- Cancer Types
Information about risk, prevention, screening, symptoms, diagnosis, treatment, and support for all cancers Cancer A to Z - Cancer Treatment
Cancer Treatment
Information about cancer treatment, including surgery, chemotherapy, radiation therapy, clinical trials, proton therapy, complementary medicine, and cutting edge technologies.
- Risk and Prevention
- Cancer Drugs
- Support
Support
Ways for cancer patients and caregivers to cope with cancer, side effects, nutrition, general cancer support issues, grief/end of life issues, and shared survivor's experiences.
- Healthcare Professionals
- Clinical Trials
My Patient Treatment Binder
OncoLink Blogs
What's My Cancer Risk?
OncoPilot: Navigating Your Cancer Journey
Community Events Calendar
OncoLink eNews
Abramson Cancer CenterNCI CANCERLIT® Search: AIDS-Related Lymphoma - September 2002
National Cancer Institute®
Last Modified: September 1, 2002
- Systemic non-Hodgkin lymphoma in HIV-infected patients with effective suppression of HIV replication: persistent occurrence but improved
- HIV-associated lymphomas: the last opportunists?
- Absolute level of Epstein-Barr virus DNA in human immunodeficiency virus type 1 infection is not predictive of AIDS-related non-Hodgkin lymphoma.
- AIDS-related primary central nervous system lymphoma: prolonged remission associated with highly active antiretroviral therapy.
- Expression of RB2/p130 tumor-suppressor gene in AIDS-related non-Hodgkin's lymphomas: implications for disease pathogenesis.
- Expression profile of MUM1/IRF4, BCL-6, and CD138/syndecan-1 defines novel histogenetic subsets of human immunodeficiency virus-related
- Expression of cyclin-dependent kinase inhibitor p27(Kip1) in AIDS-related diffuse large-cell lymphomas is associated with
- Human herpesvirus-8-associated lymphoma of the bowel in human immunodeficiency virus-positive patients without history of primary
- High dose of idarubicin-based regimen for diffuse large cell AIDS-related non-Hodgkin's lymphoma patients: a pilot study.
Table of Contents
1
UI - 12154338
AU - Gerard L; Galicier L; Maillard A; Boulanger E; Quint L; Matheron S;
TI -
Cardon B; Meignin V; Oksenhendler E
Systemic non-Hodgkin lymphoma in HIV-infected patients with effective
suppression of HIV replication: persistent occurrence but improved
survival.
SO - J Acquir Immune Defic Syndr 2002 Aug 15;30(5):478-84
AD - Service d'Immuno-Hematologie. Hopital Saint-Louis, AP-HP, Paris, France.
laurence.gerard@sls.ap-hop-paris.fr
The incidence of systemic non-Hodgkin lymphoma (NHL) has only slightly
decreased since the introduction of highly active antiretroviral therapy
(HAART), suggesting that current antiretroviral strategies do not
eliminate the lymphoma risk. This study evaluates the evolving
characteristics of HIV and NHL between the pre-HAART and the post-HAART
periods in 246 HIV-infected NHL patients from a single institution.
Major HIV-related characteristics were similar in the two periods. Most
patients in the post-HAART period presented with unknown (23%),
untreated (16%), or uncontrolled (37%) HIV infection. Despite an
increased frequency of advanced stage IV disease in the post-HAART
period (68% vs. 53%, p =.03), the overall survival has improved, with a
2-year survival probability of 61.6% versus 35.9%, (p <.001). This was
associated with an increased complete remission rate (69% vs. 55%, p
=.04) and the generalization of more intensive chemotherapy regimens.
Most patients (76%) who developed NHL in the post-HAART period had
uncontrolled HIV replication. However, 27 patients (24%) developed NHL
despite an effective viral suppression at NHL diagnosis. Patients who
were naive to any antiretroviral therapy at NHL diagnosis had an overall
survival probability very similar to that of patients with controlled
HIV replication.Improvement in the overall survival rate in the
post-HAART period was associated with more intensive chemotherapy
regimens, increased complete remission rate, and a likely benefit of
continuation or introduction of HAART.
2
UI - 12184253
AU - Lucas GM
TI -
HIV-associated lymphomas: the last opportunists?
SO - Hopkins HIV Rep 2001 Jan;13(1):11-3, 16
3
UI - 12134237
AU - Van Baarle D; Wolthers KC; Hovenkamp E; Niesters HG; Osterhaus AD;
TI -
Miedema F; Van Oers MH
Absolute level of Epstein-Barr virus DNA in human immunodeficiency virus
type 1 infection is not predictive of AIDS-related non-Hodgkin lymphoma.
SO - J Infect Dis 2002 Aug 1;186(3):405-9
AD - Department of Clinical Viro-Immunology, Sanquin Research at CLB, and
Department of Hematology, Academic Medical Center, University of
Amsterdam, 1066 CX Amsterdam, The Netherlands. D_van_Baarle@clb.nl
To study whether Epstein-Barr virus (EBV) load can be used to predict
the occurrence of acquired immunodeficiency syndrome-related non-Hodgkin
lymphoma (AIDS-NHL), we determined EBV load longitudinally for
individuals infected with human immunodeficiency virus type 1. EBV load
in peripheral blood mononuclear cells (PBMC) was high and displayed
considerable fluctuations over time, indicating that absolute EBV load
in PBMC is not predictive of the development of AIDS-NHL. EBV DNA was
also detectable in serum at some time points but at a lower level.
4
UI - 12188396
AU - Chotmongkol V; Pesee M
TI -
AIDS-related primary central nervous system lymphoma: prolonged
remission associated with highly active antiretroviral therapy.
SO - J Med Assoc Thai 2002 May;85(5):634-7
AD - Department of Medicine, Faculty of Medicine, Khon Kaen University,
Thailand.
A 36-year-old HIV-seropositive man developed progressive confusion and
unilateral tremor of the hand. His medical history included cryptococcal
meningitis and CMV colitis. CT scan revealed a single hyperdense mass
with minimal peripheral enhancement at the region of the cerebral
peduncle and pons, causing obstructive hydrocephalus. He was treated
with ventriculo-peritoneal shunt and cranial radiotherapy. He also
received treatment with highly active antiretroviral therapy (HAART). A
CD4+ cell count was increased from 2 to 345 cells/mm3. He returned to
normal function for about 32 months after treatment.
5
UI - 12196924
AU - Lazzi S; Bellan C; De Falco G; Cinti C; Ferrari F; Nyongo A; Claudio PP;
TI -
Tosi GM; Vatti R; Gloghini A; Carbone A; Giordano A; Leoncini L; Tosi P
Expression of RB2/p130 tumor-suppressor gene in AIDS-related
non-Hodgkin's lymphomas: implications for disease pathogenesis.
SO - Hum Pathol 2002 Jul;33(7):723-31
AD - Institute of Pathological Anatomy and Histology, University of Siena,
Siena, Italy.
In this study we examined 21 cases of AIDS-related lymphomas for genomic
organization and expression of RB2/p130 oncosuppressor gene and compared
the results with the proliferative features of these neoplasms. We found
no mutations in the RB2/p130 gene and unusually high percentages of
cells expressing nuclear pRb2/p130 in tumors with a high proliferative
activity, such as AIDS-related lymphomas. These findings might suggest
that a molecular mechanism usually observed in viral-linked oncogenesis
could be involved. We performed in vitro and in vivo binding assays to
investigate whether the human immunodeficiency virus (HIV) gene product
Tat and Rb2/p130 could interact. The results of these assays revealed
that the HIV-1 Tat protein binds specifically to pRb2/p130. This may
result in the inactivation of its oncosuppressive properties and the
induction of genes needed to proceed through the cell cycle including
p107, cyclin A, and cyclin B. Using single-cell polymerase chain
reaction (PCR) assay, we found HIV-1 DNA in the neoplastic cells of only
2 of the 21 cases examined, whereas PCR on whole tissue revealed HIV-1
DNA in all of the cases. Furthermore, a diffuse and nuclear stain was
observed in tissue sections with anti-Tat monoclonal antibody. These
findings are in accordance with the notion that soluble Tat protein
could function as a biologically active extracellular protein released
by infected cells and taken up readily by uninfected B cells. In
conclusion, our results seem to suggest that pRb2/p130 oncosuppressor
protein may be a target in the interaction between the HIV-1 gene
products and host proteins. Copyright 2002, Elsevier Science (USA). All
rights reserved.
6
UI - 11157493
AU - Carbone A; Gloghini A; Larocca LM; Capello D; Pierconti F; Canzonieri V;
TI -
Tirelli U; Dalla-Favera R; Gaidano G
Expression profile of MUM1/IRF4, BCL-6, and CD138/syndecan-1 defines
novel histogenetic subsets of human immunodeficiency virus-related
lymphomas.
SO - Blood 2001 Feb 1;97(3):744-51
AD - Divisions of Pathology and Medical Oncology A, Centro di Riferimento
Oncologico, Istituto Nazionale Tumori, IRCCS, Aviano, Italy.
This study was aimed at defining the histogenesis of the pathologic
spectrum of lymphoma arising in the context of human immunodeficiency
virus (HIV) infection. Toward this aim, 87 AIDS-related non-Hodgkin
lymphomas (AIDS-NHL) and 16 Hodgkin lymphomas arising in HIV+ patients
(HIV-HL) were comparatively analyzed for the expression pattern of
several B-cell histogenetic markers, including BCL-6 (expressed by
centroblasts and centrocytes), MUM1/IRF4 (expressed by late centrocytes
and post-germinal center [GC] B cells), and CD138/syn-1 (expressed by
post-GC B cells). Expression of MUM1, BCL-6, and syn-1 segregated 3
major phenotypic patterns among AIDS-NHL and HIV-HL: (1) the
BCL-6+/MUM1-/syn-1- pattern, selectively clustering with a large
fraction of AIDS-Burkitt lymphoma (17 of 19) and of systemic
AIDS-diffuse large cell lymphoma (12 of 16); (2) the BCL-6-/MUM1+/syn-1-
pattern, associated with a fraction of AIDS-immunoblastic lymphoma (8 of
24); and (3) the BCL-6-/MUM1+/syn-1+ pattern, associated with systemic
and primary central nervous system immunoblastic lymphoma (14 of 24) and
with primary effusion lymphoma (10 of 10), plasmablastic lymphoma of the
oral cavity (7 of 7), and HIV-HL (15 of 16). Analysis of nonneoplastic
lymph nodes showed that the 3 phenotypic patterns detected in AIDS-NHL
and HIV-HL correspond to distinct stages of physiologic B-cell
development-centroblasts (BCL-6+/MUM1-/syn-1-), late GC/early post-GC B
cells (BCL-6-/MUM1+/syn-1-), and post-GC B cells (BCL-6-/MUM1+/syn-1+).
Expression of the Epstein-Barr virus-encoded latent membrane protein-1
clustered with the BCL-6-/MUM1+/syn-1+ profile throughout the
clinicopathologic spectrum of AIDS-NHL and HIV-HL. Overall, these
results define novel histogenetic subsets of AIDS-NHL and HIV-HL and may
provide novel tools for refining the diagnosis of these disorders.
7
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.
8
UI - 12203218
AU - Costes V; Faumont N; Cesarman E; Rousset T; Meggetto F; Delsol G;
TI -
Brousset P
Human herpesvirus-8-associated lymphoma of the bowel in human
immunodeficiency virus-positive patients without history of primary
effusion lymphoma.
SO - Hum Pathol 2002 Aug;33(8):846-9
AD - Laboratoire d'Anatomie Pathologique, Centre Hospitalier Universitaire de
Purpan, Toulouse, France.
This report describes two cases of human herpesvirus-8
(HHV-8)-associated large cell lymphoma of the bowel in human
immunodeficiency virus (HIV)-positive men. Immunohistochemistry provides
evidence of HHV-8 infection of the lymphoma cells (LNA1+, vIL-6+). In
both cases, lymphoma cells were coinfected by the Epstein-Barr virus.
One case was of B-cell lineage, but the second one was of null phenotype
with isolated expression of the CD3 molecule. However, in the latter
case, assessment of B- or T-cell clonality remained elusive. The chief
finding for these two cases was the lack of history of primary effusion
lymphoma. There was an apparent restriction of the tumor to the large
bowel in the first case. For the second case, the bowel tumor was
preceded by lymph node and liver involvement. The cases suggest that the
incidence of HHV-8 infection in large cell lymphoma arising in the
setting of HIV infection (other than primary effusion lymphoma) may be
underestimated and that the detection of the viral gene products would
be appropriate for greater understanding of the pathogenesis of these
tumors. HUM PATHOL 33:846-849. Copyright 2002, Elsevier Science (USA).
All rights reserved.
9
UI - 11602411
AU - Gastaldi R; Martino P; Gentile G; Cafolla A; Cordone I; Giannini G;
TI -
Torromeo C; Palmisano L; Picardi V; Andreotti M; Avvisati G; Mandelli F
High dose of idarubicin-based regimen for diffuse large cell
AIDS-related non-Hodgkin's lymphoma patients: a pilot study.
SO - Haematologica 2001 Oct;86(10):1051-9
AD - Ematologia, Dipartimento di Biotecnologie Cellulari ed Ematologia,
University "La Sapienza" of Rome, via Benevento, 6 00161 Rome, Italy.
gastaldi@bce.med.uniroma1.it
BACKGROUND AND OBJECTIVES: Intensive chemotherapy (CHT) in AIDS-related
non-Hodgkin's lymphoma (AIDS-NHL patients) is a vexing problem. Our
purpose was to evaluate the feasibility of a high dose idarubicin
(HD-IDA)-based regimen in diffuse large cell (DLC) AIDS-NHL patients.
DESIGN AND METHODS: Fourteen stage I-IV untreated DLC AIDS-NHL patients
with a performance status <3 and no prior AIDS-related diseases received
CIOD: cyclophosphamide, HD-IDA (25 mg/m2 in 8 patients, 20 mg/m2 in 6
patients) vincristine and dexamethasone plus granulocyte
colony-stimulating factor (G-CSF) and prophylaxis against infections.
The outcomes measured were: rate of response, disease-free survival
(DFS), overall survival (OS) and the impact of chemotherapy on
immunologic and virological parameters. RESULTS: Complete response was
achieved in 13/14 cases (response rate: 93%). The median time of
response and survival was 33 (range 5-79) and 35.5 (range 6-84) months,
respectively. At 60 months the DFS and OS were 71% and 44%,
respectively. CIOD with idarubicin 20 mg/m2 was better tolerated than
that with 25 mg/m2 and was administered with a higher mean
average-relative-dose-intensity (95.38+/-7% vs 83.35+/-15.59%,
p=0.0001). Opportunistic infections were more frequent in patients with
a baseline CD4 <100 than those with >100 cells/microL (4/5 vs 1/9:
p=0.0229). After 3 CIOD courses the mean CD4 cells/microL was
significantly lower (p=0.001) and the mean HIV.1 RNA load was
significantly higher (p=0.045) than at baseline. INTERPRETATION AND
CONCLUSIONS: The proposed chemotherapeutic regimen for AIDS-related
non-Hodgkin's lymphoma is feasible in an outpatient setting in selected
patients with relatively well-preserved immune function.
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.
Cancer Types
Bone Cancer
Brain Tumors
Breast Cancer
Carcinoid Tumors
Endocrine System Cancers
Gastrointestinal Cancers
Gynecologic Cancers
Head and Neck Cancers
Leukemia
Lung Cancers
Lymphomas
Myelomas
Pediatric Cancers
Penile Cancer
Prostate Cancer
Sarcomas
Skin Cancers
Testicular Cancer
Thyroid Cancer
Urinary Tract Cancers
OncoLink Vet
Cancer Treatment
Biologic Therapy
Bone Marrow Transplants
Chemotherapy
Clinical Trials
Complementary Medicine
Gene Therapy
General Treatment Concerns
Hormone Therapy
PDT Center
Proton Therapy
Radiation Oncology
Surgical Oncology
Targeted Therapies
Vaccine Therapies
Cancer Support
Caregivers
Hospice Care and Bereavement
Nutrition and Cancer
Sexuality & Fertility
Side Effects
Support
Survivorship
Exercise and Cancer
Cancer Resources
Cancer News
OncoLink University
Nurses' Notes
Conferences
Newly Diagnosed Patients
Causes and Prevention
Legal and Financial Information for Patients
LGBT Resources
NCI Resources
Global Resources
Cancer Resource List
Resources for Young Adults
OncoLink Media Library
OncoLink TV
Book, Music and Video Reviews
Ask the Experts
Brown Bag Chat
Tracy's Corner
About OncoLink
About OncoLink
Giving to OncoLink
Contact Information
Usage Policy
Editorial Board
How to Partner with OncoLink
Link to OncoLink
Mission Statement
