Premalignancy and oral neoplasia in HIV-infected patients (Meeting abstract).

Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.

Premalignancy and oral neoplasia in HIV-infected patients (Meeting abstract).

CCPC-93: Second International Cancer Chemo Prevention Conference. April 28-30, 1993, Berlin, Germany, p. 73, 1993.. Unique Identifier : AIDSLINE ICDB/94696755
Langford A; Rudolf Virchow, Augustenburger Platz 1, Berlin, Germany

Abstract: 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.

Keywords: Burkitt's Lymphoma/COMPLICATIONS/IMMUNOLOGY Herpesvirus 4, Human Hodgkin's Disease/COMPLICATIONS/IMMUNOLOGY Human HIV Infections/*COMPLICATIONS/IMMUNOLOGY Lymphoma/*COMPLICATIONS/IMMUNOLOGY Lymphoma, Non-Hodgkin's/COMPLICATIONS/IMMUNOLOGY Sarcoma, Kaposi's/*COMPLICATIONS/IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY ABSTRACT
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M9450902

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