By C. Meyers
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Extra resources for AIDS-Associated Viral Carcinogenesis
This resistance can be overcome by inducing HHV-8 to reenter the lytic cycle during antiviral therapy, leading to destruction of virally infected cells. 207 Other Potential Targets Potential targets based on KS pathogenesis are the focus of many current trials. 187,208–212 Further, platelet-derived growth factor213 and c-kit214 have a role in active tumor formation. 216,217 HAART has been associated with a lengthening of time to treatment failure with either local or systemic therapy for KS. 5 years with no antiretroviral therapy to detect treatment failure among HIVinfected individuals with KS.
166–169 HHV-8 has been shown to have certain genes to be homologous to cyclin D1 and G-protein coupled receptors, which are known to contribute to oncogenesis. 150,170,171 HIV PATHOGENESIS IN KS The HIV virus itself may be an oncogene in KS development. A regulatory protein of HIV released by infected cells, called the Tat protein, guards KS cells from apoptosis,172 stimulates growth and angiogenesis,173,174 and also increases the production and release of matrix metalloproteinases (MMPs) from endothelial and inflammatory cells.
In groups with low-, low-intermediate-, and high-intermediate-risk IPI disease, 3-year overall survival rates were 20%, 22%, and 5% in the pre-HAART era and 64%, 64%, and 50% in the HAART era, respectively. TREATMENT OF AIDS-RELATED NHL The treatment for ARLs is similar to that of non-HIV-infected individuals, with some exceptions. 89 The use of hematopoetic stimulants such as granulocyte-colony stimulating factor (G-CSF) may aid in reducing chemotherapy-induced cytopenic complications. 90 The AIDS Malignancy Consortium (AMC) reported using, in 65 patients, reduced doses of cyclophosphamide and doxorubicin, combined with vincristine and prednisone (modified CHOP, mCHOP) and full doses of CHOP combined with G-CSF with concomitant HAART.
AIDS-Associated Viral Carcinogenesis by C. Meyers