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NCI CANCERLIT^® Search: AIDS-Related Kaposi's Sarcoma - August 2002

National Cancer Institute^®
Last Modified: August 1, 2002

Management of AIDS-related Kaposi's sarcoma: advances in target discovery and treatment.
Clinical trials referral resource. Clinical trials and NCI resources for cancer in HIV-positive patients.
Human herpesvirus 8 cytoviraemia rebound in a patient with Kaposi's sarcoma after a short interruption of efficient antiretroviral therapy.
In vitro and in vivo modulation of MDR1/P-glycoprotein in HIV-infected patients administered highly active antiretroviral therapy and liposomal

Table of Contents

1
UI - 12113241
AU - Dezube BJ
TI - Management of AIDS-related Kaposi's sarcoma: advances in target discovery and treatment.
SO - Expert Rev Anticancer Ther 2002 Apr;2(2):193-200
AD - Beth Isreal Deaconess Medical Center, Harvard Medical School, USA. bdezube@caregroup.harvard.edu
Kaposi's sarcoma is the most common tumor arising in HIV-infected patients and is an AIDS-defining illness by the Centers for Disease Control guidelines. Recent advances in the elucidation of the pathogenesis of KS are uncovering potential targets for KS therapies. Such targets include the processes of angiogenesis and cellular differentiation and the Kaposi's sarcoma herpesvirus/human herpesvirus-8. With the increasing recognition that effective antiretroviral regimens are associated with both a decreased proportion of new AIDS-defining Kaposi's sarcoma cases and a regression in the size of existing Kaposi's sarcoma lesions, most, if not all, Kaposi's sarcoma patients should be advised to take antiretroviral drugs that will maximally decrease HIV-1 viral load. Five agents are currently approved by the US FDA for the treatment of Kaposi's sarcoma; alitretinoin gel for topical administration; and liposomal daunorubicin, liposomal doxorubicin, paclitaxel and interferon-alpha for systemic administration. Many more agents, particularly angiogenesis inhibitors and other pathogenesis-targeted therapies are in early clinical development. Over the next 5 years, we may see even more of these pathogenesis-targeted therapies in trials and just as important we may identify, develop and validate clinically practical tools for assessing the biological effects of these therapies. The next 5 years may also bring a better understanding of the pharmacokinetic interactions among the many agents in the Kaposi's sarcoma and AIDS armamentariums.

2
UI - 11866136
AU - Black JB; Feigal EG; Gore-Langton RE
TI - Clinical trials referral resource. Clinical trials and NCI resources for cancer in HIV-positive patients.
SO - Oncology (Huntingt) 2002 Feb;16(2):200-2, 205, 207
AD - National Cancer Institute, USA.

3
UI - 11953484
AU - Parisi SG; Mazzi R; Sarmati L; Carolo G; Uccella I; Rianda A; Nicastri
TI - E; Concia E; Andreoni M Human herpesvirus 8 cytoviraemia rebound in a patient with Kaposi's sarcoma after a short interruption of efficient antiretroviral therapy.
SO - AIDS 2002 May 3;16(7):1089-91

4
UI - 12138343
AU - Lucia MB; Rutella S; Leone G; Larocca LM; Vella S; Cauda R
TI - In vitro and in vivo modulation of MDR1/P-glycoprotein in HIV-infected patients administered highly active antiretroviral therapy and liposomal doxorubicin.
SO - J Acquir Immune Defic Syndr 2002 Aug 1;30(4):369-78
AD - Department of Infectious Diseases, Catholic University, Rome, Italy.
P-glycoprotein (P-gp) transports a wide range of structurally unrelated drugs, such as HIV protease inhibitors (PIs) and cytotoxic compounds such as anthracyclines. Because modification of P-gp phenotype and function is an important underlying mechanism of drug interactions, the current study was conducted in order to evaluate whether highly active antiretroviral therapy (HAART), HIV plasma viral load (VL), or cancer chemotherapy may induce in vivo changes of P-gp phenotype in peripheral blood mononuclear cells (PBMCs) from HIV-infected treatment-naive and -experienced subjects at different stages of HIV infection and/or disease, including patients with HIV-associated Kaposi sarcoma (KS). Our results show that neither HAART nor HIV VL, nor the stage of HIV infection and/or disease, significantly alter P-gp expression on PBMCs. In particular, surface P-gp expression is expressed at low levels by T-cell subsets, B cells, and NK cells, whereas almost all monocytes are double positive and these results are not modified by HIV PI-containing regimens. By contrast, a significant phenotype modification is detected in PBMCs from AIDS/KS patients after challenge with the liposomal formulation of the anthracycline doxorubicin (L-DOX) with the higher expression reached 24 hours after the end of the drug infusion. In addition, accumulation of L-DOX is unaffected by P-gp-mediated drug efflux as documented by in vitro experiments, in sharp contrast to the kinetic of free DOX, based on HIV PI blockade experiments. Finally, P-gp expression was found in KS spindle cells from HIV-infected treatment-naive AIDS/KS patients. We conclude that P-gp phenotype in PBMCs and specific subsets is not altered by HAART and/or HIV, whereas a significant increase is induced by specific anticancer drugs such as L-DOX. Moreover, HIV PIs possess an inhibitory effect on P-gp function that may improve DOX sensitivity in KS spindle cells.

The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.

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