National Cancer Institute®
Last Modified: November 21, 2001
UI - 21245395
AU - Biggar RJ
TI - AIDS-related cancers in the era of highly active antiretroviral therapy.
SO - Oncology (Huntingt) 2001 Apr;15(4):439-48; discussion 448-9
AD - Viral Epidemiology Branch National Cancer Institute, Bethesda, Maryland, USA. Biggarb@epndce.nci.nih.gov
Highly active antiretroviral therapy (HAART) has shown great efficacy in reducing human immunodeficiency virus levels, increasing immunity, and prolonging the survival of persons with acquired immunodeficiency syndrome (AIDS). The risk of life-threatening infections has been greatly reduced. However, the impact of HAART on the incidence of malignancy has been less clear. Published studies generally show that the risk of developing Kaposi's sarcoma declined by about two-thirds between 1994 and 1995 and from 1996 onward (considered the HAART era). Even before 1994, the risk for Kaposi's sarcoma in persons with AIDS had declined considerably and this cancer has now become relatively uncommon. The mechanism by which this decline in incidence was achieved appears to involve improved immunity. Data on the reduction in the risk for non-Hodgkin's lymphoma are mixed. Several studies conducted between 1997 and 1999 found no reduction in the risk for non-Hodgkin's lymphoma, although the most recent data (from 1997 to 1999) show a 42% decrease in risk. Even with a one-third reduction, the risk for non-Hodgkin's lymphoma remains considerably elevated. This high risk may be related to the fact that HAART therapy does not restore the immune system to normalcy. The increased lymphocyte turnover, with its accompanying risk of genetic errors, may increase the risk of developing non-Hodgkin's lymphoma. Most reports have insufficient data to analyze the impact of HAART therapy on incidence of central nervous system lymphomas, but recent data (from 1997 to 1999) showed a significant reduction in that risk. The mechanism by which this might occur is unclear because the central nervous system is an immunologic sanctuary. The relatively low incidence of other cancers in persons with AIDS makes it difficult to gauge the effect of HAART on their incidence, but to date, no significant trends have been reported for specific tumor types or for the overall risk of non-AIDS-related cancers.
UI - 21443826
AU - Holkova B; Takeshita K; Cheng DM; Volm M; Wasserheit C; Demopoulos R;
TI - Chanan-Khan A Effect of highly active antiretroviral therapy on survival in patients with AIDS-associated pulmonary Kaposi's sarcoma treated with chemotherapy.
SO - J Clin Oncol 2001 Sep 15;19(18):3848-51
AD - Division of Hematology, Department of Medicine, Bellevue Hospital Center, New York University School of Medicine, New York, NY 10016, USA.
PURPOSE: Kaposi's sarcoma (KS) is the most common AIDS-related malignancy. Pulmonary involvement by KS (PKS) has carried a poor prognosis with median reported survival ranging from 3 to 10 months. We studied whether the introduction of highly active antiretroviral therapy (HAART; triple antiretroviral therapy including a protease inhibitor and two reverse transcriptase inhibitors) has been associated with improved survival for AIDS patients with PKS. PATIENTS AND METHODS: A retrospective study was performed of 37 consecutive patients with PKS and human immunodeficiency virus infection in the tumor registry at a large municipal hospital in New York City between 1994 to 1997. There were 16 patients from 1994 to 1995 (pre-HAART period) and 21 patients from 1996 to 1997 (post-HAART period). The primary end point was survival, which was defined as time from start of chemotherapy until death from any cause. RESULTS: Patients were analyzed by the date of diagnosis (pre- v post-HAART period) and whether or not they received HAART. Kaplan-Meier analysis showed significantly better survival in patients diagnosed in the post-HAART period (P =.0025). Additional Kaplan-Meier analysis indicated that patients on HAART had substantially better survival (P <.0001). Cox multivariate analyses showed that HAART therapy was associated with a reduced risk of death (hazard ratio = 0.09; 95% confidence interval, 0.03 to 0.69). CONCLUSION: In patients with AIDS-associated PKS and undergoing chemotherapy, administration of HAART was associated with increased survival.
UI - 21377983
AU - Ascherl G; Sgadari C; Bugarini R; Bogner J; Schatz O; Ensoli B; Sturzl M
TI - Serum concentrations of fibroblast growth factor 2 are increased in HIV type 1-infected patients and inversely related to survival probability.
SO - AIDS Res Hum Retroviruses 2001 Jul 20;17(11):1035-9
AD - Institute of Molecular Virology, GSF-National Research Center for Environment and Health GmbH, 85764 Neuherberg, Germany.
HIV-1-infected patients develop a generalized vasculopathy that is clinically most evident as Kaposi's sarcoma (KS), a multifocally appearing endothelial cell-derived tumor. Fibroblast growth factor 2 (FGF-2) is a potent autocrine and paracrine mitogen of endothelial cells and has been implicated in the cell proliferation and angiogenesis observed in KS. Here we determined by ELISA the FGF-2 serum concentrations in different clinical groups of HIV-1-infected patients. AIDS-KS patients (n = 53) and HIV-1-infected patients without KS (n = 39) revealed significantly increased FGF-2 serum concentrations (median, 4.5 and 4.6 pg/ml, respectively), as compared with the healthy control group (n = 22; median, 2.2 pg/ml; p < 0.01). FGF-2 concentrations were highest in untreated HIV-1-infected patients (median, 8.6 pg/ml) and were significantly decreased in patients undergoing antiretroviral therapy (AZT-median, 4.5 pg/ml; HAART-median, 2.5 pg/ml; p < 0.01). In addition, FGF-2 serum concentrations above 5.2 pg/ml were associated with a statistically significant higher risk of death in HIV-1-infected patients. Multivariate analysis showed that this effect is independent of CD4 levels, localization of KS (cutaneous or visceral), AIDS-defining opportunistic diseases, and therapy. Circulating FGF-2 may contribute to AIDS-associated vasculopathy and may be a sensitive and easily accessible surrogate marker to determine the survival time of HIV-1-infected patients and the efficacy of antiretroviral therapy.
UI - 21260406
AU - Amir H; Kaaya EE; Manji KP; Kwesigabo G; Biberfeld P
TI - Kaposi's sarcoma before and during a human immunodeficiency virus epidemic in Tanzanian children.
SO - Pediatr Infect Dis J 2001 May;20(5):518-21
AD - Department of Surgery, Muhimbili University College of Health Sciences, Dar Es Salaam, Tanzania.
BACKGROUND: With the onset of AIDS increased frequency of Kaposi's sarcoma (KS) has been reported. However, there is no case-based comparison of childhood (<14 years) KS before and during the HIV pandemic in sub-Saharan Africa. Here we report on the Tanzanian cancer registry data of pediatric KS in Tanzania and implications with regard to pathogenic factors. METHODS: One hundred fifty histologically confirmed pediatric KS (PKS) cases registered during 1968 through 1995 (28 years) were analyzed with regard to demographic and clinical characteristics before and during the AIDS epidemic. Statistical analysis was done with the Epi-Info program and chi square test. RESULTS: Of children with PKS 126 (84%) were male and 24 (16%) were female. The gender ratio was 5.1:1 and 5.4:1 during the endemic and epidemic periods, respectively. The highest occurrence of PKS was observed in the 0- to 5-years age group. Overall 73 (4.9/year) of these cases were registered during the pre and 77 (5.9/year) during the AIDS period. Over time a significant increase in anatomically disseminated KS cases was evident during the AIDS epidemic (P = 0.003). CONCLUSIONS: These observations indicate that children younger than 5 years are at high risk for developing KS, possibly reflecting low resistance to human herpesvirus (HHV) 8 infection. It is also likely that an increased susceptibility to HHV8 infection and morbidity is related to progressive immunodeficiency. The increase in AIDS PKS incidence appears to reflect a direct or indirect promoting effect of HIV on the development of KS lesions. Recognition of the high KS risk in small children warrants considerations of possible prevention measures including HIV/HHV8 vaccination and therapeutic options.
UI - 21439159
AU - Fingleton B; Matrisian LM
TI - Matrix metalloproteinases as targets for therapy in Kaposi sarcoma.
SO - Curr Opin Oncol 2001 Sep;13(5):368-73
AD - Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Acquired immune deficiency syndrome-associated Kaposi sarcoma is a progressive and occasionally fatal condition. The strong angiogenic component of this disease makes it particularly suitable for treatment with the emerging class of drugs that act as antiangiogenic agents. Matrix metalloproteinases have been shown to play prominent roles in the angiogenic process, and small molecule inhibitors of these enzymes are currently being tested as antiangiogenic agents in various malignancies. Given that matrix metalloproteinases contribute to multiple steps of the angiogenic process, inhibitors of these enzymes, either alone or in combination with other agents, may represent a particularly effective therapeutic approach for Kaposi sarcoma.
UI - 20298916
AU - Jacobson LP; Jenkins FJ; Springer G; Munoz A; Shah KV; Phair J; Zhang Z;
TI - Armenian H Interaction of human immunodeficiency virus type 1 and human herpesvirus type 8 infections on the incidence of Kaposi's sarcoma.
SO - J Infect Dis 2000 Jun;181(6):1940-9
AD - Department of Epidemiology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA. email@example.com
To determine Kaposi's sarcoma (KS) risk related to timing of human immunodeficiency virus type 1 (HIV-1) and human herpesvirus type 8 (HHV-8) infections, stored longitudinal sera from 400 homosexual men with known dates of HIV-1 seroconversion (+/-4.5 months) were tested for HHV-8 antibody. Times from HHV-8 seroconversion to KS were compared for the 69 men who became infected with HHV-8 after acquiring HIV-1 to the 182 men who were HHV-8 seropositive before their HIV-1 infection. None developed KS before coinfection. HHV-8 seroconversion after HIV-1 infection increased the risk of KS (risk ratio, 2.55; 95% confidence interval, 1.06-6.10) compared with those infected with HHV-8 before HIV-1. The KS hazards in HHV-8-infected men increased by 60% (P<.001) for each year of HIV-1 infection. Faster CD4 cell loss and higher HIV-1 RNA levels significantly predicted KS. The quicker development of KS in men acquiring HHV-8 after HIV-1 and its association with CD4 slope argues that KS is more likely if HHV-8 infection occurs in an immunocompromised person.
UI - 21192347
AU - Renwick N; Weverling GJ; Schulz T; Goudsmit J
TI - Timing of human immunodeficiency virus type 1 and human herpesvirus 8 infections and length of the Kaposi's sarcoma-free period in coinfected persons.
SO - J Infect Dis 2001 May 1;183(9):1427
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