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NCI CANCERLIT^® Search: AIDS-Related Lymphoma - August 2002

National Cancer Institute^®
Last Modified: August 1, 2002

Expression of cyclin-dependent kinase inhibitor p27(Kip1) in AIDS-related diffuse large-cell lymphomas is associated with
Small bowel intussusception caused by lymphomatous polyposis in a patient with AIDS.
[MRI of a cauda equina lymphoma]
Clinical trials referral resource. Clinical trials and NCI resources for cancer in HIV-positive patients.
Antiretroviral rounds. One patient, with another on the way.
Jejunocolic fistula: an unreported complication of acquired immunodeficiency syndrome-associated lymphoma.
Hepatitis C virus-Epstein-Barr virus interaction in patients with AIDS.
Trends in Kaposi's sarcoma and non-Hodgkin's lymphoma incidence in the United States from 1973 through 1998.

Table of Contents

1
UI - 12107101
AU - Gloghini A; Gaidano G; Larocca LM; Pierconti F; Cingolani A; Dal Maso L;
TI - Capello D; Franceschi S; Tirelli U; Libra M; Niu H; Dalla-Favera R; Carbone A Expression of cyclin-dependent kinase inhibitor p27(Kip1) in AIDS-related diffuse large-cell lymphomas is associated with Epstein-Barr virus-encoded latent membrane protein 1.
SO - Am J Pathol 2002 Jul;161(1):163-71
AD - Division of Pathology, Centro di Riferimento Oncologico, Istituto Nazionale Tumori, IRCCS, Aviano, Italy.
Knowledge of the role of cell-cycle regulators in the pathogenesis of acquired immune deficiency syndrome-related non-Hodgkin's lymphomas (AIDS-NHLs) is scarce. Here we analyzed 86 systemic AIDS-NHLs and 20 AIDS-primary central nervous system lymphomas for expression of p27(Kip1), a negative regulator of cell-cycle progression belonging to the Kip family of cyclin-dependent kinase inhibitors. In parallel, we investigated the relationship between p27(Kip1), the lymphoma proliferation index, Epstein-Barr virus status, expression of cellular cyclin D3 and cyclin D1, and B-cell differentiation stage. We report that AIDS-immunoblastic lymphomas (AIDS-IBLs), either systemic or primarily localized to the central nervous system, consistently express p27(Kip1) protein (19 of 24 and 10 of 14, respectively) despite the high proliferative rate of the lymphoma clone, suggesting a failure of p27(Kip1) to inhibit the cell cycle in AIDS-IBL. Conversely, the remaining systemic AIDS-NHLs and AIDS-primary central nervous system lymphomas preferentially fail to express p27(Kip1). Expression of p27(Kip1) in Epstein-Barr virus-positive AIDS-NHLs generally associates with latent membrane protein 1 (LMP1) expression and is related to a late stage of B-cell differentiation, characterized by the BCL-6-/MUM1+/syn-1+/- phenotypic profile, whereas it seems to be unrelated to the expression of cellular cyclins. In B cells in vitro, induction of LMP-1 expression under the control of inducible promoters up-regulates expression of p27(Kip1), thus providing a putative mechanistic explanation for the association between LMP1 and p27(Kip1) observed in vivo. Overall, these data show that AIDS-IBL pathogenesis is characterized by loss of the inverse relationship between p27(Kip1) positivity and tumor growth fraction that is otherwise generally observed in normal lymphoid tissues and in most other types of NHLs.

2
UI - 9128353
AU - Finkle HI
TI - Small bowel intussusception caused by lymphomatous polyposis in a patient with AIDS.
SO - Am J Gastroenterol 1997 Apr;92(4):726-7

3
UI - 11965182
AU - Boukriche Y; Krainik A; Rosenberg C; Guilmin F; Felce-Dachez M; Masson C
TI - [MRI of a cauda equina lymphoma]
SO - Rev Neurol (Paris) 2002 Feb;158(2):253-5
AD - Services de Neurologie, Cliniques Universitaires de Mont-Godinne, Yvoir, Belgique.

4
UI - 11866136
AU - Black JB; Feigal EG; Gore-Langton RE
TI - Clinical trials referral resource. Clinical trials and NCI resources for cancer in HIV-positive patients.
SO - Oncology (Huntingt) 2002 Feb;16(2):200-2, 205, 207
AD - National Cancer Institute, USA.

5
UI - 12170959
AU - Neu N
TI - Antiretroviral rounds. One patient, with another on the way.
SO - AIDS Clin Care 2000 May;12(5):42-3

6
UI - 11782623
AU - Kumar A; West JC; Still CD; Komar MJ; Babameto GP
TI - Jejunocolic fistula: an unreported complication of acquired immunodeficiency syndrome-associated lymphoma.
SO - J Clin Gastroenterol 2002 Feb;34(2):194-5

7
UI - 12115996
AU - Challine D; Buisson M; Cadilhac M; Germanidis G; Joab I; Eliaszewicz M;
TI - Caumes E; Flahault A; Fillet AM; Pawlotsky JM; Seigneurin JM Hepatitis C virus-Epstein-Barr virus interaction in patients with AIDS.
SO - J Med Virol 2002 Aug;67(4):510-5
AD - Department of Virology (EA 3489), Hopital Henri Mondor, Universite Paris XII, Creteil, France.
Immortalization of B cells by Epstein-Barr virus (EBV) and their subsequent proliferation leads to B-cell non-Hodgkin's lymphoma in immunocompromised patients. The role of hepatitis C virus (HCV) in B-cell non-Hodgkin's lymphoma has recently been raised, and an interaction between HCV and EBV is supported by recent in vitro experiments. The aim of this study was to investigate in vivo interactions between HCV and EBV in patients with AIDS, i.e., patients exposed to the risk of EBV-related B-cell non-Hodgkin's lymphoma. A total of 135 patients were prospectively studied. Serological and molecular markers of HCV, EBV, and human immunodeficiency virus (HIV) infection were sought. All the patients harbored latent EBV infection, and 20% had detectable HCV RNA in serum. No significant relationship was found between HIV, HCV, and EBV viral load in peripheral blood mononuclear cells or plasma. There was no difference between anti-HCV-positive and -negative patients or between HCV RNA-positive and -negative patients with regard to the prevalence of EBV markers, especially EBV replication markers. The presence of EBV replication markers was not related to HCV RNA seropositivity or to HCV viral load. Five patients subsequently developed B-cell non-Hodgkin's lymphoma, none of whom had markers of EBV or HCV replication. These results argue against an in vivo interaction between HCV and EBV in patients with AIDS, and against a role of HCV infection in the occurrence of B-cell non-Hodgkin's lymphoma in these patients. Copyright 2002 Wiley-Liss, Inc.

8
UI - 12189223
AU - Eltom MA; Jemal A; Mbulaiteye SM; Devesa SS; Biggar RJ
TI - Trends in Kaposi's sarcoma and non-Hodgkin's lymphoma incidence in the United States from 1973 through 1998.
SO - J Natl Cancer Inst 2002 Aug 21;94(16):1204-10
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
BACKGROUND: The incidence of Kaposi's sarcoma (KS) and non-Hodgkin's lymphoma (NHL) in the general population has markedly increased since the onset of the AIDS epidemic in 1981. However, during the 1990s, the dynamics of the AIDS epidemic changed, as human immunodeficiency virus (HIV) infection rates slowed and effective antiretroviral therapies were introduced. We examined the impact of these changes on the general population incidence of KS and NHL. METHODS: Age-standardized incidences for KS and NHL from 1973 through 1998 were obtained from nine population-based cancer registries that participate in the Surveillance, Epidemiology and End Results (SEER) program. RESULTS: During the mid-1990s, KS incidence declined sharply in all nine registries. Decreases in KS incidence were most evident in San Francisco, where KS rates among white men had risen from 0.5 per 100 000 people per year in 1973 to between 31.1 and 33.3 from 1987 through 1991 and then declined to 2.8 in 1998. With background NHL incidence in the general population being much higher than that for KS, changes in incidence related to the AIDS epidemic were most evident in subgroups at high risk of AIDS. In San Francisco, NHL rates among white men rose from 10.7 in 1973 to a peak of 31.4 in 1995 and then declined to 21.6 in 1998. NHL types that were most highly AIDS-associated declined most steeply, whereas the incidence of NHL types not associated with AIDS was either stable or increasing. CONCLUSION: Changes in KS and NHL incidence since the mid 1990s may reflect declines in the number of individuals with AIDS and improved immune function in such individuals following the introduction of effective antiretroviral therapies in the 1990s. Notably, non-AIDS-associated NHL incidence has continued to increase steadily through 1998.

The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.

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