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      Multi-Gene Expression in Anthracosis of the Lungs as One of the Risk Factors for Non-Small Cell Lung Cancer

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          Abstract

          Background:

          Anthracosis of the lung occurs due to the deposition of carbon and silica in the mucosa and submucosa, manifested as black lesions. The association of anthracosis with lung cancer has remained to be clearly elucidated The current study aimed to assess the P16, CDH1 and LUNX genes expression level to evaluate the association of anthracotic lesions in the lungs with the occurrence of non-small cell lung cancer.

          Methods:

          Forty biopsy samples were taken from the center and 40 from the margins of black anthracotic lesions in the lungs; RNA was extracted from the samples and cDNA was synthesized. Real-time reverse-transcription polymerase chain reaction (RT-PCR) was performed to assess the expression of P16, CDH1 and LUNX genes. All steps were performed in triplicate.

          Results:

          A significant reduction in P16 gene expression was noted at the center compared to the margins of the lesions (P<0.001).expression level of CDH1 at the center of lesions was significantly lower than margins (P<0.001). However, LUNX gene had significantly higher expressionlevel at the center compared to margins (P<0.001).

          Conclusion:

          Decreased expression of P16 and CDH1 and increased expression of LUNX tumor genes were noted at the center of anthracotic lesions. Significant increase in expression of LUNX gene in NSCLC indicates an association between anthracosis and NSCLC, according to which, anthracotic patients may carry a high risk for NSCLC.

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          Most cited references33

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          Ovarian cancer metastasis: integrating insights from disparate model organisms.

          Despite considerable efforts to improve early detection, and advances in chemotherapy, metastasis remains a major challenge in the clinical management of ovarian cancer. Studies of new murine models are providing novel insights into the pathophysiology of ovarian cancer, but these models are not readily amenable to genetic screens. Genetic analysis of border-cell migration in the Drosophila melanogaster ovary provides clues that will improve our understanding of ovarian cancer metastasis at the molecular level, and also might lead to potential therapeutic targets.
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            Carbonic anhydrase IX in oligodendroglial brain tumors

            Background Carbonic anhydrase IX is a hypoxia-induced enzyme that has many biologically important functions, including its role in cell adhesion and invasion. Methods This study was set out to investigate the role of CA IX in a series of 86 oligodendroglial brain tumors (71 primary and 15 recurrent; 48 pure oligodendrogliomas and 40 mixed oligoastrocytomas). Results 80% of the tumors showed CA IX expression by immunohistochemistry. Tumors with moderate or strong CA IX expression had decreased level of cell proliferation compared to weak or no CA IX expression (median 2.9 vs. 5.8, p = 0.015). CA IX correlated with two antioxidative enzymes, manganese superoxide dismutase (MnSOD) and regulatory gammaglutamylcysteine synthetase (GLCL-R): CA IX expression was significantly higher in MnSOD-positive tumors (p = 0.008) and decreased in GLCL-R-positive tumors (p = 0.044). In Cox multivariate analysis CA IX expression, patient age and histological component (pure oligodendroglioma vs. mixed oligoastrocytoma) showed independent prognostic values (p = 0.009, p = 0.003 and p = 0.022, respectively), CA IX positivity predicting poorer outcome. Conclusion CA IX was proved to be an independent prognostic indicator in oligodendroglial brain tumors, and it also correlates reversely with cell proliferation. It may have a role in the biology of oligodendrogliomas, and most interestingly, as it is mainly expressed in tumor tissue, CA IX could serve as a target molecule for anticancer treatments.
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              Persistent E-cadherin expression in inflammatory breast cancer.

              E-cadherin is a transmembrane glycoprotein that mediates epithelial cell-to-cell adhesion. Because loss of E-cadherin expression results in disruption of cellular clusters, it has been postulated that E-cadherin functions as a tumor suppressor protein. The role of E-cadherin in inflammatory breast cancer (IBC), a distinct and highly aggressive form of breast cancer, is largely unknown. The aim of our study was to elucidate whether E-cadherin expression contributes to the development and progression of the IBC phenotype and to investigate any differences in E-cadherin expression between IBC and stage-matched non-IBC. Forty-two breast cancer cases (20 IBC and 22 non-IBC) were identified. Strict and well-accepted criteria were used for the diagnosis of IBC. Clinical and pathologic features were studied, and formalin-fixed, paraffin-embedded tissue sections were immunostained for E-cadherin, estrogen and progesterone receptors (ER and PR, respectively), and HER2/neu. Statistical analysis was performed using Fisher's exact test. All IBC uniformly expressed E-cadherin, whereas 15 of the 22 (68%) of the non-IBC expressed the protein (P = .006). Intralymphatic tumor emboli in the IBC cases were also all E-cadherin positive. Two IBC tumors demonstrated invasive lobular histology, and both cases were positive for E-cadherin. Of the non-IBC cases, three were invasive lobular carcinomas, and all were positive for E-cadherin. No association was found between E-cadherin expression and ER, PR status, or HER2/neu overexpression. Our study demonstrates that there is a strong association between E-cadherin expression and IBC and suggests that E-cadherin may be involved in the pathogenesis of this form of advanced breast cancer. In our study, we demonstrate that circulating IBC tumor cells strongly express E-cadherin, thereby providing an important exception to the positive association between E-cadherin loss and poor prognosis in breast cancer.
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                Author and article information

                Journal
                Asian Pac J Cancer Prev
                Asian Pac. J. Cancer Prev
                Asian Pacific Journal of Cancer Prevention : APJCP
                West Asia Organization for Cancer Prevention (Iran )
                1513-7368
                2476-762X
                2017
                : 18
                : 11
                : 3129-3133
                Affiliations
                [1 ] Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Tehran, Iran
                [2 ] Craniomaxillofacial Research Center, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran
                [3 ] Oral and Maxillofacial Surgery Department, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran
                [4 ] Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Tehran, Iran
                [5 ] Tobacco Prevention and Control Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Tehran, Iran
                [6 ] Tracheal Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Tehran, Iran
                [7 ] Department of Physiology, Faculty of Basic Sciences, Hamedan Branch, Islamic Azad University, Hamedan, Iran
                [8 ] Virology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Tehran, Iran
                [9 ] Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                Author notes
                [* ] For Correspondence: mohamadnia.ar@ 123456gmail.com
                Article
                APJCP-18-3129
                10.22034/APJCP.2017.18.11.3129
                5773802
                29172290
                f32cdd75-5252-4669-ab2b-c9ed533e5a74
                Copyright: © Asian Pacific Journal of Cancer Prevention

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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                Research Article

                p16- cdh1- lunx- anthracotic- non,small cell lung cancer

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