INVITED SPEAKERS ABSTRACTS
Epidemiology and pathogenesis of Kaposi Sarcoma, what have we learnt recently?
In 1872, a Viennese dermatologist, Moritz Kaposi, described multicentric, cutaneous and extra-cutaneous neoplasms predominantly affecting older individuals with a protracted clinical course. This disease is now designated Kaposi's sarcoma (KS). Four recognized clinical subsets have been secondarily distinguished: the sporadic or classic subtype initially described by Kaposi, the endemic subtype observed in subsaharian Africans, the epidemic subtype in patients infected with human immunodeficiency virus and the iatrogenic subtype in patients treated by immunosuppressive therapy specially in organ transplant recipients. Classic Kaposi'sarcoma usually present as individual, slow growing, indolent, cutaneous lesions predominant on the legs and constrasts with epidemic KS characterized by multifocal, progressive (florid) lesions with frequent primary involvement of the oral mucosa and dissemination to the viscera and in post-transplant KS. All KS are characterized by the proliferation of spindle cells of presumed lymphatic origin and infected by HHV-8. Post-transplant KS can lead to multifocal, progressive (florid) lesions with frequent primary involvement of the oral mucosa and dissemination to the viscera.
HIV associated KS prevalence and mortality has decreased in the era of highly active retroviral therapy but remains an important problem in Africa. KS prevalence after organ transplantation varies greatly depending on the prevalence of HHV-8 infection in the general population. Most cases of pos-transplant KS develop as a result of HHV8 reactivation.
HHV8 encodes for several genes able to control cell proliferation, angiogenesis, immune reactions which shed light on KS pathogenesis and provide new therapeutic targets. Several interesting in vitro and in vivo models shall be discussed. HHV8 cofactors particularly genetic factors remain to be discovered.© 2010 Lippincott Williams & Wilkins, Inc.