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National Cancer Institute®
Ultima Vez Modificado: 1 de enero del 2002
UI - 11440037
AU - Kulasegaram R; Giersing B; Page CJ; Blower PJ; Williamson RA; Peters BS;
TI - O'Doherty MJ In vivo evaluation of 111In-DTPA-N-TIMP-2 in Kaposi sarcoma associated with HIV infection.
SO - Eur J Nucl Med 2001 Jun;28(6):756-61
AD - Biosciences Department, University of Kent, Canterbury, UK.
Matrix metalloproteinases are the major agents responsible for the degradation of extracellular matrix and are produced at high levels by transformed and tumour cells, where they participate in the metastatic process by allowing local invasion. They are also more active at sites of new normal growth and angiogenesis. In the early stages of Kaposi sarcoma (KS), in vitro studies have demonstrated that vascular invasion can be inhibited by inhibitors of matrix metalloproteinases. Imaging of visceral and cutaneous KS presents a problem and therefore the potential use of a labelled inhibitor of metalloproteinases, N-TIMP-2, with indium-111 was thought to present a possible imaging tool. The biokinetics, dosimetry and potential for imaging with 111In-DTPA-N-TIMP-2 were assessed in five patients with HIV infection and KS. Between 103.1 and 108.0 MBq of this agent was injected into each patient, and the dynamic uptake over the kidneys was assessed, whole body scans were performed and blood samples were obtained. The clearance from the blood was rapid, with a first component half-time of 16.6+/-3.4 min and a second component half-time of 9.68+/-2.68 h. Two out of five patients experienced minor shivering but one of these patients was generally unwell before the study. The last three patients had no such problems. The tracer distributed predominantly to the kidneys and did not localise in other tissues. No KS lesions were clearly identified. 111In-DTPA-N-TIMP-2 can be successfully prepared and administered to patients safely, with a biodistribution and dosimetry which would allow its use as an imaging tracer. It is unlikely to be of use for imaging KS, but may have a role in other tumours that produce matrix metalloproteinases.
UI - 11453603
AU - Nuvor SV; Katano H; Ampofo WK; Barnor JS; Sata T
TI - Higher prevalence of antibodies to human herpesvirus 8 in HIV-infected individuals than in the general population in Ghana, West Africa.
SO - Eur J Clin Microbiol Infect Dis 2001 May;20(5):362-4
AD - Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.
UI - 11673818
AU - Nunez M; Saballs P; Valencia ME; Santos J; Ferrer E; Santos I; Berrocal
TI - A; Galindo MJ; Podzamczer D; Gonzlez-Lahoz J; Caelyx/KS Spanish Study Group Response to liposomal doxorubicin and clinical outcome of HIV-1-infected patients with Kaposi's sarcoma receiving highly active antiretroviral therapy.
SO - HIV Clin Trials 2001 Sep-Oct;2(5):429-37
AD - Hospital Carlos III, Madrid, Spain. firstname.lastname@example.org
PURPOSE: HIV-associated Kaposi's sarcoma (KS) may not resolve despite highly active antiretroviral therapy (HAART). Moreover, the therapeutic goal has shifted from palliative care to long-term durable complete remission. The objective of the study was to assess the impact of liposomal doxorubicin in the treatment of HIV-associated KS in the HAART era. METHOD: In this prospective, noncomparative, multicenter study, patients with more than 10 cutaneous lesions or visceral disease were treated with 20 mg/m(2) of liposomal doxorubicin (Caelyx) every 3 weeks in addition to their antiretroviral therapy. In addition to tumor measurements and laboratory tests, human herpes virus 8 (HHV-8) polymerase chain reaction (PCR) in peripheral blood mononuclear cells (PBMC) was performed. RESULTS: Out of 79 participants enrolled in the study, 47 (59%) had stage T(1), 41 (52%) I(1), and 32 (40%) S(1). Nine individuals were not evaluable for response, 32 (40%) had complete response, 30 (38%) partial response, 5 (6%) stable disease, and 3 (4%) progression. Regression analysis did not find any statistically significant factor predicting response. HHV-8 PCR was positive in 37/53 (70%) patients with available PBMC samples, and HHV-8 viremia cleared in 14/27 (52%) without correlation with clinical response. Eleven (14%) participants experienced a relapse of KS, while at the last update of data, 49 (62%) remained stable. The only risk factor for recurrence identified was the follow-up time (odds ratio [OR] 1.21, 95% CI 1.07-1.36; p =.002). CONCLUSION: The response rate of AIDS-associated KS to liposomal doxorubicin administered with HAART was high, and most often the response was durable. HHV-8 viremia did not correlate well with clinical outcome.
UI - 11676823
AU - Pellet C; Chevret S; Blum L; Gauville C; Hurault M; Blanchard G;
TI - Agbalika F; Lascoux C; Ponscarme D; Morel P; Calvo F; Lebbe C Virologic and immunologic parameters that predict clinical response of AIDS-associated Kaposi's sarcoma to highly active antiretroviral therapy.
SO - J Invest Dermatol 2001 Oct;117(4):858-63
AD - Laboratory of Pharmacology, Hopital Saint-Louis, Paris, France.
The purpose of the work was to assess the predictive value of biologic factors on the efficacy of highly active antiretroviral therapy alone or combined with chemotherapy on AIDS-associated Kaposi's sarcoma. Twenty-six AIDS-Kaposi's sarcoma patients who started therapy with protease inhibitors were investigated. No baseline chemotherapy was associated with less severe initial clinical status. Median follow-up was 652 d. The main outcome measures were as follows: best Kaposi's sarcoma clinical response; Kaposi's-sarcoma-associated herpesviral load in peripheral blood mononuclear cells using real-time quantitative polymerase chain reaction (non-detectable if less than 100 copies per microg); human immunodeficiency viral charge in plasma (non-detectable if less than 200 copies per ml); and CD4 lymphocyte count. Time to undetectable Kaposi's-sarcoma-associated herpesviral load, time to undetectable human immunodeficiency viral charge, and time to CD4 >or= 150 per microl were also recorded over time, from 2 mo measurements. Patients were staged according to the AIDS Clinical Trials Group-based tumor, immune, systemic staging system criteria. At baseline, Kaposi's sarcoma was progressive for 25 (96%) of the 26 enrolled patients. Complete or partial response to highly active antiretroviral therapy alone or combined with chemotherapy was achieved in 22 patients (85%). Median time to clinical response was estimated at 251 d. Clinical response was faster in patients without chemotherapy at baseline (p = 0.003) as well as in patients not previously treated with reverse transcriptase inhibitors (p = 0.0012). Using univariable analyses, predictive factors of clinical response were undetectable Kaposi's-sarcoma-associated herpesviremia (p = 0.013), undetectable human immunodeficiency viremia (p = 0.03), and relative variation of CD4 lymphocytes (p = 0.004). Using multivariable analysis, undetectable Kaposi's-sarcoma-associated herpesviremia (p = 0.009) and relative variation of CD4 (p = 0.005) were independently selected as having a predictive value for clinical response. Occurrence of nondetection of either Kaposi's-sarcoma-associated herpesvirus or human immunodeficiency virus was not associated with baseline CD4 value. Kaposi's-sarcoma-associated herpesvirus quantitative viral charge is an independent predictive factor of the efficacy of highly active antiretroviral therapy on AIDS-Kaposi's sarcoma. Our results support immune reconstitution as a mechanism of response of Kaposi's sarcoma to highly active antiretroviral therapy.
UI - 11696169
AU - Suda T; Katano H; Delsol G; Kakiuchi C; Nakamura T; Shiota M; Sata T;
TI - Higashihara M; Mori S HHV-8 infection status of AIDS-unrelated and AIDS-associated multicentric Castleman's disease.
SO - Pathol Int 2001 Sep;51(9):671-9
AD - Department of Pathology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Multicentric Castleman's disease (MCD) is a clinicopathologically defined entity characterized by systemic lymphadenopathy with unique pathomorphology such as angiosclerosis, blood vessel proliferation in and around follicles, and plasmacytosis. While its pathogenesis has remained unclarified for many years, identification of the human herpesvirus 8 (HHV-8) in at least some MCD cases has opened new perspectives in this field. Because previous reports have described many inconsistencies regarding HHV-8 positivity in MCD, we intended to clarify this issue by the introduction of more convincing methodologies. For this investigation, we introduced two antibodies produced in our laboratories that recognize a latent gene product ORF73 and a lytic gene product ORF59, together with two well-recognized methods, in situ hybridization for the detection of lytic phase transcript T1.1/nut-1, and genomic polymerase chain reaction (PCR). Eighty-two cases of MCD were collected from Japan (n = 75) and France (n = 7). In three cases, the patients were suffering from acquired immunodeficiency syndrome (AIDS). Immunohistochemistry and in situ hybridization showed identical results: only three out of 82 cases were positively stained, and all the positive cases were found to be the patients with AIDS. Genomic PCR was done in 43 cases, and only one case produced positive results: the only AIDS case among the 43 cases studied by genomic PCR. Histopathologically, the HHV-8-positive cases showed the highest intensity of angiosclerosis and germinal center / perifollicular vascular proliferation, while plasmacytosis was not severe in the HHV-8-positive cases. Some of the HHV-8-negative MCD cases displayed similar histopathology, but at a far less intense level, except for the plasmacytosis. These results suggest that: (i) all three of the HHV-8-positive MCD patients in the present group are the patients with AIDS; and (ii) HHV-8-positive MCD patients develop typical but marked angiosclerosis and vascular proliferation that might be differentiated from HHV-8-negative MCD patients, who showed far less intense changes.
UI - 11720464
AU - Engels EA; Rosenberg PS; Frisch M; Goedert JJ
TI - Cancers associated with Kaposi's sarcoma (KS) in AIDS: a link between KS herpesvirus and immunoblastic lymphoma.
SO - Br J Cancer 2001 Nov 2;85(9):1298-303
AD - Viral Epidemiology Branch and Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., Rockville, MD, USA.
Kaposi's sarcoma (KS), common among persons with acquired immunodeficiency syndrome (AIDS), is caused by KS herpesvirus (KSHV) but whether KSHV causes other malignancies is uncertain. Using linked United States AIDS and cancer registries, we measured the incidence of specific malignancies in persons with AIDS (4-27 months after AIDS onset). We identified associations with KSHV by calculating a relative risk: cancer incidence in persons with KS (all were KSHV-infected) divided by incidence in persons without KS. Using Poisson regression, relative risks were adjusted for human immunodeficiency virus risk group, gender, age, race, and calendar year. We included 189 159 subjects (26 972 with KS). Immunoblastic lymphoma was significantly associated with KS (506 cases; relative risks: unadjusted 2.44, 95%CI 2.00-2.96, adjusted 1.58, 95%CI 1.29-1.93). Only one immunoblastic lymphoma had pleura as primary site. None of 37 other specified malignancies (other non-Hodgkin lymphomas, haematological malignancies, solid tumours) was significantly associated with KS. In summary, the association of immunoblastic lymphoma with KS was specific among examined malignancies and remained significant after statistical adjustment. Our findings, and the previously demonstrated presence of KSHV in the histologically related primary effusion lymphoma, suggest that KSHV is involved in the pathogenesis of some immunoblastic lymphomas. Copyright 2001 Cancer Research Campaign
UI - 11600842
AU - Mazzi R; Parisi SG; Sarmati L; Uccella I; Nicastri E; Carolo G; Gatti F;
TI - Concia E; Andreoni M Efficacy of cidofovir on human herpesvirus 8 viraemia and Kaposi's sarcoma progression in two patients with AIDS.
SO - AIDS 2001 Oct 19;15(15):2061-2
UI - 11737340
AU - Hermans P
TI - Kaposi's sarcoma in HIV-infected patients: treatment options.
SO - HIV Med 2000 Jul;1(3):137-42
AD - CHU Saint-Pierre, Division of Infectious Diseases, rue Haute, 322, B-1000 Brussels, Belgium.
Kaposi's sarcoma (KS) is the most prevalent AIDS-associated tumour, occurring in 20-30% of HIV-1-infected individuals in the early 1980s. The introduction of highly active antiretroviral therapy (HAART) has dramatically reduced the incidence of the disease and might therefore support the concept of 'opportunistic malignancies' requiring immune impairments to occur. The relationship between the immune system and the epidemiology of this virus-induced tumour is of importance in order to identify new therapeutic approaches for treating or preventing its occurrence. As a model of impaired angiogenesis, therapeutic options for treating AIDS patients with KS should therefore target cell division, anti-angiogenic processes, immune modulators, cytokines and potentially antiviral drugs.
UI - 11558892
AU - Kreuter A; Gambichler T; Schlottmann R; Altmeyer P; Brockmeyer N
TI - Psoriasiform pustular eruptions from pegylated-liposomal doxorubicin in AIDS-related Kaposi's sarcoma.
SO - Acta Derm Venereol 2001 Jun-Jul;81(3):224
UI - 11363097
AU - Prescott LM
TI - Doxil offers hope to KS sufferers.
SO - J Int Assoc Physicians AIDS Care 1995 Dec;1(11):43-4
UI - 11684936
AU - Renwick N; Weverling GJ; Halaby T; Portegies P; Bakker M; Schulz TF;
TI - Goudsmit J Kaposi's sarcoma and human herpesvirus 8 infection do not protect HIV-1 infected homosexual men from AIDS dementia complex.
SO - AIDS 2001 Nov 9;15(16):2165-9
AD - Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, The Netherlands.
OBJECTIVE: To examine the association between Kaposi's sarcoma (KS), human herpes virus 8 (HHV8) and AIDS dementia complex (ADC). DESIGN: A total of 599 HIV-1 infected homosexual men participated in a prospective cohort study (Amsterdam, 1984-1996). METHODS: The risk for ADC in patients with prior KS or HHV8 infection was estimated using the Cox proportional hazards method with adjustments for antiretroviral medication and low CD4 cell counts. RESULTS: Of the 599 participants, 290 (48.4%) had HHV8 antibodies, 99 (16.5%) had KS and 30 (5.0%) had ADC. ADC was diagnosed in 5.2% of participants with KS and 5.0% of those without KS, and in 4.8% of HHV8 seropositive compared to 5.2% seronegative individuals and thus was not associated with KS or HHV8 infection. Using a time-dependent Cox proportional hazards analysis with the date of KS as risk factor, the risk for ADC was 2.7 [95% confidence interval (CI), 0.92-7.96; P = 0.07) and when only definite ADC was considered it was 3.5 (95% CI, 1.00-12.26;P = 0.05). After adjusting for decreases in CD4 cell count and use of medication, the hazards ratio for participants with KS to develop ADC was 2.0 (95% CI, 0.66-5.77; P = 0.23) and 2.6 (95% CI, 0.73-9.12; P = 0.14), respectively. HHV8 seropositivity, adjusted for the same variables, showed a risk for ADC of 0.85 (95% CI, 0.41-1.77;P = 0.66) and for definite ADC 0.69 (95% CI, 0.27-1.73; P = 0.42). The expected neuroprotective effects of antiretroviral medication were observed. CONCLUSIONS: KS or HHV8 does not significantly influence the risk for developing ADC in a group with a uniform risk for developing KS therefore we recommend caution in searching for a KS-associated or HHV8-derived therapy for ADC.
UI - 11750207
AU - Engels EA
TI - Human immunodeficiency virus infection, aging, and cancer.
SO - J Clin Epidemiol 2001 Dec;54 Suppl 1():S29-34
AD - Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., Room 8005, Rockville, MD 20852, USA. email@example.com
HIV infection increases non-Hodgkin's lymphoma and Kaposi's sarcoma risk. Among HIV-uninfected persons, risk for these malignancies and others increases with age. As HIV-infected persons age, new patterns in cancer incidence may emerge. In this article, data from the AIDS-Cancer Registry Match study are presented on risk for Kaposi's sarcoma and lung cancer among persons with AIDS. For 132,346 homosexual men with AIDS, Kaposi's sarcoma incidence was highest for men 30-39 years old (5.0 cases/100 person-years) and declined with age (P(trend) <.0001). This trend likely arises from variation in Kaposi's sarcoma herpesvirus prevalence among homosexual men. For 239,257 adults with AIDS (all risk groups), lung cancer incidence increased with age, and was higher than in the general population (P <.0001), probably reflecting heavy smoking among HIV-infected adults. Identifying separate effects of HIV and aging on cancer risk will require detailed data on individuals' HIV infection status and exposures to known carcinogens.
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