129 research outputs found
Carcinogénèse hépatique (rôle des protéases matricielles et identification de nouveaux acteurs par analyse globale du protéome des carcinomes hépatocellulaires)
No full textLe carcinome hépatocellulaire (CHC) se développe sur cirrhose, donc sur un foie siège d'altérations stromales. Les interactions entre stroma et cellules tumorales sont donc dans ce cas une cible d'étude pertinente. Nous avons étudié le rôle des protéases matricielles et montré que les cellules tumorales hépatiques régulent la production de MMP-2 pour les myofibroblastes. In vivo, sur un modèle de carcinogenèse chimique chez le rat, la pravastatine diminue la progression et le pouvoir invasif des tumeurs en diminuant l'activation de la MMP-2. Afin d'identifier les acteurs de la carcinogenèse hépatique, nous avons analysé le protéome des CHC développés sur hépatite C et décrit 45 protéines exprimées différentiellement. Parmi ces protéines, la reptine a fait l'objet d'une analyse complémentaire. Sa surexpression dans la lignée HuH7 augmente la tumorigénicité des cellules lors de xénogreffes sur des souris immunodéprimées alors que sa sous-expression induit l'apoptose de ces cellules.Hepatocellular carcinoma (HCC) arises often in cirrhotic patients with deep stromal alterations. Then, the study of interactions between stroma and cancerous cells is of great interest. We studied the function of matrix proteases in HCC progression and we have shown that tumoral hepatocytes regulated MMP-2 production by hepatic myofibroblasts. Then, using a model of chemical hepatocarcinogenesis in rats, we have shoxn that pravastatin decrease the metastatic potential of tumors, associated with an inhibition of MMP-2 activation. Finally, a proteomic analysis of hepatocellular carcinoma developed in hepatitis C allowed us to identify 45 proteins differentially expressed. Among these proteins, we have demonstrated the involvement of reptin in hepatic carcinogenesis. Indeed, the over expression of reptin in HuH7 cells increased the tumorigenicity of these cells after injection in immunocompromised mice whereas the down-regulation of reptin led to an apoptosis of the cells.BORDEAUX2-BU Santé (330632101) / SudocSudocFranceF
Pictures of focal nodular hyperplasia and hepatocellular adenomas.
No full textThis practical atlas aims to help liver and non liver pathologists to recognize benign hepatocellular nodules on resected specimen. Macroscopic and microscopic views together with immunohistochemical stains illustrate typical and atypical aspects of focal nodular hyperplasia and of hepatocellular adenoma, including hepatocellular adenomas subtypes with references to clinical and imaging data. Each step is important to make a correct diagnosis. The specimen including the nodule and the non-tumoral liver should be sliced, photographed and all different looking areas adequately sampled for paraffin inclusion. Routine histology includes HE, trichrome and cytokeratin 7. Immunohistochemistry includes glutamine synthase and according to the above results additional markers such as liver fatty acid binding protein, C reactive protein and beta catenin may be realized to differentiate focal nodular hyperplasia from hepatocellular adenoma subtypes. Clues for differential diagnosis and pitfalls are explained and illustrated
Will the pathomolecular classification of hepatocellular adenomas improve their clinical management?
No full textImmunohistochemical pitfalls in the diagnosis of focal nodular hyperplasia and inflammatory hepatocellular adenoma
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