National Cancer Institute®
Last Modified: July 1, 2002
UI - 10853981
AU - Eberly LE; Ohman PA; Neaton JD; Price RW; Abrams DI
TI - Kaposi's sarcoma and central nervous system disease: a real association or an artifact of the control group? Terry Beirn Community Programs for Clinical Research on AIDS.
SO - AIDS 2000 May 26;14(8):995-1000
AD - Community Programs for Clinical Research on AIDS Statistical and Data Management Center, Division of Biostatistics, University of Minnesota, Minneapolis 55455-0378, USA. firstname.lastname@example.org
OBJECTIVES: To test the hypothesis that Kaposi's sarcoma (KS) protects against four central nervous system (CNS) diseases in HIV-1-infected individuals. STUDY POPULATION AND DESIGN: The study population of 9404 subjects included participants in Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA) protocols who were enrolled between METHODS: Proportional hazards regression was used to estimate adjusted relative risks for predictors of four central nervous system diseases. Covariates included occurrence of Kaposi's sarcoma, occurrence of other opportunistic infections or malignancies, baseline CD4+ count, and other baseline characteristics. RESULTS: Among the 5944 participants without progression to AIDS at entry, 451 developed a CNS disease. The adjusted relative risk of any CNS disease for those who developed Kaposi's sarcoma versus those who did not develop any AIDS-defining event was 1.41 [95% confidence interval (CI), 0.98-2.03; P = 0.06]. In contrast, the adjusted relative risk of any CNS disease for those with Kaposi's sarcoma versus those with some other non-Kaposi's sarcoma AIDS-defining event was 0.37 (95% CI, 0.24-0.57; P < 0.0001). Among the 3460 participants with progression to AIDS at entry, the adjusted relative risk of any CNS disease for those with Kaposi's sarcoma versus those with some other non-Kaposi's sarcoma AIDS-defining event was 0.71 (95% CI, 0.40-1.25; P = 0.23). CONCLUSIONS: Our analyses indicate that the risk of CNS disease associated with Kaposi's sarcoma depends strongly on the reference or control group chosen. When compared to individuals with other non-Kaposi's sarcoma AIDS-defining diseases, Kaposi's sarcoma is associated with a lower risk of CNS disease in HIV-1 positive individuals. However, when compared to individuals with no AIDS-defining disease or with a similarly mild AIDS-defining disease such as invasive candidiasis, Kaposi's sarcoma is associated with an equivalent risk of CNS disease.
UI - 11101086
AU - Dore G; Brew B
TI - Response to Eberly et al., Kaposi's sarcoma and central nervous system disease: a real association or an artifact of the control group?
SO - AIDS 2000 Nov 10;14(16):2631-2
UI - 12062994
AU - Hengge UR; Ruzicka T; Tyring SK; Stuschke M; Roggendorf M; Schwartz RA;
TI - Seeber S Update on Kaposi's sarcoma and other HHV8 associated diseases. Part 1: epidemiology, environmental predispositions, clinical manifestations, and therapy.
SO - Lancet Infect Dis 2002 May;2(5):281-92
AD - Department of Dermatology, Venereology and Allergology, University of Essen, Germany. email@example.com
Kaposi's sarcoma (KS) is a mesenchymal tumour involving blood and lymphatic vessels. Only recently has the pathogenesis of this extraordinary neoplasm been elucidated. Viral oncogenesis and cytokine-induced growth together with some state of immunocompromise represent important conditions for this tumour to develop. In 1994, a novel virus was discovered and termed human herpesvirus 8 (HHV8), also known as Kaposi's sarcoma-associated herpes virus, which can be found in all types of KS, whether related to HIV or not. In the era of highly active antiretroviral therapy (HAART), the incidence of AIDS-KS has considerably declined, probably due to enhanced immune reconstitution and anti-HHV8-specific immune responses. If HAART is able to prevent spreading of KS, local therapy of KS may become an essential component of patient management. Part 1 of the review covers the epidemiology, environmental predispositions, clinical manifestations, and therapy of KS. Newer treatments such as pegylated liposomal anthracyclines and experimental strategies are discussed. We also present rationales and graduated treatment algorithms for local and systemic therapy in patients with KS to appropriately meet the challenges of this extraordinary neoplasm. Part 2, to be published next month, will summarise recent insights in the pathogenesis of KS and will discuss other HHV8-related diseases such as Castleman's disease and primary effusion lymphoma.
UI - 12045689
AU - Paparizos VA; Kyriakis KP; Papastamopoulos V; Hadjivassiliou M;
TI - Stavrianeas NG Response of AIDS-associated Kaposi sarcoma to highly active antiretroviral therapy alone.
SO - J Acquir Immune Defic Syndr 2002 Jun 1;30(2):257-8
UI - 11984939
AU - Simon K
TI - [Etiology, pathogenesis and treatment options in Kaposi's sarcoma of HIV infection]
SO - Przegl Epidemiol 2001;55 Suppl 3():129-35
AD - Katedra i Klinika Chorob Zakaznych AM we Wroclawiu.
UI - 11168763
AU - Bezold G; Messer G; Peter R; Flaig M; Sander C
TI - Quantitation of human herpes virus 8 DNA in paraffin-embedded biopsies of HIV-associated and classical Kaposi's sarcoma by PCR.
SO - J Cutan Pathol 2001 Mar;28(3):127-30
AD - Department of Dermatology, Ludwig-Maximilians-Universitat, Munich, Germany.
BACKGROUND: Kaposi's sarcoma occurs in patients seropositive and seronegative for the human immunodeficiency virus (HIV) and has been associated with human herpes virus 8 (HHV8). The purpose of this study was to determine and to compare the amount of HHV8 DNA in formalin-fixed tissue sections of Kaposi's sarcoma. METHODS: From 27 biopsies of Kaposi's sarcoma patients, tissue sections were taken and deparaffinized. Four patients were HIV seronegative and 13 were HIV seropositive. After extraction of DNA copy numbers of HHV8 and beta-globin were determined in every sample by quantitative PCR ELISA using an internal quantitation standard. Results were expressed as HHV8 per beta-globin. RESULTS: No significant differences were found between biopsies from HIV-positive and HIV-negative patients (14.8+/-19.6 HHV8 per 1000 beta-globin in HIV-positive versus 18.0+/-23.5 in HIV-negative patients). CONCLUSIONS: These data suggest that HHV8 viral load in Kaposi's sarcoma is relatively low and does not differ in HIV-positive and HIV-negative samples. The importance of viral load determination for prognosis or treatment monitoring remains to be elucidated.
UI - 12115328
AU - Tulpule A; Groopman J; Saville MW; Harrington W Jr; Friedman-Kien A;
TI - Espina BM; Garces C; Mantelle L; Mettinger K; Scadden DT; Gill PS Multicenter trial of low-dose paclitaxel in patients with advanced AIDS-related Kaposi sarcoma.
SO - Cancer 2002 Jul 1;95(1):147-54
AD - Division of Hematology, Department of Medicine, Kenneth Norris Cancer Hospital and Research Institute, University of Southern California School of Medicine, Los Angeles, California, USA.
BACKGROUND: Treatment options are limited for patients with advanced acquired immunodeficiency syndrome (AIDS)-related Kaposi sarcoma (AIDS-KS) whose disease has progressed after receiving therapy with liposomal anthracyclines or combination chemotherapy with doxorubicin (Adriamycin), bleomycin, and vincristine (ABV). This study was performed to assess the safety and efficacy of a novel dose and schedule of paclitaxel in patients with AIDS-KS who failed to respond to previous systemic chemotherapy. METHODS: This was an open-label, multicenter Phase II study. Eligible patients had advanced AIDS-KS consisting of at least 25 mucocutaneous lesions, visceral disease, or lymphedema, and had failed to respond to at least one previous systemic chemotherapy regimen. Patients were treated with paclitaxel at a dose of 100 mg/m(2) given intravenously over 3 hours, every 2 weeks. Primary efficacy end points were tumor response, time to progression, time to treatment failure, and survival. Quality of life and adverse events were evaluated using the Symptom Distress Scale (SDS) and the World Health Organization Toxicity Criteria, respectively. RESULTS: One hundred and seven male patients with advanced AIDS-KS were enrolled from nine participating sites. The median entry CD4+ lymphocyte count was 41/mm(3) (range 0-1139). Previous treatment regimens included ABV in 52, liposomal daunorubicin in 49, and liposomal doxorubicin in 40 patients. Forty-one patients (38%) received two or more previous chemotherapy regimens. Protease inhibitor use during the study was reported by 82 (77%) patients overall; 47 patients (44%) were receiving a protease inhibitor before study entry. Complete or partial response was documented in 60 patients (56%). The median duration of response was 8.9 months. Major response rate was similar when comparing patients not on a protease inhibitor at the time of response (59%) with patients on a protease inhibitor at time of response (54%). However, protease inhibitor use had a significant impact on survival (P = 0.04). Grade 4 neutropenia was reported in 35% of patients; other life-threatening side effects were uncommon. Significant improvements were seen in the total quality of life scores measured by the SDS, including significant improvement in KS-related symptoms such as facial disease, tumor-associated edema, and pulmonary involvement. CONCLUSION: Paclitaxel given every 2 weeks induces major tumor regression in the majority of patients with advanced KS who failed to respond to previous systemic chemotherapy. Paclitaxel is associated with significant improvement in quality of life with acceptable toxicity and should be considered as an effective treatment option for patients with advanced KS. Copyright 2002 American Cancer Society.
UI - 11964546
AU - Maradona JA; Carton JA; Asensi V; Rodriguez-Guardado A
TI - AIDS-related Kaposi's sarcoma with chylothorax and pericardial involvement satisfactorily treated with liposomal doxorubicin.
SO - AIDS 2002 Mar 29;16(5):806
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