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Présentation de l'éditeur : "Les tumeurs hépatiques bénignes sont nombreuses, variées, de présentation et d'évolution différentes. Plus de cent types différents de tumeurs ont été répertoriés. Leur diagnostic comme leurs traitements peuvent être complexes, parfois mal codifiés. Trois tumeurs bénignes ont été, ces dix dernières années, au cœur de l'actualité, pour des raisons différentes. La première, l'"adénome hépatocellulaire", tumeur rare au potentiel évolutif incertain (hémorragie et transformation maligne), a été l'objet d'intenses travaux de recherche en biologie moléculaire menés par des équipes françaises. Il nous est apparu intéressant de nous interroger, quelques années après les premières publications et au travers d'une enquête, sur le diagnostic d'adénome hépatocellulaire et sur l'impact des procédés d'imagerie moderne et des outils de la biologie (moléculaire et immunohistochimique) sur sa prise en charge. La deuxième, le "cystadénome hépatobiliaire" (CHB), est une tumeur kystique très rare, au potentiel dégénératif. Le diagnostic des tumeurs kystiques du foie est difficile. En l'absence de facteurs favorisants reconnus, le diagnostic de CHB repose-t-il encore, aujourd'hui, sur l'analyse du spécimen opératoire ? Ce rapport tente, au-delà d'une indispensable analyse épidémiologique descriptive, d'établir les outils de sa prise en charge. Enfin, concernant la "polykystose hépatique", le traitement chirurgical radical par résections hépatiques apporte de très bons résultats, au prix d'une sélection rigoureuse, d'une tactique opératoire précise et d'une morbidité importante. Cette pathologie " bénigne " est de diagnostic souvent facile ; sa prise en charge est en revanche difficile, discutée et parfois discutable : nous avons essayé d'établir un état des lieux. Notre travail s'est orienté sur la collecte rétrospective d'informations à partir de périodes d'enregistrement relativement longues. Sacrifiant aux habitudes et à l'enquête monolithique, nous avons ainsi choisi de soumettre aux membres de l'AFC trois enquêtes courtes et orientées, dont les objectifs vous ont été présentés. Ce rapport est complété par des mises au point sur les plus récentes évolutions qui jalonnent le diagnostic et la gestion des angiomes, des hyperplasies nodulaires focales, des kystes biliaires et des tumeurs bénignes rares."

Liver Neoplasms

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Liver cancer is becoming one of the most frequent cancers in the world, because of lifestyle or some infections, for example hepatitis B or C even some diseases, such as cirrhosis. The frequency depends on the geographical area. In Africa, land of high endemy of hepatitis, the patients with cancer will be younger than in our regions, who will be significantly older. Prevention is therefore very important in these countries of high endemy, and for patients with a high risk of hepatitis, by vaccination against the virus or by checking the organ twice a year. Different types of treatment are available for the patients, to cure the disease or to improve the quality of life. The curative treatments are surgery or hepatic transplantation. Surgery can be applied if the liver is still working; transplantation is applied when the liver doesn’t work anymore. Then, we have the different alternatives, which are destruction with destruction with radiofrequencies, and cryosurgery. They can be applied criteria’s of location and size of the tumor. Chemoembolization destroy the tumor by asphyxiation by stopping the blood entrance, and a chemotherapy drug is injected inside the tumor. Radiotherapy is used for patients with pain and in advanced stage of the disease, also in association to obtain a synergy of different treatments. Finally, alcohol injection causes a tumoral necrosis by injection of absolute alcohol inside the tumor. Le cancer du foie est en passe de devenir un des cancers les plus fréquents au monde à cause du mode de vie que des différentes infections, comme l’hépatite B ou C ou pathologies pouvant être contractées comme la cirrhose du foie. La fréquence de ce cancer dépendra de certaines zones géographiques. En Afrique, pays à forte endémie d’hépatites, les individus présentant un cancer seront souvent les plus jeunes, alors que dans nos régions les patients seront nettement plus âgés. La prévention est donc de mise dans les pays à forte endémie et chez les patients à risque existent pour soit guérir le patient, soit pour améliorer sa qualité de vie. Les traitements curatifs sont la chirurgie ou la transplantation hépatique. La chirurgie peut être appliquée si le foie fonctionne encore normalement, la greffe est de choix si le foie ne fonctionne plus. Ensuite viennent les alternatives à la chirurgie qui sont la destruction par radiofréquence et la cryochirurgie, applicable selon les critères de taille et de localisation de tumeur. La chimio-embolisation permet de détruire la tumeur par asphyxie en empêchant l’arrivée dans le sang et en injectant un médicament de chimiothérapie. La radiothérapie est plutôt utilisée chez les patients douloureux en stade avancé, et aussi en association pour obtenir une synergie des traitements. Enfin l’alcoolisation de tumeur permet une nécrose tumorale par injection d’alcool absolu.

Liver Neoplasms --- Liver Cirrhosis, Alcoholic

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Previous studies have shown that a synergistic effect by the association of ascorbate (vitamin C) and menadione ( vitamin K3) results in cell death in a wide variety of cancer cell types. A redox cycling between ascorbate and menadione generates the formation of reactive oxygen species (ROS) inducing an oxidative stress and leads to cancer cell death. Oxidative stress by provoking DNA strand breaks leads to an energy impairment followed by cell death.Our work on Transplantable liver Tumor cells (TLT), a murine hepatocarcinoma, show the involvement of PARP (Poly ADP Ribose Polymerase) activation and subsequent glycolysis inhibition in the process of cell death. The inhibitory effect obtained by using the antioxidant N-acetylcystein, reinforces the main role of oxidative stress in CK mediated cytotoxicity. The involvement of protein phosphorylation in cytotoxicity observed by using two H²O²­ generating systems, namely CK3 and xanthine oxidase, is suggested by the protective effects obtained by a tyrosine kinase inhibitor (tyrphostine 46), and by a tyrosine phosphatase inhibitor (Et-3,4-dephostatin).We would like to suggest that Ca2+ may also plays an active role by triggering or amplifying some processes leading to cell death, as suggested by the delayed toxicity seen with Bapta-AM, a Ca2+ chelator. lndeed in the presence of Bapta-AM, both processes poly ADP ribosylation of proteins and yH2AX phosphorylation were delayed, thus confirming the involvement of PARP activation and NAD+ depletion in the mechanism leading to energetic crisis during an oxidative stress. Furthermore, the use of Bapta also allows to observe a delay in the activation of an ER stress as well as a reduction in the amount of carbonylated protein. ln conclusion we suggest that further studies are required to clarify the involvement of calcium in this cell death.

Liver Neoplasms, Experimental --- Liver Neoplasms, Experimental --- Vitamin K 3 --- Oxidative Stress --- Mice --- Ascorbic Acid --- Cell Death

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Previous studies demonstrated a synergistic cytotoxic effect by ascorbate-menadione on various types of cancer cells. When used in combination, ascorbate and menadione are entering a redox cycle leading to hydrogen peroxide production, which seems to be the basis of this cytotoxicity. Recent studies suggest that oxidative stress generated by ascorbate/menadione affects Hsp90 leading to the degradation of some critical proteins and cell death. Moreover, this association leads to the appearance of an additional Hsp90 protein band of about 70 kDa, suggesting Hsp90 cleavage,in the K562 leukemia myelogenous chronic cells.ln this study, we first confirmed the presence of the additional Hsp90 protein band induced by ascorbate/menadione in murine hepatocarcinoma cells (Transplantable liver tumor).Secondly, by using two modulators of oxidative stress, N-acetylcysteine and 3-aminotriazole, we showed the implication of oxidative stress in the Hsp90 cleavage.Thirdly, by using two calcium chelating agents, namely Bapta-AM and EGTA, we showed that intracellular calcium may be implicated in this cleavage.Finally, by using some metabolic inhibitors of Hsp90, we founded that both the cleavage of Hsp90 and the cytotoxicity induced by ascorbate/menadione are not necessarily correlated. That means that Hsp90 cleavage is not the only expianation of cell death. As conclusion, given the key role played by Hsp90 in cancer cells stabilizing mutated proteins critical for their survival, we would like to propose ascorbate/menadione as a new non toxic adjuvant anticancer therapy, without presenting any supplementary risk for the patients.

Oxidative Stress --- HSP90 Heat-Shock Proteins --- Liver Neoplasms, Experimental --- Vitamin K 3 --- Ascorbic Acid --- Mice --- Liver Neoplasms, Experimental

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Oncology. Neoplasms --- Gastroenterology --- Carcinogenesis --- Liver cells --- Cell transformation --- Cell culture --- Congresses --- Differentiation --- Carcinogens. --- Cell Differentiation. --- Cell Transformation, Neoplastic. --- Cells, Cultured. --- Liver Neoplasms, Experimental --- Liver --- -Cell culture --- -Cell transformation --- -Liver cells --- -#Lilly --- Hepatic cells --- Hepatocytes --- Cells --- Culture alteration (Cytology) --- Transformation of cells --- Tissue culture --- Cultures (Biology) --- Cytology --- Cancer --- Oncogenesis --- Pathogenesis of cancer --- Tumorigenesis --- Pathology --- Genetic toxicology --- Cultured Cells --- Cell, Cultured --- Cultured Cell --- Organ Culture Techniques --- Coculture Techniques --- Cell Culture Techniques --- Culture Techniques --- Human Umbilical Vein Endothelial Cells --- Neoplastic Cell Transformation --- Transformation, Neoplastic Cell --- Tumorigenic Transformation --- Neoplastic Transformation, Cell --- Cell Neoplastic Transformation --- Cell Neoplastic Transformations --- Cell Transformations, Neoplastic --- Neoplastic Cell Transformations --- Neoplastic Transformations, Cell --- Transformation, Cell Neoplastic --- Transformation, Tumorigenic --- Transformations, Cell Neoplastic --- Transformations, Neoplastic Cell --- Transformations, Tumorigenic --- Tumorigenic Transformations --- Cell Line, Transformed --- Differentiation, Cell --- Cell Differentiations --- Differentiations, Cell --- Embryo, Mammalian --- Gene Expression Regulation --- Cell Lineage --- Oncogens --- Tumor Initiators --- Tumor Promoters --- Initiators, Tumor --- Promoters, Tumor --- Benzidines --- chemically induced. --- cytology. --- -Congresses --- Technique --- Pathogenesis --- Carcinogens --- Cell Differentiation --- Cells, Cultured --- Cell Transformation, Neoplastic --- #Lilly --- Differentiation&delete& --- chemically induced --- cytology --- Carcinogen --- Oncogen --- Tumor Initiator --- Tumor Promoter --- Initiator, Tumor --- Promoter, Tumor --- Carcinogenesis - Congresses --- Liver cells - Differentiation - Congresses --- Cell transformation - Congresses --- Cell culture - Congresses