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Версія від 06:11, 25 грудня 2016, створена Iranchild1 (обговореннявнесок) (Створена сторінка: The remaining control cases showed a high score of immunoreactivity for CK34bE12, while negative or low for CK5, CD44 and p63. In conclusion, immunoreactivity C...)

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The remaining control cases showed a high score of immunoreactivity for CK34bE12, while negative or low for CK5, CD44 and p63. In conclusion, immunoreactivity CK5 and CD44 commonly immunostained NV/MV and some invasive high grade UC. Other basal cell markers (CK34bE12 and p63) appear to be non specific or non sensitive. NV and MV and some UC likely represent a subset of UC displaying immunohistochemical features of urothelial basal cells. They had tendency of endophytic growth and early invasion despite the innocuous cytologic appearance. ""ADAM23, a member of a disintegrin and metalloprotease (ADAM) family, has been reported to be expressed in several types of tumours. The exact role of ADAM23 and the possible mechanisms in which it is involved in non-small-cell lung carcinoma (NSCLC) remains unclear. Therefore, selleck chemicals this study was designed to explore the expression of ADAM23 and its correlation with promoter methylation in NSCLC. Immunohistochemistry and RT-PCR together with Western blotting methods were used to analyse the expression of ADAM23 in 52 cancer tissue samples and eight benign pulmonary lesions as well as four cell lines. The methylated status of ADAM23 gene was determined with methylation-specific PCR (MSP). The results of immunohistochemistry showed that the expression of ADAM23 protein was lower in NSCLC Selleckchem Pifithrin�� than that in corresponding normal tissues and benign pulmonary lesions (38.5%vs. 86.5% and 87.5%, P?Temsirolimus (CCI-779, NSC 683864) the rate of ADAM23 gene methylation was 50.3% (17/32). ADAM23 expression and its promoter methylation were negatively associated (r?=??0.328, P?=?0.017). Moreover, weak expression of ADAM23 in methylated cancer cells increased after treatment with 5-aza-2��-deoxycytidine (5-Aza-2��-dC), confirming that methylation was responsible for the gene downregulation. Our results demonstrate that the expression level of ADAM23 is likely to be involved in the progression of NSCLC and its downregulation is probably correlated with promoter methylation. These findings may provide potential diagnostic and prognostic information about NSCLC. ""Chronic tendon pathology is a common and often disabling condition, the causes of which remain poorly understood. The continuum model of tendon pathology was proposed to provide a model for the staging of tendon pathology and to assist clinicians in managing this often complex condition (Br. J. Sports Med., 43, 2009, 409). The model presents clinical, histological and imaging evidence for the progression of tendon pathology as a three-stage continuum: reactive tendinopathy, tendon disrepair and degenerative tendinopathy.