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MASSIMO PIGNATELLI DRIVER
Forgotten password Please enter your email address below and we'll send you a link to reset your password. Not you? Written in an accessible and easy to read format and featuring such topics as the implementation of digital histology, molecular pathology of massimo pignatelli cancer and the big bang theory of tumour development: how cancers start, each chapter provides a comprehensive overview, and emphasises the salient points of interest. Serrated lesions of colon and rectum. In addition, during those years, he was the Dean of the Faculty of Engineering. He also nurtured a number of national and international partnerships in the field of education, research, and innovation entrepreneurship.
Professor Adesida has published more than peer-reviewed articles and has made more than presentations at massimo pignatelli conferences.
Executive Management - Nazarbayev University
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- Massimo Pignatelli, MD, PhD, FRCPath — Nazarbayev University
- Massimo Pignatelli - Nazarbayev University
- Recent Advances in Histopathology: 24
- ISBN 13: 9781853156496
- Executive Management
Recent Advances in Histopathology: Experience Required: All academic ranks may apply. Related Pages.
Property Lawyer. The importance of the E-cadherin-catenin complex in the maintenance of massimo pignatelli epithelial homoeostasis: More than intercellular glue? Dec Gut.
Adhesion massimo pignatelli Opportunities for modulation and a paradigm for novel therapeutic approaches in cancer. Nov Expert Opinion massimo pignatelli Investigational Drugs. In the past decade, there have been major advances in the elucidation of processes underlying tumour invasion and metastasis, in which adhesion molecules play a critical role.
Massimo pignatelli advances have revolutionised our ability to devise novel approaches for cancer treatment. This review gives an insight into the adhesion pathways, and highlights the current status of adhesion molecules as potential therapeutic targets.
Aberrant E-Cadherin and?? Aug Cancer Research. E-cadherin maintains the normal differentiated phenotype in epithelial cells; this function is partly mediated by alpha-catenin, which links E-cadherin to the cell cytoskeleton. Dysfunction of E-cadherin in vitro and in vivo is associated with an invasive phenotype. However, the role of alpha-catenin is largely undetermined. We analyzed the expression of E-cadherin and alpha-catenin in prostate cancer massimo pignatelli assess the relationship of abnormal expression to stage, grade and survival. E-cadherin expression was evaluated in 99 prostate cancers. In 79 of those specimens, alpha-catenin was also assessed.
In benign prostatic epithelium, both E-cadherin and alpha-catenin were expressed uniformly at the cell membrane.
Multivariate regression analysis showed that the prognostic value of E-cadherin was independent of tumor grade but not of metastasis. These results suggest that perturbation of cell-cell adhesion is involved in the progression of prostate cancer and that analysis of E-cadherin expression may be clinically useful. Jun International Journal of Cancer. We have previously shown that expression of gpMR6, a molecule that is functionally associated with the interleukin-4 receptor IL-4Ris lost from breast carcinoma cells as malignancy increases. Here we have analysed a series of colorectal carcinoma cell lines and show a similar decrease with massimo pignatelli malignancy. Moreover, analysis of the HRA cell line, which can exhibit a poorly or a well-differentiated phenotype according to culture conditions, shows that gpMR6 massimo pignatelli weakly expressed on the former but strongly expressed on the latter.
Functional analysis using either IL-4 or monoclonal antibody MAb MR6 and the well-differentiated cell line SW revealed that MAb MR6 acts as an agonist for IL-4, with both reagents causing a dose-dependent inhibition of cell division, but greatly enhancing the glandular differentiation of SW in three-dimensional collagen gels. These observations suggest that the gpMR6 molecule may act as the product of a tumour suppressor gene and that its loss may be a primary event in tumourigenesis.
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Fibroblast growth factor 1 and fibroblast growth factor 2 immunoreactivity in gastrointestinal tumours. Acidic and basic fibroblast growth factors FGF-1 and FGF-2 massimo pignatelli mitogenic polypeptides that may play a role in autocrine and paracrine growth control of malignant tumours.
We have examined the expression of FGF-1 and FGF-2 in a series of 41 colorectal tumours 24 adenomas, 17 adenocarcinomas massimo pignatelli 50 massimo pignatelli adenocarcinomas 23 intestinal, 27 diffuseusing immunohistochemistry. FGF-1 immunoreactivity was detected in all samples per centwhereas FGF-2 immunoreactivity was seen in 17 adenomas 71 per cent13 colorectal carcinomas 76 per centand 29 gastric carcinomas 58 per cent. Compared with the normal mucosa, FGF-1 was overexpressed in 42 per cent of colorectal adenomas, 76 per cent of colorectal cancers, and 54 per cent of gastric cancers. Conversely, FGF-2 expression was reduced in 16 66 per cent8 47 per centand 40 80 per cent adenomas and colorectal and gastric samples, respectively.
Recent Advances in Histopathology: 23 - Massimo Pignatelli, Patrick Gallagher - Google книги
We found a significant correlation only between reduced FGF-2 and massimo pignatelli tumour grade. These data indicate that FGF-1 overexpression occurs in a large proportion of human colorectal and gastric cancers. This may play a role in massimo pignatelli progression of these tumours.School of Medicine. Nazarbayev University / School of Medicine / Massimo Pignatelli. Massimo Pignatelli. Department. School of Medicine.
Massimo Pignatelli, MD, PhD, FRCPath
Title. Dean. Email. Erratum: Abnormal expression and function of the E-cadherin-catenin complex in gastric carcinoma cell lines (British Massimo pignatelli of Cancer 80 .