Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-10 (IL-10) is mainly an anti-inflammatory cytokine produced by a number of cells including normal and neoplastic B cells. It has been implicated in autoimmunity, transplantation tolerance and tumourigenesis. Polymorphisms in the IL-10 gene promoter genetically determine inter-individual differences in IL-10 production. The aim of this study was to determine whether polymorphisms in the IL-10 gene promoter play a role in predisposing an individual to lymphoma. We analysed the frequencies of three single base substitutions in the IL-10 promoter in patients with aggressive lymphoma (B-cell DLCL n = 46, other aggressive histologies n = 17), Hodgkin's disease (n = 44) or low/intermediate grade lymphoma (n = 46), compared to healthy controls. The frequency of the low-IL-10 producing AA allele (at position -1082) was significantly higher in patients with aggressive lymphoma compared to controls (p = 0.0344, Odds ratio 1.974, 95% C.I 1.066-3.655). Similarly, the frequency of the low IL-10 producing ATA or the intermediate-IL-10- producing ACC haplotype was significantly higher in patients with aggressive disease compared to controls (p = 0.0255, Odds ratio 1.647, 95% C.I 1.077-2.518). No association was found between IL-10 genotypes and Hodgkin's disease or less aggressive forms of lymphoma. Thus, polymorphisms in the IL-10 gene promoter which are associated with a low IL-10 producing phenotype may influence susceptibility to aggressive forms of lymphoma or may contribute to the pathogenesis of this disease.
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PMID:Polymorphisms in the interleukin 10 gene promoter are associated with susceptibility to aggressive non-Hodgkin's lymphoma. 1268 41

The association of Non-Hodgkin Lymphoma (NHL) and HIV-infection was soon recognized and the Center of Disease Control (CDC) has classified some types of NHL as AIDS-defining illnesses (ADI). Hodgkin's disease (HD) represents the most common type of non ADI malignancy in HIV-infected cases. Commonly, data on malignant lymphoma in this population is collected in known HIV-positive patients or in autopsy-series. This registration study was designed to estimate the incidence of HIV-positivity in patients with newly diagnosed malignant lymphoma. A registration of all patients with newly diagnosed malignant lymphoma and their HIV-status was performed in every center of the Swiss Group for Clinical Cancer research (SAKK) from January 1, 1991 to July 31, 1993. Among 474 eligible patients, HIV-status was evaluated in 400 and 52 were tested positive (13%), 42 (81%) of them males. Three of them were newly detected cases (after lymphoma-diagnosis). Three hundred and forty patients (72%) presented with NHL, 42 (12.4%) of them HIV-positive; 33 out of these had aggressive lymphoma. B-symptoms were significantly more frequent in HIV-positive patients. In the 134 patients with HD, 10 (7.5%) tested HIV-positive, mostly presenting with stage IV disease (7), B-symptoms (9) and extranodal disease (7). In conclusion, 13% out of 400 evaluated patients with newly diagnosed malignant lymphoma tested HIV-positive. The study confirms the predominance of aggressive lymphoma histologies and frequent presentation with B-symptoms in HIV-positive patients with NHL. Male gender, young age (26-35 years) and B-symptoms are prognostic factors for HIV-positivity in NHL.
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PMID:HIV-testing and newly-diagnosed malignant lymphomas. The SAKK 96/90 registration study. 1269 Nov 53

Mantle cell lymphoma (MCL) accounts for approximately 6% of non-Hodgkin's lymphomas. Patients usually present with advanced disease, with a tendency for extranodal involvement. MCL is an aggressive lymphoma with moderate chemosensitivity, but it remains one of the most difficult therapeutic challenges. Complete response rates to chemotherapy range from 20% to 40%, with median survivals of 2 1/2 to 3 years. Anthracycline-containing regimens do not prolong survival compared with nonanthracycline regimens. Single-agent rituximab (Rituxan) has produced response rates of about 30%, and when combined with an anthracycline-containing regimen, response rates increase to above 90%; however, an impact on survival has not yet been demonstrated. More intensive regimens such as hyperCVAD (hyperfractionated cyclophosphamide [Cytoxan, Neosar], vincristine, doxorubicin [Adriamycin], dexamethasone, methotrexate, cytarabine) with either stem cell transplant or rituximab have been associated with promising results.
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PMID:Mantle cell lymphoma: clinicopathologic features and treatments. 1284 28

We conducted a randomized trial to compare the intensive conventional chemotherapy regimen ACVBP (doxorubicin, cyclophosphamide, vindesine, bleomycin, prednisone) with standard CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) in previously untreated patients with poor-risk aggressive lymphoma. Patients aged 61 to 69 years who had aggressive non-Hodgkin lymphoma with at least one prognostic factor of the age-adjusted international prognostic index (IPI) were included. ACVBP consisted of an induction phase of intensified chemotherapy and central nervous system (CNS) prophylaxis followed by a sequential consolidation phase. Of the 708 patients registered for the study, 635 were eligible. The rate of complete response was 58% in the ACVBP group and 56% in the CHOP group (P =.5). Treatment-related death occurred in 13% of the ACVBP group and 7% of the CHOP group (P =.014). At 5 years, the event-free survival was 39% in the ACVBP group and 29% in the CHOP group (P =.005). The overall survival was significantly longer for patients treated with ACVBP, at 5 years it was 46% compared with 38% for patients treated with CHOP (P =.036). CNS progressions or relapses were more frequent in the CHOP group (P =.004). Despite higher toxicity, the ACVBP regimen, used as first-line treatment for patients with poor-risk aggressive lymphoma, is superior to standard CHOP with regard to both event-free survival and overall survival.
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PMID:Intensive conventional chemotherapy (ACVBP regimen) compared with standard CHOP for poor-prognosis aggressive non-Hodgkin lymphoma. 1292 37

Immunotherapy with the anti-CD20 monoclonal antibody rituximab has been shown in clinical trials to be effective in the treatment of both indolent and aggressive non-Hodgkin's lymphomas (NHL). Recent studies have demonstrated improved clinical benefit with extended dose and maintenance therapies in patients with indolent lymphomas and chronic lymphocytic leukemia. Rituximab's label was recently expanded to include treatment of bulky disease, retreatment of patients previously treated with rituximab, and an eight-week extended treatment schedule. Rituximab has also been effectively combined with chemotherapy, resulting in higher response rates and longer response durations in randomized trials in patients with aggressive lymphoma. Studies continue to evaluate and expand the role of rituximab in the treatment of NHL, including its use in combined immunotherapy approaches and autologous stem cell transplant as well as in the treatment of autoimmune disorders. Radioimmunotherapy with the rituximab and ibritumomab tiuxetan (Zevalin) regimen was recently approved for the treatment of relapsed or refractory low-grade, follicular or CD20+ transformed NHL, including rituximab refractory follicular NHL. The regimen is delivered on an outpatient basis over the course of a week. Studies are currently exploring sequential dose therapy, radioimmunotherapy with rituximab maintenance, and ibritumomab tiuxetan radioimmunotherapy as part of autologous stem cell transplant. Current understanding of the mechanisms of action of rituximab and the use of rituximab and ibritumomab tiuxetan in patients with indolent and aggressive NHL will be discussed.
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PMID:Rituxan immunotherapy and zevalin radioimmunotherapy in the treatment of non-Hodgkin's lymphoma. 1452 25

The advent of highly active antiretroviral therapy (HAART) and its co-administration with chemotherapy in patients with human immunodeficiency virus (HIV)-related lymphoma has lead to the exploration of potentially curative combination chemotherapy and myeloablative therapy followed by autologous haematopoietic stem cell transplantation (ASCT). Applying the same principles used for patients with HIV-negative aggressive lymphoma, in 1998 we developed a program of high-dose therapy and ASCT at City of Hope for patients with HIV-related lymphoma and Hodgkin's disease. Our studies have primarily included patients with chemosensitive lymphoma in relapse or first remission with poor-risk features at diagnosis. Filgrastim (G-CSF)-primed peripheral blood stem cell mobilization and apheresis have been successful while patients were receiving HAART and chemotherapy. To date, ASCT has been performed in 19 patients with HIV-related lymphoid malignancies, representing the largest single-institution experience reported to date. Most patients received a chemotherapy-based conditioning regimen consisting of high-dose carmustine, etoposide and cyclophosphamide. Early infections, namely bacteremias and neutropenic fever were similar to those observed in the HIV-negative transplant setting. Opportunistic infections were rare and easily treatable. There were three early deaths, two from relapsed lymphoma and one from multi-organ failure in an older patient. The remaining 16 patients are alive and in remission. In summary, ASCT is well tolerated, can result in long-term remissions, and is potentially curative in selected HIV-related lymphoma patients with chemosensitive relapse and high-risk disease in first remission defined by the age-adjusted International Prognostic Index criteria (i.e., two or three of the following: elevated LDH, advanced stage, and poor performance status). Acquisition of resistance to HAART remains as a potential problem for HIV-positive patients who are cured of their lymphoma.
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PMID:Treatment of human immunodeficiency virus-related lymphoma with haematopoietic stem cell transplantation. 1455 80

This study was designed to determine the value of 2-[fluorine-18]-fluoro-2-deoxy- d-glucose positron emission tomography (FDG-PET) in the early assessment of therapy response in lymphoma patients. We studied 20 patients with pathologically proven lymphoma, including 17 patients with aggressive non-Hodgkin's lymphoma and three patients with Hodgkin's lymphoma. All patients underwent whole-body FDG-PET imaging at baseline and after 1-2 cycles of chemotherapy. PET images were analysed visually and quantitatively by calculating the standardised uptake value (SUV). In each patient, we measured the SUV of the tumour demonstrating the highest FDG uptake at baseline study and the SUV of the same tumour after 1-2 cycles of therapy. The achievement of complete response was assessed on the basis of a combination of clinical findings and the results of conventional imaging modalities. Follow-up of progression-free survival (PFS) was obtained for the validation of PET data. Of the 20 patients, ten achieved complete remission at the completion of chemotherapy and the other ten did not respond to chemotherapy. Of the ten responders, four are still in remission (PFS 24-34 months) while the other six have relapsed (PFS 8-16 months). For the prediction of 24-month clinical outcome, visual analysis of PET after 1-2 cycles showed high sensitivity (87.5%) and accuracy (80%) but low specificity (50%). Comparison with the baseline SUVs revealed that the responders showed a significantly greater percent reduction in SUV after 1-2 cycles of therapy as compared with the non-responders (81.2%+/-9.5% vs 35.0%+/-20.2%, P<0.001). In addition, using 60% reduction as a cut-off value, the responders were clearly separated from the non-responders, with the exception of one non-responder. In conclusion, when performed early during chemotherapy, FDG-PET may be predictive of clinical outcome and allows differentiation of responders from non-responders in cases of aggressive lymphoma.
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PMID:Early therapy monitoring with FDG-PET in aggressive non-Hodgkin's lymphoma and Hodgkin's lymphoma. 1457 14

Occurrence of an aggressive lymphoma in patients with chronic lymphocytic leukemia (CLL), clinically referred to as Richter's syndrome, occasionally manifests as a lymphoproliferation resembling Hodgkin's lymphoma (HL) and often containing the Epstein-Barr virus (EBV). Only a limited number of HL variants have been subject to informative analysis regarding their clonal relationship to the CLL, with evidence of a same clonal origin in some cases and of clonally unrelated neoplasms in other cases. In this paper, we performed a detailed pathologic, virologic, and molecular analysis of two cases of Richter's syndrome with HL features. The first case occurred in a 65-year-old man with a 5-year history of CLL as a mediastinal and supraclavicular mass histologically diagnosed as lymphocyte depleted HL with no background CLL. The second case occurred in a 78-year-old woman with a 4-year history of CLL as an inguinal mass with a composite histologic appearance comprising areas of CLL, areas of CLL with Hodgkin Reed-Sternberg cells, and areas of HL. Both patients had received fludarabine therapy. The HRS cells were CD20-/CD30+/CD15-/J-chain- in case no. 1 and CD20+/-/CD30+/CD15-/J-chain- in case no. 2. In both cases, the Hodgkin's Reed-Sternberg cells (HRS) were positive for type A EBV, and a 30-bp deletion of the LMP-1 gene was detected in case no. 2. Using microdissection and polymerase chain reaction amplification of the immunoglobulin heavy chain gene (IgH) complementarity determining region III of each cell type, we demonstrated a distinct clonal origin for the CLL cells and the HRS in both cases. These cases bring support to the hypothesis that EBV+ HL in CLL patients occurs as unrelated secondary neoplasms most likely as the result of the immune depression associated with CLL and also raise the question of a possible causal role of fludarabine.
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PMID:Distinct clonal origin in two cases of Hodgkin's lymphoma variant of Richter's syndrome associated With EBV infection. 1510 59

Second malignancies are frequent complications in patients with chronic lymphocytic leukemia (CLL). Patients with this leukemia may develop large cell lymphoma (LCL) known as Richter's syndrome (RS). RS occurs in CLL patients of about 3% and may develop in a single lymph node or more often in a group of nodes. However, in some patients extranodal localization of aggressive lymphoma in RS has been observed. Besides LCL, Hodgkin's disease, prolymphocytoid leukemia, multiple myeloma and acute lymphoblastic leukemia may also occur as RS variants. The origin of lymphoid cells in RS remains tentative. However, CLL and RS originate from the same clone for some patients, whereas, in other patients cells of aggressive lymphoma do not have the features of the same clone as the CLL cells. The prognosis of RS is poor. Survival in different studies will be usually 2-5 months. The secondary development or coexistence of myeloproliferative disorders or myelodysplastic syndrome and solid tumors have also been rarely documented in CLL patients. It is of great concern that therapy may further increase the risk of a second neoplasm. However, until now, there are no clear evidence that alkylating agents or purine nucleoside analogs may be associated with an increased incidence of second malignancies in patients with CLL. In this review, epidemiology, biology, clinical characteristic and treatment approaches in RS and other secondary neoplasms in patients with CLL are discussed.
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PMID:Second malignancies and Richter's syndrome in patients with chronic lymphocytic leukemia. 1576 79

Parameters of the erythroid, granulocytic, and megakaryocytic hemopoietic stems were compared in 87 patients with aggressive and indolent non-Hodgkin's lymphomas before and 6 months after the start cytostatic therapy. Before chemotherapy anemia was detected in 46% patients with aggressive and 49% patients with indolent lymphomas. Hemoglobin content, peripheral blood erythrocyte count, and total count of erythroid cells in the bone marrow increased during chemotherapy in the indolent lymphoma group. Increased count of erythroid cells in the myelogram was due to decreased count of lymphoid cells in the bone marrow, which was associated with complete or partial remission. In aggressive lymphoma chemotherapy decreased the mean level of hemoglobin and mean erythrocyte count in the peripheral blood, but the total count of erythroid cells in the bone marrow increased; no relationship was detected between lymphocyte count in the bone marrow and erythropoiesis characteristics. Lymphocytosis >50% in the myelogram before chemotherapy was less frequent in this group in comparison with indolent non-Hodgkin's lymphomas.
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PMID:Erythropoiesis in patients with aggressive and indolent non-Hodgkin's lymphomas. 1613 22


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