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Pathogenesis of AIDS-associated Kaposi's sarcoma
B Ensoli1, G Barillari, R C Gallo
1Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Hematology/Oncology Clinics of North America
|April 1, 1991
Summary
Kaposi's sarcoma (KS) pathogenesis is being uncovered using new models. HIV-Tat protein may play a key role in the development and progression of this mesenchymal tumor in infected individuals.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Kaposi's sarcoma (KS) is a mesenchymal tumor with complex origins, frequently affecting individuals with HIV.
- Epidemic KS lesions exhibit mixed cellularity, spindle cell proliferation, and new blood vessel formation.
- Spindle cells, the presumed tumor cells, originate from mesenchymal cells and share traits with endothelial and smooth muscle cells.
Purpose of the Study:
- To investigate the pathogenesis of Kaposi's sarcoma using established in vitro and in vivo models.
- To explore the role of specific cytokines and the HIV Tat protein in KS development and progression.
Main Methods:
- Utilized AIDS-KS cell cultures for in vitro studies.
- Employed a transgenic mouse model for in vivo investigations.
- Assessed autocrine and paracrine growth activities of AIDS-KS cells.
- Examined the effect of exogenous Tat protein on KS cell proliferation.
Main Results:
- AIDS-KS cells exhibit autocrine and paracrine growth activities, producing specific cytokines that may explain lesion histology.
- Inoculation of cultured AIDS-KS cells into nude mice induced KS-like lesions, suggesting KS is an inducible disease.
- Tat-transgenic mice developed KS-like lesions, and Tat protein induced proliferation of AIDS-KS cells.
Conclusions:
- Kaposi's sarcoma is an inducible disease, with significant implications for understanding its development in HIV-infected individuals.
- The HIV Tat protein is strongly implicated as a factor in the development or progression of Kaposi's sarcoma.
- Further research into KS pathogenesis can benefit from the established cell culture and transgenic mouse models.