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• W1499688817 abstract "The aim of my thesis was an example of human renal cell carcinoma to investigate the Makrophageninfiltrate terms of their distribution and density of occurrence of hypoxia and the possible influence on the expression and function of iNOS. Furthermore, the morphological relationship between vascular density, hypoxia and spontaneous tumor necrosis was characterized. Also played a large role in the investigation of the expression of nitric oxide, especially of iNOS, taking into account the α-actinin-4 expression, the Stickstoffmonoxidsynthasefunktion and hypoxia.Renal cell carcinoma was used as a tumor model, because it belongs both to the most heavily infiltrated by immune cells, tumors and other sharply defined against the tumor-free normal kidney tissue. In addition, the vessels are formed within the tumor neoangiogenesis all about.Renal cell carcinomas were examined 23 nephrectomized patients, including 16 men and seven women, with an average age at surgery of about 67 years.A subdivision of the tumors occurred in the histological qualification, the degree of malignancy, organ or tumor stage, presence of necrosis and tumor size.The quantification of Makrophageninfiltrate was morphometrically by light microscopy using CD68-stained tissue sections by immunohistochemistry. It was found that tumors recruit statistically with necrosis, depending on the histological grade of malignancy, in contrast to tumors without necrosis, significantly more CD68-positive macrophages, which accumulate in particular perinekrotischen border.For evaluation of tissue hypoxia in carcinoma of the morphological relationship between vascular density, hypoxic areas and presence of necrosis were characterized. The vessel distances were measured on computer-assisted CD31 immunohistochemically stained tissue sections. Hypoxic areas were shown by immunohistochemistry using HIF-1α and with the assistance of the IRS evaluated by light microscopy. Necrosis were computer assisted using H.-E.-stained tissue sections determined. The present results show that significantly increases the vascular necrosis increased distances. He also showed that HIF-1α was expressed in both tumor-free normal kidney tissue as well as diffusely in the tumor. Only in some carcinomas perinekrotisch a corresponding upregulation could be observed.A second observation is that HIF-1α is expressed in both tumor-free normal kidney tissue as well as diffusely in the tumor. However, a corresponding upregulation perinekrotisch could be observed in some cancers.The expression of nitric oxide synthase, iNOS was specifically taking into account the α-actinin-4 expression at the protein level determined by immunohistochemistry and evaluated by light microscopy according to the IRS. Moreover, the determination of relative mRNA expression of iNOS and α-actinin-4 on the basis of quantitative RT-PCR. The nitrite content in the tumor and tumor-free kidney normal tissue was determined by Griess reaction and served as proof of the Stickstoffmonoxidsynthasefunktion.iNOS was expressed at the protein level in the tumor compared to normal kidney tumor-free tissue significantly increased, regardless of the incidence of necrosis. In the α-actinin-4 expression is in sharp contrast, no significant also vary significantly from the mRNA level could still be detected in iNOS-α-actinin-4 expression was a significant difference in either the. eNOS was expressed in perinekrotischen Tumorendothelien significantly reduced. Nitrotyrosine was expressed in both tumor and normal tissue in tumor-free kidneys appeared diffuse and thus neither the incidence nor the degree of tumor necrosis and the associated hypoxic areas correlate. The nitrite concentration was significantly increased in Tumorwebe, but significantly reduced in tumors with necrosis compared with tumors without necrosis.Summarizing the data, then one shows the relationship between a decreased vascular density, the presence of tumor necrosis and an increased Makrophageninfiltrat. Renal cell carcinoma has a higher density specially on infiltration of TAM accumulate perinekrotisch. Inhibited by the prevailing there hypoxia in their tumor cytotoxicity, the cells are still able to attack specifically the vasculature and in the course of tumor growth, vascular regression and ultimately to induce tumor hypoxia, because the supply of the tumor can not be maintained. Other tumor necrosis are the result, which in turn recruited macrophages. The cells thus modulate the one hand, the stroma but also promote tumor cell growth or development hypoxiestabiler, metastasis viable cell clones. HIF-1α is in renal cell carcinoma is not a reliable Hypoxiemarker opinions expressed in some carcinomas perinekrotische observed upregulation suggests that in these tumors, HIF-1α as a result of mutations in the VHL gene is not expressed and therefore degrades relatively strong. Under hypoxia, the activity of nitric oxide, especially of iNOS, suppressed, whereas the expression of iNOS and -actinin-4 is not affected. Main reason for this seems to be a dissociation of α-actinin-4 binding to be mediated to the cytoskeleton. Secretion of cytotoxic concentrations of nitric oxide is prevented under hypoxia. The aim of further investigations must be to substantiate the hypothesis of vascular regression, experimental morphology and to identify the inducers of regression." @default.
• W1499688817 created "2016-06-24" @default.
• W1499688817 creator A5029607997 @default.
• W1499688817 date "2022-02-20" @default.
• W1499688817 modified "2023-09-25" @default.
• W1499688817 title "Makrophageninfiltration, Hypoxie und Stickstoffmonoxidsynthasen im humanen Nierenzellkarzinom" @default.
• W1499688817 doi "https://doi.org/10.53846/goediss-1128" @default.
• W1499688817 hasPublicationYear "2022" @default.
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