Pulmonary Pathology
Sotoudeh Mohammadi; Mitra Rezaei; Fatemeh Shojaeian; Mihan Pourabdollah; Leila Mohammadi Ziazi; Sharareh Seifi; Atousa Doroodinia; Babak Salimi; Adnan Khosravi; Mohammad Amin Farhangnasab
Abstract
Background & Objective: Various studies showed the use of epidermal growth factor receptors (EGFRs) gene mutations in the therapeutic plan of patients with advanced lung cancer. This study aimed to investigate the frequency and types of EGFR gene mutations among Iranian patients with lung adenocarcinoma ...
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Background & Objective: Various studies showed the use of epidermal growth factor receptors (EGFRs) gene mutations in the therapeutic plan of patients with advanced lung cancer. This study aimed to investigate the frequency and types of EGFR gene mutations among Iranian patients with lung adenocarcinoma referred to a specialized lung diseases hospital from 2014 to 2019.Methods: The data of all patients with lung adenocarcinoma referred to the Molecular Department of Masih Daneshvari Hospital Laboratory (National Research Institute of Tuberculosis and Lung Diseases) from 2014 to 2019 for EGFR mutation tests were collected. Patients' characteristics data and information on the frequency and types of EGFR gene mutations were obtained from the hospital information system (HIS). The collected data were analyzed using SPSS 25.Results: A total of 570 individuals (Mean age of 58.74, 51.6% Male) were included in the study; 113 out of 570 patients (19.8%) were diagnosed with gene mutation. In terms of the type of mutation, 65 participants (57%) showed deletion, 48 patients (42.1%) were diagnosed with replacement, and one (0.9%) case demonstrated both. Notably, the mutation rate detected among the female patients was significantly higher than the male ones (P=0.001); in particular, deletion type of mutation was found more among women, although both genders were the same in terms of the replacement frequency. However, the age had no effect on the mutation in this study (P=0.05).Conclusion: Among Iranian patients with lung adenocarcinoma, 19.8% harbored EGFR gene mutation. This mutation was found in association with lung cancer and could affect the patient's therapeutic plan.
Oral Pathology
Mehdi DehghanNezhad; Noushin Jalayer Naderi; Hasan Semyari
Abstract
Background & Objective: Micronucleus assay of buccal mucosa cells is a simple bio- monitoring method for diagnosing the genetic damages of toxic agents. The aim was to study the genotoxic effect of waterpipe smoking on buccal mucosa cells using micronucleus assay. Methods: This was a case control. ...
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Background & Objective: Micronucleus assay of buccal mucosa cells is a simple bio- monitoring method for diagnosing the genetic damages of toxic agents. The aim was to study the genotoxic effect of waterpipe smoking on buccal mucosa cells using micronucleus assay. Methods: This was a case control. A total of 30 male waterpipe smokers and 30 non-smokers were included in the study. The exfoliated buccal mucosa cells were scrapped using wooden spatula and were spread over glass slides. The mean number of micronuclei was determined using Feulgen-stained slides. The number of micronuclei per 1000 cells was calculated and compared between the two groups of smokers and non-smokers. Result: The mean number of micronuclei in waterpipe smokers and non-smokers was 1.94±0.39 and 1.68±0.35, respectively. The micronuclei count in waterpipe smokers was significantly higher than non-smokers (P=0). The difference between the number of waterpipe smoking and micronuclei count was significantly different (P=0). Conclusion: The mean number of micronuclei in buccal mucosa cells of waterpipe smokers was significantly higher than non-smokers. The genotoxicity effect of waterpipe was dose-dependent.
Noushin Jalayer Naderi
Abstract
Dear Editor, Cigarette smoking has destructive effect on periodontal tissue. The rates of loss of periodontal attachment and recession of gingival are higher in smokers than non-smokers (1-2). Previous studies on the inflammatory immune responses in smokers’ periodontitis have mainly focused on ...
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Dear Editor, Cigarette smoking has destructive effect on periodontal tissue. The rates of loss of periodontal attachment and recession of gingival are higher in smokers than non-smokers (1-2). Previous studies on the inflammatory immune responses in smokers’ periodontitis have mainly focused on the role of neutrophils. Tumor necrosis factor–α, prostaglandin E2 and matrix metalloproteinase-8 have been shown to rise in smokers with periodontitis (3-4). Different functions of mast cells and eosinophils in inflammatory immune responses make them distinctive cells in disease pathogenesis (5-6). In an investigation, our team examined the effect of smoking on mast cells density in chronic periodontitis. The study showed that the mean number of mast cells in smokers was significantly lower compared to the non-smokers. Based on the literature, no research was found regarding the effect of cigarette smoking on eosinophil cells in human periodontitis. Eosinophils and mast cells regulate the hypersensitivity reactions by affecting each other function (5). Thus, in the next study, we examined this issue on the same samples. The results revealed that the number of eosinophil count in smokers was significantly lower than non-smokers. Considering the findings of both studies on decreased number of mast cells and eosinophils in the same samples, it seems that cigarette smoke had an apoptotic function on extra-vascular immune inflammatory related cells in human periodontitis. According to our opinion, with the death of mast cells and eosinophils, a cascade of different events occurs in the microenvironment of gingiva which causes more tissue damage in the smokers. The apoptotic effect of cigarette smoke on gingival connective tissue must be studied in the enzymatic level.The Heme Oxygenase-1 (HO-1)/Carbon Monoxide (CO) system demand to explain the pathogenesis of diseases by using the basic metabolism and enzymatic activities. HO-1 has a regulatory action on inflammatory signaling programs. CO is an end-product of HO-1. CO affects the apoptosis and cellular inflammation by modulating the inflammatory related cytokines. Modulating the HO-1 and application of CO-releasing molecules are new therapeutic strategies in inflammatory diseases (7). Based on our previous findings, we suggest that further study on HO-1/CO can probably determine the effect of cigarette smoke on inflammatory immune cells in human chronic periodontitis. The system can be potentially considered as a therapeutic target in inflammatory disease of periodontium in cigarette smokers. Conflict of Interest The authors declared no conflict of interest regarding the publication of this article.