Mashhad, Iran
Mashhad, Iran

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Gholamin M.,Mashhad University of Medical Sciences | Moaven O.,Mashhad University of Medical Sciences | Farshchian M.,Mashhad University of Medical Sciences | Mahmoudi M.,Immunology Research Center | And 6 more authors.
BMC Cancer | Year: 2010

Background: Dendritic Cells (DC) are potent antigen presenting cells with the ability to prime naïve T cells and convert them to cytotoxic T-lymphocytes (CTL). We evaluated the capability of autologous DCs transfected with total tumor and normal RNA to induce cytotoxic CTL as the preliminary step to design a DC-based vaccine in the esophageal squamous cell carcinoma (ESCC).Methods: Monocytes-derived DCs were electroporated with either total tumor RNA or normal RNA. T cells were then primed with tumor RNA transfected DCs and lytic effects of the generated CTL were measured with Cytotoxicity assay and IFN-γ Release Elispot assay.Results: Cytotoxicity was induced against DCs loaded with tumoral RNA (%24.8 ± 5.2 SEM) while in normal RNA-loaded DCs, it was minimal (%6.1 ± 2.4 SEM) and significantly lower (p < 0.05). INF-γ secretion was more than 2-folds higher in tumoral RNA-loaded DCs when compared with normal RNA-loaded DCs (p < 0.05).Conclusion: Electroporating DCs with tumor RNA generated tumor antigen presenting cells which in turn enhanced cytotoxic effects of the T cells against ESCC. This may be a useful autologous ex vivo screening tool for confirming the lytic effects of primed T cells on tumors and evaluate probable further adverse effects on noncancerous tissues. These data provide crucial preliminary information to establish a total tumor RNA-pulsed DC vaccine therapy of ESCC. © 2010 Gholamin et al; licensee BioMed Central Ltd.


Taghavi N.,Iran National Institute of Genetic Engineering and Biotechnology | Taghavi N.,Tehran University of Medical Sciences | Biramijamal F.,Iran National Institute of Genetic Engineering and Biotechnology | Sotoudeh M.,Tehran University of Medical Sciences | And 6 more authors.
BMC Cancer | Year: 2010

Background: Tumor suppressor genes p53 and p16INK4aand the proto-oncogene MDM2 are considered to be essential G1 cell cycle regulatory genes whose loss of function is associated with ESCC carcinogenesis. We assessed the aberrant methylation of the p16 gene and its impact on p16INK4aprotein expression and correlations with p53 and MDM2 protein expressions in patients with ESCC in the Golestan province of northeastern Iran in which ESCC has the highest incidence of cancer, well above the world average.Methods: Cancerous tissues and the adjacent normal tissue obtained from 50 ESCC patients were assessed with Methylation-Specific-PCR to examine the methylation status of p16. The expression of p16, p53 and MDM2 proteins was detected by immunohistochemical staining.Results: Abnormal expression of p16 and p53, but not MDM2, was significantly higher in the tumoral tissue. p53 was concomitantly accumulated in ESCC tumor along with MDM2 overexpression and p16 negative expression. Aberrant methylation of the p16INK4agene was detected in 31/50 (62%) of esophageal tumor samples, while two of the adjacent normal mucosa were methylated (P < 0.001). p16INK4aaberrant methylation was significantly associated with decreased p16 protein expression (P = 0.033), as well as the overexpression of p53 (P = 0.020).Conclusions: p16 hypermethylation is the principal mechanism of p16 protein underexpression and plays an important role in ESCC development. It is associated with p53 protein overexpression and may influence the accumulation of abnormally expressed proteins in p53-MDM2 and p16-Rb pathways, suggesting a possible cross-talk of the involved pathways in ESCC development. © 2010 Taghavi et al; licensee BioMed Central Ltd.


Delirezh N.,Urmia University | Majedi L.,Urmia University | Rezaei S.A.,Urmia University | Ranjkeshzadeh H.,Omid Hospital
Iranian Biomedical Journal | Year: 2011

Background: Dendritic cells (DC) induce tumor or pathogen-specific T cell responses in humans. Several laboratories have developed culture systems, including maturation factors for human DC from peripheral blood monocytes. We comprehensively compared standard maturation stimulus, an autologous monocyte-conditioned medium (MCM), with heparin for their ability to promote uniformly mature DC that elicit T cell responses. Methods: A short (4-day) priming of plastic adherent monocytes with granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-4 with or without heparin was followed by 48-hour incubation in MCM to generate fully mature and stable DC. Phenotypic and functional analyses were carried out using anti-CD14 and anti-CD83 monoclonal antibodies, and mixed lymphocyte reaction, respectively. Results: We found that fully matured DC with a large amount of cytoplasm and copious dendritic projections were visible at the end of culturing period in the presence of MCM, heparin and MCM plus heparin. Thus, DC generated with these maturation factors are nonadherent and have typical satellite morphology. Flow cytometric analysis using anti-CD14 (monocyte marker) and anti-CD83 (mature DC marker) revealed that expression of CD14 decreased in MCM plus heparin-treated DC, and the expression of CD83 was increased when heparin and MCM used as a maturation factor. Functionally, MCM and MCM plus heparin-treated DC showed stronger mixed leukocyte reaction than heparin alone. Conclusion: These results support the use of the MCM with heparin as maturation factor that could result in functionally mature monocyte-derived DC in comparison to either MCM or heparin alone.


Forghanifard M.M.,Islamic Azad University at Tehran | Forghanifard M.M.,Mashhad University of Medical Sciences | Gholamin M.,Mashhad University of Medical Sciences | Farshchian M.,Mashhad University of Medical Sciences | And 9 more authors.
Cancer Biology and Therapy | Year: 2011

Cancer-testis antigens (CTAs) are often specifically expressed in cancer cells and under normal conditions are only considered to be expressed in the germ line cells and the placenta. CTAs are potential targets for cancer immunotherapy and therefore necessitates their expression profiling. The expression profile of LAGE1, MAGE-A4 and NY-ES O1, their possible correlations and interaction, and the clinicopathological associations of each marker were studied. RNA was extracted from fresh esophagectomy tissues of 41 esophageal squamous cell carcinoma (ES CC) patients prior to any other therapeutic intervention. The relative mRNA expression of LAGE1, MAGE-A4 and NY-ES O1 was assessed with the real-time reverse transcription-polymerase chain reaction (RT-PCR) 5′ nuclease assay. The overexpression of LAGE1, MAGE-A4 and NY-ES O1 was found in 39, 90.2 and 41.4% of ES CC samples respectively. Of the patients, 97.5% showed an overexpression of at least one CTA. The relative expression of MAGE-A4 was directly associated with lymph node metastasis and the stage of the tumor (p < 0.05). A significant direct correlation was also detected between the MAGE-A4/LAGE1 and MAGE-A4/NY-ES O1 levels of gene expression. MAGE-A4 is identified as a specific biomarker of ES CC with a possible oncogenic role contributing to tumor progression. Interactions between MAGE-A4, LAGE1 and NY-ES O1 and their significant clinical consequences introduce these CTAs as appropriate targets for a polyvalent cancer vaccine. © 2011 Landes Bioscience.


Ghorbani N.,Mazandaran University of Medical Sciences | Cherati J.Y.,Mazandaran University of Medical Sciences | Anvari K.,Mashhad University of Medical Sciences | Ghorbani N.,Omid Hospital
Journal of Mazandaran University of Medical Sciences | Year: 2015

Background and purpose: The aim of this study was to estimate the disease-free survival rate, in female patients with breast cancer and determining the level of influencing factors. Materials and methods: In a retrospective cohort study, the records of 377 patients attending Mashhad Omid hospital, Iran, spanning the years 2006 to 2011 were selected using convenience sampling. The patients were followed up until April 2014. Data analyses were done in SAS (ver.9.3) applying Cox’s semi-parametric regression method. The time after surgery until first recurrence or metastasis was considered as the dependent variable. Results: From 377 patients (mean age: 49 years) 249 (0.66%) were found to have no any metastasis, while 128 (34%) had metastasis. Using Kaplan-Meier’s nonparametric method, the probability of the disease-free survival in 2920 days (8 years) follow-up was estimated to be 52.5% (mean time: 6 years and 3 months). There were significant differences between disease-free survivals in different tumor sizes and the involved lymph nodes and type of invasive breast cancer Also, increase of recur risk or metastasis was found to be associated with increases in size of tumor, in number of involved lymph nodes and in the level of cancer anti-gene CA 15-3 before first recur. The hazard ratio of the chance of metastasis occurrence while controlling other variables increased 19% against per unit increase in the size of tumor, 10% per involved number of lymph nodes, and 0.6% per unit increase in CA 15-3 antigen. Conclusion: The CA 15-3 antigen was determined as the prognostic factor for occurrence of metastasis alongside tumor size and the number of involved nodes. © 2015, Mazandaran University of Medical Sciences. All rights reserved.


Toussi M.S.,Omid Hospital | Bagheri R.,Mashhad University of Medical Sciences | Anvari K.,Omid Hospital | Sheibani S.,Mashhad University of Medical Sciences
Asian Cardiovascular and Thoracic Annals | Year: 2013

Background: For patients with lung metastases from soft-tissue sarcoma, pulmonary metastasectomy is considered to be the only chance of possible cure. In this survey, we analyzed some potential prognostic factors affecting the outcome in these patients. Patients and methods: 34 patients who underwent pulmonary metastasectomy for soft-tissue sarcoma from April 1996 to April 2007, were enrolled in our study. The median follow-up period was 26 months. Survival curves, factors affecting the outcome, and treatment success rate were evaluated. Results: Complete resection was achieved in 88.2% of patients. There was no perioperative mortality. The median overall survival and median disease-free survival were 42 and 27 months, respectively. Incomplete resection and bilateral lung metastases had significant adverse effects on overall survival. Shorter disease-free interval (<18 months) was a significant predictor of survival on multivariate analysis. Metastasectomy was attempted in 12 cases of whom 50% remained disease-free to the end of follow-up. Conclusion: Complete resection is the most important defining factor of success rate and survival. Patients with bilateral lung metastases or a shorter disease-free interval have significantly lower success rates. Repeat metastasectomy is curative in many patients. © 2012 The Author(s).


Rostami A.,Mashhad University of Medical Sciences | Toossi M.T.B.,Mashhad University of Medical Sciences | Sazgarnia A.,Mashhad University of Medical Sciences | Soleymanifard S.,Mashhad University of Medical Sciences | Soleymanifard S.,Omid hospital
Radiation and Environmental Biophysics | Year: 2016

Due to biocompatibility and relative non-toxic nature, gold nanoparticles (GNPs) have been studied widely to be employed in radiotherapy as radio-sensitizer. On the other hand, they may enhance radiation-induced bystander effect (RIBE), which causes radiation adverse effects in non-irradiated normal cells. The present study was planned to investigate the possibility of augmenting the RIBE consequence of applying glucose-coated gold nanoparticles (Glu-GNPs) to target cells. Glu-GNPs were synthesized and utilized to treat MCF7 and QUDB cells. The treated cells were irradiated with 100 kVp X-rays, and their culture media were transferred to non-irradiated bystander cells. Performing MTT cellular proliferation test and colony formation assay, percentage cell viability and survival fraction of bystander cells were determined, respectively, and were compared to control bystander cells which received culture medium from irradiated cells without Glu-GNPs. Glu-GNPs decreased the cell viability and survival fraction of QUDB bystander cells by as much as 13.2 and 11.5 %, respectively (P < 0.02). However, the same end points were not changed by Glu-GNPs in MCF-7 bystander cells. Different RIBE responses were observed in QUDB and MCF7 loaded with Glu-GNPs. Glu-GNPs increased the RIBE in QUDB cells, while they had no effects on RIBE in MCF7 cells. As opposed to QUDB cells, the RIBE in MCF7 cells did not change in the dose range of 0.5–10 Gy. Therefore, it might be a constant effect and the reason of not being increased by Glu-GNPs. © 2016 Springer-Verlag Berlin Heidelberg


Toossi M.T.B.,Mashhad University of Medical Sciences | Mohebbi S.,Mashhad University of Medical Sciences | Samani R.K.,Mashhad University of Medical Sciences | Soleymanifard S.,Mashhad University of Medical Sciences | Soleymanifard S.,Omid Hospital
Journal of Medical Physics | Year: 2014

Radiation damages initiated by radiation-induced bystander effect (RIBE) are not limited to the first or immediate neighbors of the irradiated cells, but the effects have been observed in the cells far from the irradiation site. It has been postulated that bystander cells, by producing bystander factors, are actively involved in the propagation of bystander effect in the regions beyond the initial irradiated site. Current study was planned to test the hypothesis. MRC5 and QU-DB cell lines were irradiated, and successive medium transfer technique was performed to induce bystander effects in two bystander cell groups. Conditioned medium extracted from the target cells was transferred to the bystander cells (first bystander cells). After one hour, conditioned medium was substituted by fresh medium. Two hours later, the fresh medium was transferred to a second group of non-irradiated cells (second bystander cells). Micronucleated cells (MC) were counted to quantify damages induced in the first and second bystander cell groups. Radiation effect was observed in the second bystander cells as well as in the first ones. Statistical analyses revealed that the number of MC in second bystander subgroups was significantly more than the corresponding value observed in control groups, but in most cases it was equal to the number of MC observed in the first bystander cells. MRC5 and QU-DB bystander cells can produce and release bystander signals in the culture medium and affect non-irradiated cells. Therefore, they may contribute to the RIBE propagation. © 2014 Journal of Medical Physics.


Forghanifard M.M.,Islamic Azad University at Tehran | Forghanifard M.M.,Islamic Azad University at Dāmghān | Moaven O.,Harvard University | Farshchian M.,Mashhad University of Medical Sciences | And 7 more authors.
Annals of Surgical Oncology | Year: 2012

Background. Epithelial-mesenchymal transition has recently attracted great attention in studying the malignant progression of cells through a converging pathway of oncogenesis and metastasis. Twist1 and Mastermind-like 1 (MAML1) are major regulators of EMT through different pathways. The aim of this study was to investigate the clinicopathological relevance of the expression of MAML-1 and Twist1 genes in esophageal squamous cell carcinoma (ESCC). Methods. Tumoral and corresponding normal tissues from 55 treatment-naive ESCC patients were subjected for expression analysis with quantitative real-time RT-PCR. Results. Overexpression of MAML-1 and Twist1 were significantly associated with lymph node metastasis and the surgical staging of tumor. Overexpression of Twist1 was associated with tumor depth of invasion. Mean relative expression (MRE) of MAML1 was significantly higher in patients with metastasis to lymph nodes (3.07 ± 0.51 vs. 0.86 ± 0.58, P = .008). MRE of Twist1 was significantly higher in patients with invasion of tumor to adventitia (T3, T4) (1.97 ± 0.29 vs. 0.39 ± 0.73, P = .036). In advanced stages of tumor (stage III, IV), a significantly higher MRE of Twist1 (2.47 ± 0.41 vs. 1.25 ± 0.36, P = .035) and MAML1 (3.05 ± 0.45 vs. 1.07 ± 0.59, P = .021) mRNA was observed. Conclusions. We introduce Twist1 and MAML1 as new molecular markers of advanced tumor, which determine the characteristics and aggressive behavior of ESCC. Along with the emerging evidence of their role in different cellular processes and aberrations in various cancers, they are suggested as potentially interesting therapeutic targets to reverse a broad spectrum of functional aberrations that promote ESCC development. © Society of Surgical Oncology 2011.


PubMed | Omid Hospital
Type: Journal Article | Journal: Asian cardiovascular & thoracic annals | Year: 2014

For patients with lung metastases from soft-tissue sarcoma, pulmonary metastasectomy is considered to be the only chance of possible cure. In this survey, we analyzed some potential prognostic factors affecting the outcome in these patients.34 patients who underwent pulmonary metastasectomy for soft-tissue sarcoma from April 1996 to April 2007, were enrolled in our study. The median follow-up period was 26 months. Survival curves, factors affecting the outcome, and treatment success rate were evaluated.Complete resection was achieved in 88.2% of patients. There was no perioperative mortality. The median overall survival and median disease-free survival were 42 and 27 months, respectively. Incomplete resection and bilateral lung metastases had significant adverse effects on overall survival. Shorter disease-free interval (<18 months) was a significant predictor of survival on multivariate analysis. Metastasectomy was attempted in 12 cases of whom 50% remained disease-free to the end of follow-up.Complete resection is the most important defining factor of success rate and survival. Patients with bilateral lung metastases or a shorter disease-free interval have significantly lower success rates. Repeat metastasectomy is curative in many patients.

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