagnosed among women worldwide. Genetic background and lifestyle/environment play a significant role in the disease etiology. According to Genome-wide association studies, some single-nucleotide polymorphisms such as 2q35-rs13387042-(G/A) have been introduced to be associated with breast cancer risk and features. In this study, we aimed to evaluate the association between this variant and the risk of breast cancer in a cohort of Iranian women.Demographics and clinical information were collected by interview and using patients' medical records, respectively. DNA was extracted from 506 blood samples, including 184 patients and 322 controls, and genotyping was performed using allele specific-PCR. SPSS v16 was used for statistical analysis.Statistically significant association was observed between AA genotype and disease risk in all patients [pThere is a statistically significant association between 2q35-rs13387042 and breast cancer risk. rs13387042-AA genotype might be a risk-conferring factor for breast cancer development in the Iranian population. However, further consideration is suggested to confirm its role in risk assessment and probable association with other genetic markers.

Pancreatic ductal adenocarcinoma (PDAC) is an incidence rate nearly equal to its mortality rate. The poor prognosis of the disease can be explained by the absence of effective biomarkers for screening and early detection, together with the aggressive behavior and resistance to the currently available chemotherapy. The therapeutic failure can also be attributed to the inter-/intratumor genetic heterogeneity and the abundance of tumor stroma that occupies the majority of the tumor mass. Gemcitabine is used in the treatment of PDAC; however, the response rate is less than 12%. A recent phase III trial revealed that the combination of oxaliplatin, irinotecan, fluorouracil, and leucovorin could be an option for the treatment of metastatic PDAC patients with good performance status, although these approaches can result in high toxicity level. Further investigations are required to develop innovative anticancer agents that either improve gemcitabine activity, within novel combinatorial approaches or acts with a better efficacy than gemcitabine. The aim of the current review is to give an overview of preclinical and clinical studies targeting key dysregulated signaling pathways in PDAC.

Background: CC chemokine receptor 5 (CCR5) is introduced as an immune response modulator. The activity of CCR5 influences breast tumour development in a p53-dependent manner. This study aimed to investigate the frequency of CCR5delta32 and its association with the risk of breast cancer in 1038 blood samples in North East of Iran. Methods: In this case-control study, we genotyped 570 control samples and 468 breast cancer patients by a gel electrophoresis-based gap-polymerase chain reaction (gap-PCR) method Mashhad, Iran. The data were analyzed using the SPSS software. Results: Of 570 controls included, 542 (95.09%) had CCR5delta32 wild/wild (W/W) genotype, 28 samples (4.91%) had CCR5delta32 wild/deletion (W/D) genotype and none of them were CCR5delta32 deletion/deletion (D/D) genotype (0%). While 428 samples of patients (91.45%) had CCR5delta32 W/W genotype, 40 samples (8.55%) had CCR5delta32 W/D and CCR5delta32 D/D homozygous was nil (0%) amongst cases. All samples were in the Hardy–Weinberg equilibrium (P>0.05). According to the allele frequency, D allele, as a risky allele, in the cases was more than the control samples (0.0427 vs 0.0245, respectively) (P=0.0206). Hence, W/D genotype may confer a risk effect (OR=1.77, CI: 1.09-2.90; P=0.0206) compared with WW genotype between case and control groups. Conclusion: There is a statistically significant association between CCR5W/D and breast cancer risk. CCR5 may be regarded as a target for the prevention of breast cancer in certain conditions such as interaction with p53 variants, which remains to be further investigated.

Background: Cervical cancer is a preventable cancer with various risk factors. In this study, we assessed different risk factors involved in invasive cervical cancer in the Northeast of Iran. Methods: In a case-control study, 99 patients with advanced cervical cancer were compared to 102 healthy, normal women. Cervical cancer risk factors were documented for these groups using a questionnaire and available medical notes. Univariate analysis was done for each risk factor, followed by multivariate regression analysis, to evaluate the most powerful risk factors after adjustment. Results: Multivariate model indicated that sexual transmitted diseases (STD) [p

Breast cancer as the most common cancer worldwide is influenced by genetic and physiological factors. Based on some evidence indicating the role of estrogen receptor 1 gene (ESR1) in breast cancer development, in this study, the association of three common variations in ESR1 gene with breast cancer and density in an Iranian population was evaluated. In a case-control study, 400 blood samples were collected for DNA extraction and genotyping. Breast density was assessed using mammography. ESR1 rs6915267 (G/A), rs2077647 (C/T) and rs1801132 (C/G) were genotyped using ARMS-PCR method. PHASE program was used to estimate the haplotypes frequencies. Our data analysis showed rs6915267 GA genotype in the heterozygous (GA) as well as co-dominant models was associated with lower mammographic density. None of the three variations were associated with the breast cancer risk. Haplotype analysis indicated G-T-C haplotype of rs6915267, rs2077647 and rs1801132 [OR = 0.54, 95% CI (0.31-0.92), p = 0.025] and G-T/G-T diplotype of rs6915267-rs2077647 [OR = 0.38, 95% CI (0.17-0.86), p = 0.019] were associated with a decreased risk of breast cancer. ESR1 may affect density of the breast and its haplotypes may modulate breast cancer risk.

Background Bipolar I disorder (BID) is a severe psychiatric disease with a confirmed strong hereditary pattern. However, the genetic component is not completely clear to design the diagnostic tests. In this pilot study, we aimed to evaluate the association of haplotypes, including four polymorphisms in the IL-1 region, with BID in a sample of the Iranian population. Methods In a case-control study, genotyping of 95 subjects (48 BID and 47 healthy samples) were performed using PCR-based methods for IL-1α (rs1800587), IL-1b +3954 (rs1143634), IL-1b −511 (rs16944) and IL-1RN (VNTR; rs2234663) loci. PHASE was used for haplotyping, and data were analyzed using SPSS 16. Results Out of 55 haplotypes and 121 diplotypes, three haplotypes including two SNPs (C-T of rs1800587-rs16944, p = 0.007, T-C of rs1143634-rs16944, p = 0.044 and T-A1 of rs16944-rs2234663, p = 0.030) and one haplotype including three SNPs (C-C-T of rs1800587-rs1143634-rs16944, p = 0.012) and one diplotype including two SNPs (C-T/C-T of rs1800587-rs16944, p = 0.032) were identified to be associated with the risk of the disease. In addition, several haplotypes and diplotypes were associated with the disease's features, including the age of onset, the type of first episode and the history of depressive episodes. Conclusion Our findings suggest a diagnostic role of the interleukin-1 region in the BID. The risky haplotypes may carry one or more susceptibility alleles, and the evaluation of their action will aid individual-level risk prediction.

Ischaemic stroke, which is mostly caused by atherosclerosis, is one of the most widely causes of mortality and morbidity. One of the most important enzymatic activities of paraoxonase-1 (PON1) in association with high-density lipoprotein (HDL) is the prevention of low-density lipoprotein (LDL) oxidation, which gives it an anti-atherogenic activity. PON1 expression and activity is influenced by various factors; the most important of which is genetic polymorphism, mainly single nucleotide polymorphisms (SNPs). The results of various studies in different populations indicate that some SNPs of the PON1 gene are associated with stroke. Therefore, in this review we studied various researches, in which the association of PON1 SNPs with stroke had been investigated in different populations.

A growing body of evidence has shown that extracellular vesicles can be efficient as experimental therapeutics in pre-clinical models of skin wounds, but there is a significant unmet need to translate this to clinical utilization. The objectives of the current systematic review were to identify the strength of the therapeutic effects of EVs derived from stem cells in cutaneous wounds and to assess which EV-mediated mechanisms could be involved in the therapeutic response. PubMed, ISI Web of Science, and Scopus databases were systematically searched. We retrieved English-language articles published through June 2020. In vivo studies which applied stem cell-derived EVs were included for further analysis. The Risk of bias was assessed by the SYRCLE tool. We identified thirty-nine pre-clinical studies that evaluated the effects of EVs on the wound healing process. The included studies varied greatly in EVs isolation techniques, route of administration, EVs producing cells, and follow-up time. In vivo application revealed beneficial effects of EVs on accelerating wound closure and re-epithelialization in a dose-dependent manner. Elevated angiogenesis was reported in twelve eligible studies through multiple signaling pathways such as PI3K/Akt, MAPK/ERK, and JAK/STAT. The well-known signaling pathway to inhibit scar formation was TGF-β2/SMAD2. However, all included studies were not blinded enough which may have introduced bias. Therefore, the transition of EV's efficacy into the clinics is deeply rooted in the following important factors: 1) pre-clinical studies with a lower risk of bias and longer follow-up time, and 2) consistent, reproducible, and feasible manufacturing of EVs production in a large-scale commercial program.

Brain-derived neurotrophic factor (BDNF) is a potent neurotrophic factor that has been shown to stimulate breast cancer cell growth and metastasis via tyrosine kinase receptors TrkA, TrkB, and the p75NTR death receptor. The aberrant activation of BDNF/TrkB pathways can modulate several signaling pathways, including Akt/PI3K, Jak/STAT, NF-kB, UPAR/UPA, Wnt/β-catenin, and VEGF pathways as well as the ER receptor. Several microRNAs have been identified that are involved in the modulation of BDNF/TrkB pathways. These include miR-206, miR-204, MiR-200a/c, MiR-210, MiR-134, and MiR-191; and these may be of value as prognostic and predictive biomarkers for detecting patients at high risk of developing breast cancer. It has been also been demonstrated that a high expression of genes involved in the BDNF pathway in breast cancer is associated with poor clinical outcome and reduced survival of patients. Several approaches have been developed for targeting this pathway, for example TKr inhibitors (AZD6918, CEP-701) and RNA interference. The aim of the current review was to provide an overview of the role of BDNF/TrkB pathways in the pathogenesis of breast cancer and its value as a potential therapeutic target. J. Cell. Biochem. 118: 2502-2515, 2017. © 2017 Wiley Periodicals, Inc.

Caspase 8 (CASP8) gene plays a key role in the regulation of apoptotic cell death. Expression variation in this gene has been associated with the risk of breast cancer. The aim of this study was to investigate the association of rs3834129 and rs3769821, as functional variants, and their haplotypes with molecular profile as well as the risk of breast cancer in an Iranian population. A case-control study was conducted on 812 participants including 293 breast cancer patients and 519 healthy controls. Genotyping was performed by polymerase chain reaction-based methods. Statistical analysis was performed using SPSS Ver16. The association between polymorphisms and haplotypes with the risk of breast cancer was estimated by calculating odds ratios (OR) and chi-square (χ2 ) tests. In comparison with ins allele (I) of rs3834129, carriers of del allele (D) showed a lower risk of breast cancer (OR, 0.65; 95% confidence interval [CI], 0.49-0.87; P = 0.004). The multivariate logistic regression model indicated DD genotype as an independent factor for a decreased risk of breast cancer in our population (OR, 0.18; 95% CI, 0.06-0.58; P = 0.004). Also, the C allele of rs3769821 was associated with a 43% increased risk of breast cancer (P = 0.005); however, after adjustment for confounding factors, no association with rs3769821 and breast cancer was observed. In addition, D-T haplotype and diplotype presented protective effects (P < 0.05). Our results indicate that genetic variations in the promoter region of CASP8 gene, especially rs3834129, may serve as a genetic risk factor for breast cancer in an Iranian population.

Background Introduction: Breast Cancer is one of the most common cancer in Iranian women. Whole genome association study of breast cancer have recognized various single nucleotide polymorphisms (SNPs) that are related with increased breast cancer risk in the population. This study aimed at assessing the correlation between caspase-8 (CASP8) gene polymorphisms (rs3754934 and rs12990906) and the pathogenesis of breast cancer in Northeast of Iran. Methods In a case- control study a total of 450 breast cancer cases and 553 healthy subjects were included in this study. Polymorphisms were genotyped by amplification-refractory mutation system (ARMS). The chi-squared test was used to calculate Odds ratio (OR) with 95% confidence interval to determine the relationship between CASP8 polymorphisms and breast cancer risk. Results According to the results, after adjustment for confounding factors, rs3754934 in dominant model (CA+AA vs. CC) [p = 0.004, OR = 0.49 95% CI (0.27-0.78)] and rs12990906 in allelic model (T vs. C) [p = 0.026, OR = 1.27, 95%CI (1.03-1.58)] were associated with the risk of breast cancer in this population. We did not find any association with breast cancer risk factors, clinical and pathologic features and prognosis and considered polymorphisms. Conclusions Polymorphisms of CASP8 gene may have a crucial role in association with the risk of breast cancer. However, further larger studies can confirm such findings. An understanding of the mode of action of these variants will aid individual-level breast cancer risk prediction. Legal entity responsible for the study Mashhad University of Medical Sciences. Funding Mashhad University of Medical Sciences. Disclosure All authors have declared no conflicts of interest.

Brain-derived neurotrophic factor (BDNF) is a potent neurotrophic factor that has been shown to stimulate breast cancer cell growth and metastasis via tyrosine kinase receptors TrkA, TrkB, and the p75

Background Breast cancer is the most common cancer among women in Iran and the world. Multiple environmental factors and genetic variations such as genetic polymorphisms are of its main causes. p53 gene plays an important role in conserving and sustaining the genome as a tumor suppressing gene. Change and polymorphism at codon 72 of p53 gene are correlated with increased risk of lung, mouth, endometrial, prostate, and colorectal cancers, and could be considered an indicator of susceptibility to breast cancer. Methods Twelve studies (1,190 cases and 1,145 control studies with evaluation of three types of Arg/Arg, Arg/Pro, and Pro/Pro genotypes) have been conducted using keywords, such as polymorphism at codon 72, gene p53 polymorphisms, and the relation between polymorphisms and breast cancer, from databases in Iran, including Magiran, Medlibe, Sid, and Iranmedex, as well as Latin databases such as PubMed, Google Scholar, Science Direct, and Scopus. Results The OR for Arg/Arg is 1.58 (95% CI: 2.45 to 1.01), the OR for Arg/Pro is 0.75 (95% CI: 1.10 to 0.51), and the OR for Pro/Pro is 0.62 (95% CI: 0.93 to 0.42). p53 gene polymorphism at codon 72 is statistically significant in Arg/Arg and Pro/Pro genotypes. Conclusions Arg/Arg genotype can be considered as a risk factor for breast cancer, and Pro/Pro genotype can be accounted for as a protective factor against breast cancer.

Background Breast cancer prognosis is influenced by several histopathology and clinical factors including expression of Ki67 which may have a predictive role in lymph node negative breast cancer patients. The aim of this study was to assess Ki67 expression in breast cancers without axillary lymph node involvement and to evaluate its prognostic value with regard to disease-free survival. Materials and methods Subjects were selected from non-metastatic invasive breast cancer patients who were referred to the oncology department of Ghaem hospital during 1 April 2001 to 1 April 2008. Ki67 levels were measured using immunohistochemistry (IHC) and compared with clinicopathological features. The relation of Ki67 expression with disease-free survival was also analysed. Results A total of 106 women with a mean age of 49 were examined. Some 94.3% were classified as having invasive ductal carcinomas and the mean tumour diameter at the time of diagnosis was 2.8 cm. Some 50.9% of cases were ER positive and 47.2% were PR positive. P53 expression was positive in 48.1% of the cases. According to the IHC results, only 8.5% of the patients were Her2/neu positive. Ki67 was positive in 66 (62.3%) with a significant relation to lower age (p=0.0229) and P53 positivity (p=0.005). After an average of 40-months follow up, 13 (12.3%) demonstrated recurrence, most commonly systemic. Of 13 cases with relapse, 10 patients (77%) were Ki67 positive. Conclusions In our population Ki67 appeared to be an independent prognostic factor for three-year survival. However, we stress that a survival study with a bigger sample size would help to support this conclusion.

Addendum: Amplification, Sequencing and Cloning of Iranian Native Bacillus subtilis Alpha-amylase Gene in Saccharomyces cerevisiae [published in Jundishapur J Microbiol. 2013;6(8):e7371] Fahimeh Afzal-Javan ; Mohsen Mobini-Dehkordi ; Behnaz Saffar 1,2 1Department of Genetics, Faculty of Science, University of Shahrekord, Shahrekord, IR Iran 2Research Institute of Biotechnology, University of Shahrekord, Shahrekord, IR Iran *Corresponding author: Mohsen Mobini-Dehkordi, Department of Genetics, Faculty of Science , University of Shahrekord, Shahrekord, IR Iran. Tel/Fax. +98-3814424419, E-mail: mmobinid@gmail.com

Background: Alpha-amylases are digestive enzymes which hydrolyze starch glycosidic bonds to glucose, maltose, maltotriose and dextrin which have diverse applications in a wide range of industries such as food, textile, paper, detergents representing approximately 30% of the world enzyme production. Objectives: In this study, the gene encoding the alpha-amylase enzyme of native isolated Bacillus subtilis was amplified with specific primers containing of NotI and AscI restriction sites by PCR and then sequenced. Purified PCR product and shuttle episomal vector p316TDH3 were cut by restriction enzymes and cloned into Escherichia coli and yeast hosts. Materials and Methods: The haploid auxotroph (ura3-) strain of S. cerevisiae and p316TDH3 were used as the host and vector for cloning and expression of the alpha amylase gene, respectively. In native Bacillus sp. the amyE gene without signal sequence was amplified with specific primers that introduced AscI and NotI restriction sites. After constructing the recombinant plasmid, it was transformed into E. coli competent cells. Then, colonies selection and confirmation were performed and the extracted plasmid was introduced to competent yeast cells using carrier sperm DNA. Recombinant yeast cells could grow on minimal media and produce extracellular enzyme. Results: The presence of alpha-amylase gene in recombinant bacteria was certificated by colony-PCR method. After extraction of recombinant vector from E. coli, the competent S. cerevisiae cells were transformed using polyethylene glycol and carrier sperm DNA. The recombinant yeast strains were screened by URA3 auxotrophic marker and analyzed for alpha-amylase gene existence. In the other hand, the amylase gene length of native B. subtilis was1887base pairs (bp) with an approximately93.65% similarity with standard bacterial strain. Conclusions: Based on this similarity and our bioinformatics evaluations, this mentioned alpha-amylase gene can be expressed in S. cerevisiae as extracellular enzyme.