In order to promote carcinogenesis multiple factors must be orchestrated. Since that time, several case-control studies have investigated this hypothesis with overall positive associations (2, 3). Moreover, technological advances have led to the discovery of previously unknown and unsuspected oncogenic infections in recent years, prompting the idea that additional infection-associated cancers might still be discovered. The project also includes studies of cancer cofactors of importance to people with HIV/AIDS, including human herpesvirus 8, the causative agent of Kaposi sarcoma. Of these, 2 of 3 MCCs (67%) were positive for MCV. Also involved in tumor progression is the dysregulation of cellular processes by viral proteins, and we describe how this has been investigated by studies in cell culture and in experimental animals and by molecular cellular approaches. Results: RT-PCR demonstrated the presence of v-cyclin D mRNA in biopsy specimens of AIDSrelated Kaposi’s sarcoma, in earlypassage spindle cells from classical (i.e., not AIDS-related) Kaposi’s sarcoma, and in spindle cells isolated from the peripheral blood of patients with AIDS-related Kaposi’s sarcoma.
In situ hybridization indicated that mRNAs for v-cyclin D and kaposin, an HHV-8 latency-associated gene, were present in approximately 1% of the spindle cells in early patch lesions and approximately 60% of the spindle cells in late nodular lesions of Kaposi’s sarcoma. Spindle cells of Kaposi’s sarcoma, which have been regarded as the tumor cells of this cancer, contain v-cyclin D mRNA. The resultant tumors grew rapidly, metastasized, and continued to express ORF74.