National Cancer Institute®
Last Modified: July 1, 2002
1
UI - 9863882
AU - Dore GJ; Grulich A; Law MG; Brew BJ; Kaldor JM
TI -
Kaposi's sarcoma and protection from AIDS dementia complex.
SO - AIDS 1998 Dec 3;12(17):2354-5
2
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. lynn@biostat.umn.edu
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.
3
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
4
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. ulrich.hengge@uni-essen.de
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.
5
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
6
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.
7
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.
8
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.
9
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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