National Cancer Institute®
Last Modified: June 1, 2002
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.
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.
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. email@example.com
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. firstname.lastname@example.org
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.
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.
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.
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. email@example.com
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.
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.
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. firstname.lastname@example.org
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.
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.
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.
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. email@example.com
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.
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
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.
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. firstname.lastname@example.org
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.
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. email@example.com
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).
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.
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.
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.
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.
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. firstname.lastname@example.org
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.
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. email@example.com
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.
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.
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