Introduction: The proto-oncogene HER2 plays a key role in the control of cellular proliferation. Its overexpression has been reported to be associated with a poor prognosis in cancer, particularly in breast cancer.Materials and Methods: In the present study, serum HER2 levels were investigated in patients diagnosed with Epithelial ovarian cancer. Serum HER2 levels were detected by an ELISA commercial kit in 51 patients and 33 healthy individuals.Results: The mean serum HER2 level was found to be significantly higher in patients than healthy controls (P=0.005). In 29% of patients, serum HER2 levels were higher than the cut-off value. HER2 serum level was not associated with tumor stage at diagnosis.Conclusion: Elevation of HER2 in a high proportion of patients with Epithelial ovarian cancer further strengthens the importance of this molecule in the pathogenesis of ovarian cancer.

Background: ovarian cancer is the most common fatal gynecologic malignancy in women. The BRCA2 gene has a role in regulation of cell cycle during proliferation, differentiation and DNA repair. Changes in the methylation of BRCA2 may be an effective mechanism for ovarian cancer.Objectives: The aim of the present study was to evaluate the association between ovarian cancer and methylation status of BRCA2.Materials and Methods: In this study, methylation changes of BRCA2 genes in 44 tissue samples from patients with ovarian cancer and 44 adjacent normal ovarian tissue samples were studied as the control group. After primer design and amplification of the BRCA2 gene sequence by the Polymerase Chain Reaction (PCR), gene methylation levels were evaluated using an enzymatic digestion method, Restriction Fragment Length Polymorphism (RFLP).Results: According to the study of the methylation status of subjects, status changes were observed only in three cases. The results did not show a correlation between BRCA2 gene promoter methylation in ovarian cancer patients and healthy subjects.Conclusions: According to the results obtained in this study, changes in the methylation status of BRCA2 cannot be the decisive factor to ascertain the development of ovarian cancer.

Introduction: Hypodontia is the congenital absence of one or more deciduous and/or permanent teeth. Hypodontia is the most common developmental anomaly in humans and is frequently associated with several other oral abnormalities. Tooth agenesis is correlated to the DNA–binding capacity of the mutated PAX9 proteins, which supports this hypothesis that DNA binding is responsible for the genetic defects. Objective: Genetic analysis of the genes of interest is necessary to explore similarities between hypodontia and the other abnormalities in other parts of the body such as Epithelial ovarian cancer (EOC). An association could allow hypodontia to serve as a potential risk marker for EOC.Materials and Methods: In this case, controlled study, 21 subjects with EOC and 24 control subjects that did not have EOC were evaluated.Clinical, dental and radiographic examination performed on each subject to detect hypodontia. To do statistical analysis ANOVA and chi-square tests were used.Results: The kind of hypodontia was similar between the two groups. Lateral incisors of maxilla and second premolars of mandible and maxilla were the most affected teeth. The prevalence of hypodontia was 21% for EOC patients and 3% for control patients. This difference implied that women with EOC are 7 times more likely to have hypodontia compare with women without EOC (CI 95%: 1.79-23.44).Conclusion: Hypodontia of the permanent dentition and EOC had statistical association. Genetic analysis of PAX9 gene is the next step in this research to survey and explore similarities between EOC and hypodontia is recommended. Hypodontia has a potential risk marker for EOC.

Background: EOC is one of the most lethal gynecological malignancy worldwide. Although the majority of EOC patients achieve clinical remission after induction therapy, over 80% relapse and succumb to the chemoresistant disease. Previous investigations have demonstrated the association of EGFR with resistance to cytotoxic chemotherapies, hormone therapy, and radiotherapy in the cancers. These studies have highlighted the role of EGFR as an attractive therapeutic target in cisplatin-resistant EOC cells. Methods: The human ovarian cell lines (SKOV3 and OVCAR3) were cultured according to ATCC recommendations. The MTT assay was used to determine the chemosensitivity of the cell lines in exposure to cisplatin and erlotinib. The qRT-PCR was applied to analyze the mRNA expression of the desired genes. Results: Erlotinib in combination with cisplatin reduced the cell proliferation in the chemoresistant EOC cells in comparison to monotherapy of the drugs (p < 0. 05). Moreover, erlotinib/cisplatin combination synergistically decreased the expression of anti-apoptotic and also increased proapoptotic genes expression (p < 0. 05). Cisplatin alone could increase the expression of MDR genes. The data suggested that EGFR and cisplatin drive chemoresistance in the EOC cells through MEKK signal transduction as well as through EGFR/MEKK pathways in the cells, respectively. Conclusion: Our findings propose that EGFR is an attractive therapeutic target in chemoresistant EOC to be exploited in translational oncology, and erlotinib/cisplatin combination treatment is a potential anti-cancer approach to overcome chemoresistance and inhibit the proliferation of the EOC cells.