National Cancer Institute®
Last Modified: November 21, 2001
1
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.
2
UI - 21413351
AU - Vilchez RA; Kozinetz CA; Butel JS
TI -
The changing incidence of four AIDS-related malignancies in a large
urban center.
SO - AIDS Patient Care STDS 2001 Aug;15(8):405-6
3
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.
4
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.
5
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.
6
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.
7
UI - 21443114
AU - Anonymous
TI -
Bibliography. Current World Literature. Cancer in AIDS.
SO - Curr Opin Oncol 2001 Sep;13(5):B139-42
8
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. ljacobso@jhsph.edu
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.
9
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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