Les Tumeurs Malignes De La Parotide

Buts : Analyser les divers aspects cliniques, histologiques et thérapeutiques des tumeurs malignes de la parotide. Méthode : Étude rétrospective portant sur 17 cancers parotidiens opérés dans le service d\'ORL de la Rabta entre 1994 et 2006. Résultats : Sur une période de13 ans, suite à 77 parotidectomies pour tumeur parotidienne, nous avons diagnostiqué 17 cas de cancers parotidiens soit un pourcentage de 22% de l\'ensemble des tumeurs parotidiennes, réparties en 6 types histologiques. L\'âge moyen des patients est de 49 ans avec des extrêmes allant de 16 à 86 ans et un pic à la 7ème décade de vie. Le sex-ratio est égal à 1,8. Quatre cas de Paralysies faciales (PF) transitoires et un cas de PF définitive ont été déplorés. Deux cas de récidive ont été notés et repris chirurgicalement. Conclusion : Les cancers de la parotide se caractérisent par une grande diversité histologique. Le pronostic dépend du type histologique, du stade évolutif et du traitement.Aim : to analyse clinical, histopathologic and therapeutic aspects of parotid cancers. Method : data from a retrospective study of 17 cases treated in the ENT department of Rabta hospital between 1994 and 2006. Result : in this period 77 patients were operated of parotid tumors, 17 of them were malignants (22%) divided on 6 different histological types. Mean age was 49 years and sex ratio was 1.8. Transitory facial pulsy was observed in 4 patients. Only one definitive facial palsy was observed. Recurrence was observed in 2 patients.They were operated and received a complement of radiptherapy. Conclusion : Parotid cancers are caracterised by great histopathological variety. Their prognosis depends on histological type, tumor stage and treatment Keywords: Parotid gland, cancer, parotid tumor. Journal Tunisien d\'ORL et de chirurgie cervico-faciale Vol. 18 2007: pp. 25-2

Small-molecule inhibitors of macrophage migration inhibitory factor(MIF) as an emerging class of therapeutics for immune disorders

Macrophage migration inhibitory factor (MIF) is an important cytokine for which an increasing number of functions is being described in the pathogenesis of inflammation and cancer. Nevertheless, the availability of potent and druglike MIF inhibitors that are well-characterized in relevant disease models remains limited. Development of highly potent and selective small-molecule MIF inhibitors and validation of their use in relevant disease models will advance drug discovery. In this review, we provide an overview of recent advances in the identification of MIF as a pharmacological target in the pathogenesis of inflammatory diseases and cancer. We also give an overview of the current developments in the discovery and design of small-molecule MIF inhibitors and define future aims in this fiel

Les facteurs predectifs des echecs de la pharyngotomie au cours de la rhonchopathie chronique

No Abstract. Journal Tunisien d\'ORL et de chirurgie cervico-faciale Vol. 17 2006: pp. 25-2

Manifestations ORL revelatrices de leucemie aigue a propos de trois observations

No Abstract. Journal Tunisien d\'ORL et de chirurgie cervico-faciale Vol. 17 2006: pp. 60-6

Isothiocyanates inhibit proteasome activity and proliferation of multiple myeloma cells

Isothiocyanates (ITCs), including benzyl isothiocyanate (BITC), phenethyl isothiocyanate (PEITC) and sulforaphane, compounds found in cruciferous vegetable, are highly effective in inducing cell cycle arrest and apoptosis in a variety of cancer cells and animal models. Although some studies indicate that ITC-induced reactive oxygen species (ROS) generation may underlie apoptosis induction, our recent studies show that covalent binding to target proteins may be an important event triggering apoptosis. In this study, we report that BITC and PEITC significantly inhibit proteasome activity in a variety of cell types. Further studies show that ITCs inhibit both the 26S and 20S proteasomes, presumably through direct binding, and that this inhibition is unrelated to either ROS generation or ITC-induced protein aggregation. The potency of ITC-induced proteasome inhibition correlates with the rapid accumulation of p53 (tumor suppressor) and IκB nuclear factor-kappaB (nuclear factor-kappaB inhibitor). Finally, our results demonstrate that BITC and PEITC, the two strongest proteasome inhibitors, significantly suppress growth of multiple myeloma (MM) cells through induction of cell cycle arrest at G2/M phase and apoptosis. This study suggests that proteasome, like tubulin, is a potential molecular target of ITCs, thus providing a novel mechanism by which ITCs strongly inhibit growth of MM cells and new leads in identifying compounds with therapeutic and preventative efficacies for MM. It also supports the future studies of ITCs as therapeutic and preventive agents for MM