Epidermal growth factor receptor (EGFR), cyclin D1 and KRAS proto-oncogene, GTPase (KRAS) genes serve roles in the occurrence and development of tumors. The aim of the current study was to investigate the expression levels of EGFR, cyclin D1 and KRAS in laryngocarcinoma tissues and their association with clinical features. In addition, correlation between the expression levels of EGFR, cyclin D1 and KRAS was analyzed in laryngocarcinoma tissues. The expression levels of EGFR, cyclin D1 and KRAS in 46 patients with laryngocarcinoma and 20 patients with vocal cord polyps as the control group were determined using Super Vision immunohistochemical staining assay kits. The differences in clinical and pathological parameters between groups were statistically analyzed using SPSS software version 16.0. The expression rates of EGFR, cyclin D1 and KRAS were 71.7, 52.2 and 39.1%, respectively in laryngocarcinoma tissues, and 10.0, 5.0 and 10.0%, respectively in vocal cord polyps. There was a positive correlation between the expression levels of EGFR, cyclin D1 and KRAS. The expression of these genes was also closely associated with the clinical stage, treatment response and prognosis of patients with laryngocarcinoma. Multivariate analysis of prognosis using the Cox regression model indicated that EGFR expression in laryngocarcinoma tissues and the clinical stage of patients with laryngocarcinoma were closely associated with patient prognosis. The results of the current study indicated that EGFR, cyclin D1 and KRAS were synergistically involved in the occurrence and development of laryngocarcinoma, directly affecting the prognosis of patients. Additionally, high expression of EGFR, cyclin D1 and KRAS facilitated the invasion and metastasis of laryngocarcinoma cells. The expression of EGFR in laryngocarcinoma tissues and clinical stage were two independent risk factors affecting the prognosis of patients.
The aim of the present study was to investigate the functional status of dendritic cells (DCs) in nasal polyps (NP) and their interactions with T lymphocytes. The interactions between DC and T lymphocytes in the pathogenesis of NP was also studied. The expression of cluster of differentiation (CD)1a and CD83 in NP was detected using immunohistochemistry and the ratio of CD83 DC/CD1a+DC was counted. The distribution of DCs in NP and normal inferior turbinate mucosa (nITM) was evaluated using double immunostaining (CD1a/CD40) and low illumination fluorescence microscopy. The number of CD1a+ cells, CD83+ cells and CD1a/CD40-dual positive cells in was significantly higher in NP tissues compared with nITM. Furthermore, the density of DCs observed in NP was significantly greater than that observed in nITM. The ratio of CD83 DC/CD1a+DC in NP was significantly higher compared with in nITM tissues. The results of the present study revealed significant infiltration of DCs in NP, with the majority being mature DCs. DCs are able to interact with T cells via the CD40/CD40L costimulatory factor, thus serving an important role in the development and progression of NP.
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