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Abramson Cancer CenterNCI CANCERLIT® Search: Hodgkin's Lymphoma - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
- Another patient with neck irradiation and increased susceptibility to acute mountain sickness.
- Cytoplasmic aggregation of TRAF2 and TRAF5 proteins in the Hodgkin-Reed-Sternberg cells.
- Hodgkin's disease of the head and neck in human immunodeficiency virus-infected patients.
- International note: second malignant neoplasms in children: a multicenter study of the Polish Pediatric Leukemia/Lymphoma Group.
- Is escalated BEACOPP a standard therapy for advanced Hodgkin's disease?
- Analysis of octamer-binding transcription factors Oct2 and Oct1 and their coactivator BOB.1/OBF.1 in lymphomas.
- ICAM-3 expression on endothelium in lymphoid malignancy.
- Granulomatous Pneumocystis carinii pneumonia in patients with malignancy.
- Dorothy Reed and Hodgkin's disease: a reflection after a century.
- Lymphocyte-predominant Hodgkin disease in children.
- Loss of PU.1 expression is associated with defective immunoglobulin transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin
- Expression of a mutated form of the p85alpha regulatory subunit of phosphatidylinositol 3-kinase in a Hodgkin's lymphoma-derived cell line
- Adapting a transforming growth factor beta-related tumor protection strategy to enhance antitumor immunity.
- Activated Notch1 signaling promotes tumor cell proliferation and survival in Hodgkin and anaplastic large cell lymphoma.
- Expression of survival receptors in Hodgkin disease cell lines.
- The bone marrow in Hodgkin's disease--a two year study.
- West Nile virus meningoencephalitis complicated by motor aphasia in Hodgkin's lymphoma.
- Fine needle aspiration in Hodgkin's disease.
- [Lymphomas in childhood]
- [Risk factors for Hodgkin's lymphomas]
- [Successful chemotherapy of cancer. Remission of Hodgkin's disease. IV]
- [Hodgkin lymphomas: current understanding of pathogenesis and pathomorphology]
- Polymorphic tumor necrosis factors microsatellite TNFa4 is associated with resistance of Hodgkin lymphoma to chemotherapy and with replapses
- [Treatment regimen for children and adolescents with Hodgkin's disease designed to decrease late complications of radiotherapy]
- A population-based study of intensive multi-agent chemotherapy with or without autotransplant for the highest risk Hodgkin's disease patients
- Treatment of refractory Hodgkin's disease with modified Stanford V program.
- [Hodgkin lymphoma]
Table of Contents
1
UI - 11990158
AU - Basnyat B; Litch J
TI -
Another patient with neck irradiation and increased susceptibility to
acute mountain sickness.
SO - Wilderness Environ Med 1997 Aug;8(3):176
2
UI - 12000717
AU - Horie R; Watanabe T; Ito K; Morisita Y; Watanabe M; Ishida T;
TI -
Higashihara M; Kadin M; Watanabe T
Cytoplasmic aggregation of TRAF2 and TRAF5 proteins in the
Hodgkin-Reed-Sternberg cells.
SO - Am J Pathol 2002 May;160(5):1647-54
AD - Division of Pathology, Department of Cancer Research, The Institute of
Medical Science, The University of Tokyo, Tokyo, Japan.
We previously reported that ligand-independent signaling by highly
expressed CD30 in Hodgkin-Reed-Sternberg (H-RS) cells is responsible for
constitutive activation of NF-kappa B. In the present study, we
characterize the intracellular localization of tumor necrosis factor
(TNF) receptor associated factor (TRAF) proteins in H-RS cells. Confocal
immunofluorescence microscopy of cell lines derived from H-RS cells and
HEK293 transformants highly expressing CD30 revealed aggregation of
TRAF2 and TRAF5 in the cytoplasm as well as clustering near the cell
membrane. In contrast, TRAF proteins were diffusely distributed in the
cytoplasm in cell lines unrelated to Hodgkin's disease (HD) and control
HEK293 cells. Furthermore, the same intracellular distribution of TRAF
proteins was demonstrated in H-RS cells of lymph nodes of HD, but not in
lymphoma cells in lymph nodes of non-Hodgkin's lymphoma.
Dominant-negative TRAF2 and TRAF5 suppressed cytoplasmic aggregation
along with constitutive NF-kappa B activation in H-RS cell lines.
Confocal immunofluorescence microscopy also revealed co-localization of
IKK alpha, NIK, and I kappa B alpha with aggregated TRAF proteins in
H-RS cell lines. These results suggest involvement of TRAF protein
aggregation in the signaling process of highly expressed CD30 and
suggest they function as scaffolding proteins. Thus, cytoplasmic
aggregation of TRAF proteins appears to reflect constitutive CD30
signaling which is characteristic of H-RS cells.
3
UI - 11791243
AU - Poluri A; Shah KG; Carew JF; Shaha AR; Har-El G; Lucente FE; Singh B
TI -
Hodgkin's disease of the head and neck in human immunodeficiency
virus-infected patients.
SO - Am J Otolaryngol 2002 Jan-Feb;23(1):12-6
AD - Department of Otolaryngology, State University of New York-Health
Sciences Center at Brooklyn, Brooklyn, NY.
INTRODUCTION: Hodgkin's disease can occur in immunocompromised patients.
However, the head and neck manifestations of Hodgkin's disease in human
immunodeficiency virus (HIV)-infected patients remain ill defined. The
aim of this study was to describe Hodgkin's disease of the head and neck
in HIV-infected patients and compare it with noninfected patients.
MATERIALS AND RESULTS: Sixteen patients presented with Hodgkin's disease
of the head and neck to the King's County Hospital Center, Brooklyn, New
York, beginning in January of 1991. Five patients were infected with
HIV. Hodgkin's disease involved the head and neck regions in 90.5% of
cases, occurring in 100% of HIV-infected and in 81% of noninfected
patients. Manifestations of Hodgkin's disease were isolated to the head
and neck region in only 20% of HIV-infected and in 27% of noninfected
patients. Lymphatic structures were involved in all cases with head and
neck involvement. Systemic or group B symptoms (fever, night sweats,
fatigue, and weight loss of more than 10% of normal body weight) were
present in 40% of HIV-infected patients and in 27% of noninfected
patients. Advanced stage disease (Stage III/IV) was diagnosed in 80% of
HIV-infected patients compared with 45% of noninfected patients. The
mixed cellularity subtype was most common in HIV-infected patients
(75%), whereas the nodular sclerosis subtype predominated in noninfected
patients (50%). CONCLUSIONS: The data combined with our report of the
literature suggest that the course, presentation, and outcome of
Hodgkin's disease is markedly altered in HIV-infected patients. An
aggressive approach to the diagnosis and management is suggested in this
patient population.
4
UI - 11984804
AU - Kowalczyk JR; Nurzynska J; Armata J; Boguslawska-Jaworska J;
TI -
Rokicka-Milewska R; Sonta-Jakimczyk D; Balwierz W; Chybicka A;
Kaczmarek-Kanold M; Kolecki P; Matysiak M; Pawelec K; Polish Pediatric
Leukemia/Lymphoma Group
International note: second malignant neoplasms in children: a
multicenter study of the Polish Pediatric Leukemia/Lymphoma Group.
SO - Med Pediatr Oncol 2002 Jun;38(6):421-3
AD - Department of Pediatric Hematology/Oncology, University Children's
Hospital, Lublin, Poland. jkowalcz@dsk.lublin.pl
5
UI - 11920203
AU - Carde P; Cavalli F; Diehl V; Franklin J
TI -
Is escalated BEACOPP a standard therapy for advanced Hodgkin's disease?
SO - Hematol J 2000;1(4):282-90
AD - Institute Gustav-Roussy, Villejuif, France. carde@igr.fr
6
UI - 11904338
AU - Saez AI; Artiga MJ; Sanchez-Beato M; Sanchez-Verde L; Garcia JF; Camacho
TI -
FI; Franco R; Piris MA
Analysis of octamer-binding transcription factors Oct2 and Oct1 and
their coactivator BOB.1/OBF.1 in lymphomas.
SO - Mod Pathol 2002 Mar;15(3):211-20
AD - Molecular Pathology Program, Centro Nacional de Investigaciones
Oncologicas Carlos III, Madrid, Spain.
Oct1 and Oct2 are transcription factors of the POU homeo-domain family
that bind to the Ig gene octamer sites, regulating B-cell-specific
genes. The function of these transcription factors is dependent on the
activity of B-cell-restricted coactivators such as BOB.1/OBF.1.
Independent studies of the expression of these proteins in non-Hodgkin's
lymphoma have been restricted to single markers, and most lack data
concerning immunohistochemical expression. Thus, we have investigated
the expression of Oct1, Oct2, and BOB.1/OBF.1 in human reactive lymphoid
tissue and in a series of 140 Hodgkin and non-Hodgkin's lymphomas. None
of these proteins was found to be restricted to B cells, although only B
cells expressed high levels of all three markers. Additionally, germinal
center B cells showed stronger Oct2 and BOB.1/OBF.1 staining.
Consequently, most B-cell lymphomas showed reactivity for all three
antibodies. Oct2 expression was significantly higher in germinal
center-derived lymphomas, although other B-cell lymphomas also displayed
a high level of Oct2 expression. Although T-cell lymphomas and Hodgkin's
lymphomas expressed some of these proteins, they commonly exhibited less
reactivity than B-cell lymphomas. Despite not being entirely
cell-specific, the strong nuclear expression of Oct2 and BOB.1/OBF.1 by
germinal center- derived lymphomas makes these antibodies a potentially
useful tool in lymphoma diagnosis.
7
UI - 8214000
AU - Doussis-Anagnostopoulou I; Kaklamanis L; Cordell J; Jones M; Turley H;
TI -
Pulford K; Simmons D; Mason D; Gatter K
ICAM-3 expression on endothelium in lymphoid malignancy.
SO - Am J Pathol 1993 Oct;143(4):1040-3
AD - Nuffield Department of Pathology, John Radcliffe Hospital, Oxford,
United Kingdom.
Intercellular adhesion molecule-3 (ICAM-3), the third receptor for
lymphocyte function-associated antigen molecule-1 and a new member of
the immunoglobulin superfamily has been recently characterized using
specific monoclonal antibodies. In the present study, we show
immunocytochemically that ICAM-3 is present on T and B cells in the
mantle zones and on a subpopulation of follicular center cells in
reactive lymph nodes and only occasionally in endothelium. In 52 cases
of Hodgkin's disease, ICAM-3, although present on the majority of the
reactive lymphoid cells, was absent from the Reed-Sternberg cells and
their variants. However, in 28 cases (54%), there was prominent
endothelial staining in small vessels. Similar findings were noted in 16
out of 49 cases (33%) of non-Hodgkin's lymphomas. This finding suggests
that analogous to ICAM-1 and ICAM-2, ICAM-3 expression can be induced on
endothelial cells in lymphoid neoplasms, probably by an as yet
unidentified cytokine-mediated mechanism.
8
UI - 11978921
AU - Bondoc AY; White DA
TI -
Granulomatous Pneumocystis carinii pneumonia in patients with
malignancy.
SO - Thorax 2002 May;57(5):435-7
AD - Memorial Sloan Kettering Cancer Center and Weill Medical College of
Cornell University, 1275 York Avenue, New York, NY 10021, USA.
BACKGROUND: A review was undertaken of the clinical features and results
of diagnostic tests in non-HIV infected patients who developed
granulomatous Pneumocystis carinii pneumonia (PCP). METHODS: A
retrospective review was performed of the charts and radiographs of
patients with a granulomatous reaction to P carinii identified from
computerised pathology records at Memorial Sloan Kettering Cancer
Center, a university affiliated tertiary care hospital. RESULTS: Three
cases were identified; the incidence of granulomatous PCP was 3%. All
patients had risk factors for PCP and had received high dose
corticosteroids which had been stopped. Two patients had received
chemotherapy. Presentation was insidious with only mild symptoms; only
one patient had fever. Chest radiographs showed a reticulonodular
pattern. Bronchoscopy was negative for PCP in all cases and open lung
biopsy was necessary. CONCLUSION: A granulomatous pathological reaction
to PCP occurs rarely in patients with malignancy. In these cases the
clinical presentation may be atypical and bronchoscopy can be
non-diagnostic.
9
UI - 12023141
AU - Zwitter M; Cohen JR; Barrett A; Robinton ED
TI -
Dorothy Reed and Hodgkin's disease: a reflection after a century.
SO - Int J Radiat Oncol Biol Phys 2002 Jun 1;53(2):366-75
AD - Institute of Oncology, Ljubljana, Slovenia. mzwitter@onko-i.si
It has now been 100 years since Dorothy Reed, at the age of 28, wrote
her paper on Hodgkin's disease. Her biography reveals the difficult
lives of women entering the hitherto male-dominated field of medicine,
let alone medical research. Her historic paper on Hodgkin's disease is
remarkable for its brilliant observations and concise scientific
reasoning. Nevertheless, she was told that as a woman she could not hope
for a career as an academic pathologist. After marriage to Charles
Elwood Mendenhall, Professor of Physics at the University of Wisconsin
and after giving birth to four children, the second part of her career
began. Motivated by the loss of her firstborn, she began a study of
infant mortality, an interest that lasted throughout her career. In
1926, Mendenhall undertook a survey comparing infant and maternal
mortality rates in Denmark and the United States. This influential study
concluded that American mortality rates were higher because of
unnecessary interference in the natural process of childbirth and
recommended the education of midwives follow the Danish model. In 1937,
her efforts were rewarded when Madison, WI received recognition for
having the lowest infant mortality of any city in the United States.
Reading Reed's paper on Hodgkin's disease, we see that her observations
go far beyond a description of a specific cell. Her presentation of
macroscopic and microscopic features is remarkable for the distinction
between "young" and "old" growths: Reed saw Hodgkin's disease as a
process, rather than the spreading of a cancer. She was the first to
note that those most commonly affected are boys or young adults,
especially those whose general health before the disease had been
excellent. She was also the first to note anergy to tuberculin. Dorothy
Reed defined Hodgkin's disease in relation to tuberculosis, described
its pathologic features, and offered comments on its pathogenesis,
epidemiology, and immunology that still deserve to be discussed.
10
UI - 11972094
AU - Sandoval C; Venkateswaran L; Billups C; Slim M; Jayabose S; Hudson MM
TI -
Lymphocyte-predominant Hodgkin disease in children.
SO - J Pediatr Hematol Oncol 2002 May;24(4):269-73
AD - Department of Pediatrics, New York Medical College, Valhalla, New York
10595, USA. Claudio_sandoval@nymc.edu
PURPOSE: To describe the clinicobiological features, treatment,
treatment outcome, and sequelae of children with lymphocyte-predominant
Hodgkin disease. PATIENTS AND METHODS: The authors performed a
retrospective chart review of 754 patients with Hodgkin disease
diagnoses at New York Medical College and St. Jude Children's Research
Hospital from 1962 to 2000 to identify those with lymphocyte-predominant
histology. Hematopathologists at the treating institutions reviewed
stored tissue specimens and reconfirmed the histopathology of each case.
RESULTS: Fifty-one children (44 boys, 7 girls) were identified. The
median age was 10.5 years (range 3.2-18.5); five children were younger
than age 60 months. The median duration of lymphadenopathy before
diagnosis was 4 months (range 0.5-30). Thirty-six children had stage 1
disease, eight had stage 2 disease, four had stage 3 disease, and three
had stage 4 disease. Fifteen children underwent staging laparotomy, and
four of these were upstaged. Treatment comprised combined modality
therapy (n = 27), radiation therapy alone (n = 17), and chemotherapy
alone (n = 7). Four children had a Hodgkin disease recurrence.
Forty-eight (94%) patients were alive and disease-free at a median
follow-up of 8 years (range 0.4-32.6). Eleven patients had long-term,
therapy-related adverse effects (cardiac, infertility, pulmonary, and
second malignant neoplasms). Three patients died. Two died of
complications of second malignant neoplasms and one died of infectious
complications after Hodgkin disease recurrence. CONCLUSIONS: Children
with lymphocyte-predominant Hodgkin disease respond favorably to a
variety of treatment modalities and are ideal candidates for less toxic
therapy.
11
UI - 11929801
AU - Jundt F; Kley K; Anagnostopoulos I; Schulze Probsting K; Greiner A;
TI -
Mathas S; Scheidereit C; Wirth T; Stein H; Dorken B
Loss of PU.1 expression is associated with defective immunoglobulin
transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin
disease.
SO - Blood 2002 Apr 15;99(8):3060-2
AD - Charite, Robert-Rossle-Klinik, Humboldt University of Berlin, Germany.
fjundt@mdc-berlin.de
Immunoglobulin transcription is impaired in Hodgkin and Reed-Sternberg
(HRS) cells of classical Hodgkin disease (cHD). We recently demonstrated
that defective immunoglobulin promoter transcription correlates with the
down-regulation of the B-cell transcription factors Oct2 and
BOB.1/OBF.1. These results prompted us to investigate whether
immunoglobulin enhancer activity is also impaired in HRS cells and
whether as yet unidentified factors could be necessary for
immunoglobulin enhancer activity in HRS cells of cHD. Here we analyzed
30 cases of cHD for expression of the Ets family member PU.1 that is
known to collaborate with multiple transcription factors and to regulate
expression of immunoglobulin genes. We show that PU.1 is not expressed
in primary and cultured HRS cells. Reintroduction of PU.1 and Oct2 in
cultured HRS cells restored the activity of cotransduced immunoglobulin
enhancer constructs. Our study identifies PU.1 deficiency as a recurrent
defect in HRS cells that might contribute to their impairment of
immunoglobulin transcription.
12
UI - 11986952
AU - Jucker M; Sudel K; Horn S; Sickel M; Wegner W; Fiedler W; Feldman RA
TI -
Expression of a mutated form of the p85alpha regulatory subunit of
phosphatidylinositol 3-kinase in a Hodgkin's lymphoma-derived cell line
(CO).
SO - Leukemia 2002 May;16(5):894-901
AD - Institut fur Medizinische Biochemie und Molekularbiologie, Abteilung fur
Zellulare Signaltransduktion, Universitatsklinikum Hamburg-Eppendorf,
Universitat Hamburg, Martinistrasse 52, 20246 Hamburg, Germany.
Phosphatidylinositol (PI) 3-kinase plays an important role in a variety
of biological processes, including proliferation and apoptosis.
PI3-kinase is a heterodimer consisting of an 85 kDa adapter protein
(p85) containing one SH3 domain and two SH2 domains and a 110 kDa
catalytic subunit (p110). Recently an oncogenic form of p85 named
p65-PI3K lacking the C-terminal SH2 domain has been cloned from an
irradiation-induced murine thymic lymphoma and transgenic mice
expressing p65-PI3K in T lymphocytes develop a lymphoproliferative
disorder. Here we describe the cloning of a C-terminal truncated form of
p85 expressed in a human lymphoma cell line (CO) with a T cell phenotype
derived from a patient with Hodgkin's disease. As a result of a
frame-shift mutation at amino acid 636, p76 is lacking most of the
C-terminal SH2 domain, but contains the inter-SH2 domain and is
associated with an active form of PI3-kinase. A PI3-kinase-dependent
constitutive activation of Akt was detected in CO cells which was only
partially reduced after serum starvation. Treatment of CO cells with the
PI3-kinase inhibitor wortmannin resulted in a concentration-dependent
inhibition of cell proliferation associated with an increased number of
apoptotic cells. This is the first detection of a mutated form of the
p85 subunit of PI3-kinase in human hematopoietic cells further
underlining a potential role of PI3-kinase/Akt signaling in human
leukemogenesis.
13
UI - 11964281
AU - Bollard CM; Rossig C; Calonge MJ; Huls MH; Wagner HJ; Massague J;
TI -
Brenner MK; Heslop HE; Rooney CM
Adapting a transforming growth factor beta-related tumor protection
strategy to enhance antitumor immunity.
SO - Blood 2002 May 1;99(9):3179-87
AD - Center for Cell and Gene Therapy, Department of Pediatrics, Baylor
College of Medicine, Houston, TX 77030, USA.
Transforming growth factor beta (TGF-beta), a pleiotropic cytokine that
regulates cell growth and differentiation, is secreted by many human
tumors and markedly inhibits tumor-specific cellular immunity. Tumors
can avoid the differentiating and apoptotic effects of TGF-beta by
expressing a nonfunctional TGF-beta receptor. We have determined whether
this immune evasion strategy can be manipulated to shield tumor-specific
cytotoxic T lymphocytes (CTLs) from the inhibitory effects of
tumor-derived TGF-beta. As our model we used Epstein-Barr virus
(EBV)-specific CTLs that are infused as treatment for EBV-positive
Hodgkin disease but that are vulnerable to the TGF-beta produced by this
tumor. CTLs were transduced with a retrovirus vector expressing the
dominant-negative TGF-beta type II receptor HATGF-betaRII-Deltacyt.
HATGF-betaRII-Deltacyt- but not green fluorescence protein
(eGFP)-transduced CTLs was resistant to the antiproliferative and
anticytotoxic effects of exogenous TGF-beta. Additionally,
receptor-transduced cells continued to secrete cytokines in response to
antigenic stimulation. TGF-beta receptor ligation results in
phosphorylation of Smad2, and this pathway was disrupted in
HATGF-betaRII-Deltacyt-transduced CTLs, confirming blockade of the
signal transduction pathway. Long-term expression of
TGF-betaRII-Deltacyt did not affect CTL function, phenotype, or growth
characteristics. Tumor-specific CTLs expressing HATGF-betaRII-Deltacyt
should have a selective functional and survival advantage over
unmodified CTLs in the presence of TGF-beta-secreting tumors and may be
of value in treatment of these diseases.
14
UI - 11964309
AU - Jundt F; Anagnostopoulos I; Forster R; Mathas S; Stein H; Dorken B
TI -
Activated Notch1 signaling promotes tumor cell proliferation and
survival in Hodgkin and anaplastic large cell lymphoma.
SO - Blood 2002 May 1;99(9):3398-403
AD - Charite, Robert-Rossle-Klinik, Humboldt University of Berlin, Germany.
fjundt@mdc-berlin.de
Notch signaling controls cell fate decisions of hematopoietic
progenitors by inhibiting certain steps of differentiation and inducing
either self-renewal or differentiation toward lymphoid or myeloid
lineages. In addition, truncated Notch1 alleles could be associated with
10% of all cases of human T lymphoblastic leukemia and, when introduced
into mouse bone marrow stem cells, cause T-cell neoplasms. However,
functional links between the abundant expression of intact Notch1 and
oncogenesis are still lacking. Here we show that Notch1 is highly
expressed in B- and T-cell-derived tumor cells of Hodgkin and anaplastic
large cell lymphoma. We demonstrate a novel mechanism for the oncogenic
capacity of Notch1 by showing that the interaction between intact Notch1
on tumor cells and its ligand Jagged1 dramatically induces proliferation
and inhibition of apoptosis in vitro. We further provide evidence that
in Hodgkin and anaplastic large cell lymphoma, Jagged1 is expressed in
malignant and in bystander cells colocalizing with Notch1-positive tumor
cells. Notch1 signaling may therefore be activated in tumor cells by
Jagged1 through homotypic or heterotypic cell-cell interactions, and it
seems likely that these interactions contribute to lymphomagenesis in
vivo. Thus, our data suggest that activated Notch1 signaling plays an
important role in the pathobiology of Hodgkin and anaplastic large cell
lymphoma and that it might be a potential new target for treatment.
15
UI - 12001908
AU - Bosshart H
TI -
Expression of survival receptors in Hodgkin disease cell lines.
SO - Blood 2002 May 1;99(9):3484-5; discussion 3485-6
16
UI - 12018570
AU - Ananthamurthy A; Kurien A; Ramnarayan K
TI -
The bone marrow in Hodgkin's disease--a two year study.
SO - Indian J Cancer 2000 Dec;37(4):173-83
AD - Department of Pathology, Kasturba Medical College, Manipal, Karnataka,
India.
A total of forty bone marrow trephine biopsies and aspirates were
studied from thirty five patients suffering from Hodgkin's disease
during the two year period 1994 and 1995. Of these twenty five were at
the time of diagnosis of the disease and fifteen after treatment. The
biopsies were studied for incidence of involvement as well as associated
findings in both the positive and negative biopsies. A comparison of the
trephine biopsy with marrow aspirate with respect to yield of positivity
was made. Five patients (20%) at the time of diagnosis and two (13.33%)
after treatment showed involvement of the marrow. None of the seven
corresponding aspirates were positive for involvement showing that
biopsies were superior to aspirates in detecting marrow infiltration in
Hodgkin's disease. Suppression of the marrow, fibrosis and lymphocytic
aggregates were the other findings in positive biopsies. Eosinophilia
and myelosuppression were notable changes in the negative biopsies. One
biopsy also showed granulomas. The probable significance of these
findings are also discussed.
17
UI - 12023183
AU - Spiegel R; Miron D; Gavriel H; Horovitz Y
TI -
West Nile virus meningoencephalitis complicated by motor aphasia in
Hodgkin's lymphoma.
SO - Arch Dis Child 2002 Jun;86(6):441-2
AD - Pediatric Department A', Ha'Emek Medical Center, Afula, Rappaport School
of Medicine, Technion, Haifa, Israel. spiegelr@internet-zahav.net
A 4 year old boy with Hodgkin's lymphoma was admitted to the paediatric
ward with meningoencephalitis dominated by generalised seizures and
motor aphasia. Serum IgM specific antibodies to West Nile virus were
positive. In view of ongoing neurological deterioration and
immunocompromised state he was treated with oral ribavirin for 14 days.
A gradual improvement was noted within two weeks of therapy initiation,
and with intensive supportive care he recovered completely after four
months.
18
UI - 12040667
AU - Oertel YC
TI -
Fine needle aspiration in Hodgkin's disease.
SO - Acta Cytol 2002 May-Jun;46(3):617
19
UI - 11676892
AU - Sanchez De Toledo Codina J
TI -
[Lymphomas in childhood]
SO - An Esp Pediatr 2001 Sep;55(3):195-7
20
UI - 11676899
AU - Ferris Tortajada J; Garcia Castell J; Lopez Andreu JA; Clar Gimeno S;
TI -
Berbel Tornero O
[Risk factors for Hodgkin's lymphomas]
SO - An Esp Pediatr 2001 Sep;55(3):239-43
AD - Unidad de Oncologia Pediatrica. Hospital Infantil Universitario La Fe,
Spain. ferris_jos@gva.es
OBJECTIVE: To divulge the risk factors associated with Hodgkin's
lymphoma (HL) in children and adults among pediatricians. METHODS: We
performed a literature review of the last 25 years through the Medline,
IAR Cancer, and Cancerlit databases. The search profile was "HL risk
factors". The most interesting papers, as well as those cited and
published more than 25 years prior to the search, were selected.
RESULTS: The following risk factors for HL were reported with greater or
lesser evidence: a) genetic (variation in the HLA class II region); b)
viral infections (Epstein-Barr virus); c) childhood environment and
socio-economic status; d) congenital and acquired immunodeficiency; e)
medical conditions and f) occupational exposure (the wood industry and
its derivatives). CONCLUSIONS: The etiology of most HL is unknown. The
most important risk factors are: 1) genetic; 2) Epstein-Barr virus
(infectious mononucleosis); 3) congenital and acquired immunodeficiency;
4) occupational exposure (the wood industry).
21
UI - 11692542
AU - Lopez M
TI -
[Successful chemotherapy of cancer. Remission of Hodgkin's disease. IV]
SO - Clin Ter 2001 May-Jun;152(3):203-6
AD - Istituto Regina Elena per lo Studio e la Cura dei Tumori, Roma, Italia.
22
UI - 11975042
AU - Pajor L
TI -
[Hodgkin lymphomas: current understanding of pathogenesis and
pathomorphology]
SO - Orv Hetil 2002 Mar 31;143(13):651-61
AD - Pecsi Tudomanyegyetem, Altalanos Orvostudomanyi Kar, Patologiai Intezet.
Brief summary of the history of Hodgkin disease as well as presentation
of the current REAL/WHO classification of the Hodgkin lymphoma actually
including two diseases entities is given. Beside the morphological,
phenotypical and clinicopathological characterization of the classical
as well as the nodular lymphocyte predominant Hodgkin lymphoma emphasis
is placed on the differential diagnostics of the two basic types of
Hodgkin lymphomas as well as on that of nodular paragranuloma versus
nodular lymphocyte rich classical Hodgkin lymphoma. Summarizing the last
decade's progress in research the current understanding of the
pathogenesis of Hodgkin lymphomas is presented. The key elements of it
is that although the tumor cells of both Hodgkin lymphomas arise from
B-cells having passed the germinal center phase and exhibiting somatic
hypermutation, the tumor cells of classical Hodgkin lymphoma do not have
a functional immunoglobulin gene, but show a thorough phenotypic change,
whereas the tumor cells of nodular paragranuloma preserve the
B-phenotype and being under antigen selection pressure. The role of
Epstein-Barr virus in the etiology is also introduced.
23
UI - 12014672
AU - Libura J; Bettens F; Radkowski A; Tiercy JM; Piguet PF
TI -
Polymorphic tumor necrosis factors microsatellite TNFa4 is associated
with resistance of Hodgkin lymphoma to chemotherapy and with replapses
after therapy.
SO - Anticancer Res 2002 Mar-Apr;22(2A):921-6
AD - Center of Oncology, Maria Curie-Sklodowska Memorial Institute, Cracow,
Poland.
BACKGROUND: The response of tumors to chemotherapy (CHT) exhibits wide
individual variations. PATIENTS AND METHODS: We examined the incidence
of polymorphic TNF genes in 61 patients treated for Hodgkin lymphoma.
RESULTS: During treatment, the patients were divided as responders or
non-responders, depending upon the amount of CHT required for a clinical
eradication of the tumor. The incidence of TNFa4, a microsatellite
allele associated with low TNF production in leukocytes, was
significantly higher in responders than in non-responders (25.7% vs 0 %,
p=0.04). We also examined the incidence of tumor relapses 2-5 years
after treatment. The incidence of TNFa4 was also significantly higher in
patients with relapses, than in those without relapses (41.1% vs 9.3%,
p=0.007). CONCLUSION: These results indicate that TNFa4 is a marker of
resistance of Hodgkin lymphoma to chemotherapy and most probably is a
marker of bad prognosis.
24
UI - 12004149
AU - Balwierz W; Moryl-Bujakowska A; Depowska T; Klekawka T; Rokicka-Milewska
TI -
R; Sopylo B; Kolakowska-Mrozowska B; Chybicka A; Boguslawska-Jaworska J;
Pisarek J; Ras M; Sonta-Jakimczyk D; Janik-Moszant A; Kolecki P;
Kaczmarek-Kanold M; Kowalczyk J; Odoj T; Matysiak M; Newecka-Samol T;
Balcerska A; Adamkiewicz-Drozynska E; Wysocki M; Kurylak A
[Treatment regimen for children and adolescents with Hodgkin's disease
designed to decrease late complications of radiotherapy]
SO - Med Wieku Rozwoj 2001 Jul-Sep;5(3 Suppl 1):25-35
AD - Klinika Hematologii i Onkologii Dzieciecej, Polsko-Amerykanski Instytut
Pediatrii Collegium Medicum, Uniwersytet Jagielonski, Wielicka 265,
30-663 Krakow, Poland.
Between 1997 to 1999 in 9 centres of the Polish Paediatlic
Leukemia/Lymphoma Study Group, 167 children and adolescents (aged 2-19
years) with stage 1 to IV Hodgkin's disease (HD) were treated according
to a regimen with a limited use of radiotherapy (RT). All patients
received B-DOPA and MVPP chemotherapy. The number of cycles of
chemotherapy was adjusted in respective risk groups. In 13 children with
stage IA and IIA disease with favourable prognostic factors chemotherapy
alone was used. In other patients the dose of RT applied to lymphatic
regions was 15-46,4 Gy. In case of a small tumour at presentation and
good response to initial chemotherapy the RT dose was 15-16 Gy. In other
cases doses of 25-30 Gy were planned. The use of higher doses,
particularly exceeding 35 Gy, in eleven patients, was not justified.
Among all the 167 patients, three oftliem (1.2%) with advanced disease
(Stage III-1V) did not achieve first remission. The 4-year overall
survival (OS), relapse free survival (RFS) and event free survival (EPS)
were 99%. 93% and 90%, respectively. Relapses occurred in 8 children
(first remission lasted for 4-29 (median = 9 months). All 13 children in
whom chemotherapy alone was used remain in first remission. In the group
of children who received RT in the dose of 15-16 Gy relapse occurred in
one child. Our preliminary analysis indicates that limited use of RT in
selected cases of HD in children and adolescents did not show worse
results of treatment. However, the assessment of possible influence of
this regimen on the decreased rate of late complications requires longer
follow-up.
25
UI - 11937314
AU - Proctor SJ; Mackie M; Dawson A; White J; Prescott RJ; Lucraft HL; Angus
TI -
B; Jackson GH; Lennard AL; Hepplestone A; Taylor PR
A population-based study of intensive multi-agent chemotherapy with or
without autotransplant for the highest risk Hodgkin's disease patients
identified by the Scotland and Newcastle Lymphoma Group (SNLG)
prognostic index. A Scotland and Newcastle Lymphoma Group study (SNLG HD
III).
SO - Eur J Cancer 2002 Apr;38(6):795-806
AD - Department of Haematology, Royal Victoria Infirmary, Newcastle upon Tyne
NE1 4LP, UK. s.j.proctor@ncl.ac.uk
The aim of the study was to identify all patients with poor risk
Hodgkin's disease (HD) using a numerical prognostic index in a defined
population and to recruit them into a trial of intensive chemotherapy
prednisolone, vinblastine, doxorubicin, chlorambucil, etoposide,
bleomycin, vincristine, procarbazine (PVACE-BOP)x3+autotransplant (Arm
A) versus PVACE-BOPx5 (Arm B) in first remission. In 10 years, the
Scotland and Newcastle Lymphoma Group (SNLG) registered 930 patients
with HD of whom 178 (19%) were identified as 'poor risk' by the SNLG
index and were aged 16-59 years. 126/178 (71%) entered the study. Of the
120 confirmed poor risk HD cases, all completed PVACE-BOPx3 with a 93%
Complete Response/unconfirmed Complete Response (CR/CRu) rate. Only
65/107 in CR accepted the randomisation. With a median follow-up of 6
years, both arms of the trial have a similar time to treatment failure
(TTF) (Arm A 79%+/-11 versus 85%+/-7 Arm B, P=0.35). Advanced stage
'good risk' patients not included in the trial receiving standard
therapy with CLVPP or ABVD had a 75% 5-year survival. The study
demonstrates that PVACE-BOP therapy in the poorest risk group (58% had
an IPI>/=3) produces excellent CR rates (93%) and overall survival with
minimal toxicity, and that the substitution of autotransplant in first
CR does not improve outcome. The use of the objective SNLG index
accurately helped in the selection of the poorest risk group in this
population study. The placing of a randomised control trial within the
context of a population-based study of HD enhances the validity of the
outcome.
26
UI - 11918452
AU - Aviles A; Neri N; Garcia EL; Talavera A; Diaz-Maqueo JC
TI -
Treatment of refractory Hodgkin's disease with modified Stanford V
program.
SO - Med Oncol 2001;18(4):261-7
AD - Oncological Research Unit, Oncology Hospital, National Medical Center,
IMSS, Mexico, DF. agaviles@avantel.net
This study analyzes the results using an Stanford V modified program in
the treatment of refractory Hodgkin's disease (RHD). We used
cyclophosphamide instead of mechloretamine, and epirubicin instead of
doxorubicin to avoid the risk of acute and late side effects associated
with this drugs. Seventy-one patients with RHD were treated. All were at
an advanced stage at therapy and had associated adverse prognostic
factors. The complete response (CR) rate was 84% (60 patients; 95%
confidence interval [CI]: 72-91%). At 5 yr, actuarial overall survival
(CS) is 71% (95% Cl: 59-78%) and event-free survival (EFS) is 70% (95%
CI: 59-79%). Only the duration of the initial complete response (> 12
mo) influenced the duration of EFS and OS. Toxicity was mild.
Granulocyte colony-stimulating factor to ameliorate the presence of
severe myelosuppression was used only in a few patients. Cardiac
function was not affected and, until now, late side effects has not been
observed. Thus, the use of this modified Stanford program retains the
usefulness of the original scheme both with less frequent and less
severe acute and late side effects. A controlled clinical trial in
untreated patients comparing the Stanford program with standard
chemotherapy is warranted to define the role of this therapeutic option
in patients with Hodgkin's disease.
27
UI - 12043226
AU - Itami J
TI -
[Hodgkin lymphoma]
SO - Nippon Igaku Hoshasen Gakkai Zasshi 2002 Apr;62(5):215-20
In the newly published WHO classification for tumors of the
hematopoietic and lymphoid tissues, Hodgkin's disease has been renamed
Hodgkin lymphoma, which reflects the recent confirmation of its germinal
center B-cell origin. In the classification, nodular
lymphocyte-predominant Hodgkin lymphoma has been added as a new entity
with an excellent prognosis. For management of the disease, a
risk-adapted classification is employed without staging laparotomy. In
limited stages without risk factors, subtotal nodal irradiation with
sophisticated techniques can cure more than 80% of patients.
Multimodality therapy with chemo- plus radiotherapy can improve
disease-free survival, but overall survival remains unchanged. In the
intermediate stages with risk factors, chemo- plus radiotherapy is
standard, with 3-4 cycles of ABVD and involved field irradiation. In
advanced stages, chemotherapy plays a decisive role, with radiation
therapy used as an adjuvant for bulky and/or slowly responding tumors.
Long-term follow-up of cured Hodgkin patients has revealed increased
incidences of solid malignancies and ischemic heart disease more than 15
years after therapy. Breast cancer and ischemic heart disease appear to
be related to mantle irradiation, although sophisticated modern
radiation therapy techniques are demonstrated to lower the incidence of
these long-term morbidities. Meticulous radiation therapy remains the
most effective tool for local control of Hodgkin lymphoma.
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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