Document 0085
 DOCN  M9440085
 TI    Premalignancy and oral neoplasia in HIV-infected patients (Meeting
       abstract).
 DT    9404
 AU    Langford A; Rudolf Virchow, Augustenburger Platz 1, Berlin, Germany
 SO    CCPC-93: Second International Cancer Chemo Prevention Conference. April
       28-30, 1993, Berlin, Germany, p. 73, 1993.. Unique Identifier : AIDSLINE
       ICDB/94696755
 AB    Generally, HIV-infected patients are at greater risk for developing
       malignancies. The prime causative factor seems to be their
       immune-suppressed state. Immuno-dysregulation and a failure of immune
       surveillance to recognize oncogenic agents and/or malignant cells is a
       principal assumption in the development of cancer. Depression of natural
       killer cell function has been shown to result in decreased tumor-cell
       elimination and increased formation of experimental and spontaneous
       metastasis. Other cofactors such as chemical agents certainly promote
       carcinogenesis. In HIV-infected patients another mechanism may be
       oncogene activation that allows elective growth of certain cells. In
       order to define possible premalignant lesions in the setting of
       HIV-infection, one has to note the types of malignancies emerging in
       AIDS patients. Compared to the average population, HIV-infected patients
       are at increased risk for neoplasias associated with infections,
       especially with DNA or RNA viruses. In the setting of HIV infection and
       long-lasting immunosuppression, co-viral and chronic microbial infection
       or reactivation may predispose to premalignant/malignant lesions.
       Microbially induced growth factors may sustain proliferation of specific
       cell populations. In Kaposi's sarcoma, the most common HIV-associated
       neoplasm, definitive identification of a virus has not yet been
       sustained, but there is increasing evidence of a sexually transmitted
       etiologic factor, resulting in multifocal cellular proliferation. The
       relation between Epstein-Barr virus infection and non-Hodgkin's
       lymphoma, the second most common malignancy, has been frequently
       documented. The current pathogenetic hypothesis describes these B-cell
       lymphomas as the result of a complex interaction of EBV infection,
       antigenic stimulation, and T-cell dysfunction. In addition, the
       occurrence of other malignancies in HIV-infected patients is reported
       with increasing frequency, including Hodgkin's disease, squamous cell
       carcinomas and malignant melanomas.
 DE    Burkitt's Lymphoma/COMPLICATIONS/IMMUNOLOGY  HIV
       Infections/*COMPLICATIONS/IMMUNOLOGY  Herpesvirus 4, Human  Hodgkin's
       Disease/COMPLICATIONS/IMMUNOLOGY  Human
       Lymphoma/*COMPLICATIONS/IMMUNOLOGY  Lymphoma,
       Non-Hodgkin's/COMPLICATIONS/IMMUNOLOGY  Sarcoma,
       Kaposi's/*COMPLICATIONS/IMMUNOLOGY  T-Lymphocytes/IMMUNOLOGY  MEETING
       ABSTRACT

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).