Kaposi's sarcoma: Advances and perspectives
Identifieur interne : 00BE47 ( Main/Exploration ); précédent : 00BE46; suivant : 00BE48Kaposi's sarcoma: Advances and perspectives
Auteurs : Robert A. Schwartz [États-Unis]Source :
- Journal of the American Academy of Dermatology [ 0190-9622 ] ; 1996.
Abstract
Kaposi's sarcoma (KS) is an unusual neoplasm that has proved to be an enigma in many ways since its original description by Kaposi in 1872. Its epidemiology has stimulated tremendous interest, amplified markedly in 1981 when it became known as an original defining part of the complex of immune disorders now known as AIDS. The cell of origin, etiology, and therapy for both AIDS-associated and AIDS-unassociated KS continue as matters of intense investigation. In fact, whether it is a reactive hyperplasia or a true malignancy is still a matter of debate, as is the concept of multicentricity versus metastases. Epidemiologic studies suggest that a separate agent apart from HIV-1 may cause KS. A newly postulated KS-associated herpes virus may be linked. The role of the HIV-1 tat gene product, basic fibroblast growth factor, scatter factor, oncostatin M, and other factors that regulate the growth of KS cells are discussed, as well as therapeutic options.
Url:
DOI: 10.1016/S0190-9622(96)90018-3
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Kaposi's sarcoma (KS) is an unusual neoplasm that has proved to be an enigma in many ways since its original description by Kaposi in 1872. Its epidemiology has stimulated tremendous interest, amplified markedly in 1981 when it became known as an original defining part of the complex of immune disorders now known as AIDS. The cell of origin, etiology, and therapy for both AIDS-associated and AIDS-unassociated KS continue as matters of intense investigation. In fact, whether it is a reactive hyperplasia or a true malignancy is still a matter of debate, as is the concept of multicentricity versus metastases. Epidemiologic studies suggest that a separate agent apart from HIV-1 may cause KS. A newly postulated KS-associated herpes virus may be linked. The role of the HIV-1 tat gene product, basic fibroblast growth factor, scatter factor, oncostatin M, and other factors that regulate the growth of KS cells are discussed, as well as therapeutic options.</div>
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