Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we present the results of the distribution of a cell surface protein with molecular weight 104-110 kDa (p104-110) detected by monoclonal antibody made in our laboratory. The protein is expressed by a number of cell lines belonging to B lymphoid cells, but not to the other blood cell lineages. In healthy donors the expression of p104-110 is restricted to a minor population of human peripheral blood mononuclear cells shared by both CD20(+) and CD20(-) subpopulation. No expression of p104-110 has been found on resting and activated T cells as well as on monocytes and polymorphonuclear cells. FACS analysis of mononuclear cells derived from normal human bone marrow has revealed the presence of p104-110 on committed CD34(-); CD38(+) mononuclear cell subset that composes only the minor part of mature CD20(+) B cells being mostly CD20 negative. Furthermore, CD19(+)CD5(+)CD20(-) malignant cells derived from the patients with chronic lymphoid leukemia express p104-110 at high level. Similarly, it has been shown that some patients with malignant non-Hodgkin's lymphomas can have the increased contents of CD20(+) cells bearing that surface antigen. Possible associations of p104-110 expression on human B lymphoid cells with their differentiation and activation are discussed.
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PMID:Expression of the Protein with Molecular Weight 104-110 kDa by Normal and Malignant Human B Lymphoid Cells. 1268 16

Reactivation of hepatitis is one of the most serious complications of chemotherapy in lymphoma patients who are carriers of the hepatitis B virus (HBV). Glucocorticoids are linked to increased risk of HBV reactivation. This study seeks to clarify whether removal of glucocorticoids from chemotherapy regimens may decrease the risk of HBV reactivation. Eligible patients were seropositive for hepatitis B surface antigen (HBsAg) and had histologically proven non-Hodgkin's lymphomas for which intensive chemotherapy was indicated. Patients were randomized to receive either ACE (epirubicin, cyclophosphamide, and etoposide) or PACE (prednisolone + ACE). A total of 50 patients were enrolled, 25 each for the ACE and PACE arms. The cumulative incidence of HBV reactivation at 9 months after starting chemotherapy was 38% and 73% for ACE and PACE arm, respectively (P =.03). The degree of clinical hepatitis was significantly more severe in the PACE arm: 11 patients (44%) in the PACE and 3 patients (13%) in the ACE arm had ALT elevation more than 10-fold of normal (P =.025), and 7 patients (28%) in the PACE and 1 patient (4%) in the ACE arm had icteric hepatitis (P =.049). Complete remission of tumors occurred in 11 (46%) patients in the PACE and 8 (35%) patients in the ACE arm (P =.556). The estimated overall survival rate at 46 months was 68% in the PACE arm and 36% in the ACE arm, respectively (P =.18). In conclusion, steroid-free chemotherapy decreases the incidence and severity of HBV reactivation in HBsAg-positive lymphoma patients. However, further research is needed to evaluate whether steroid-free chemotherapy may confer a less satisfactory control of lymphoma.
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PMID:Steroid-free chemotherapy decreases risk of hepatitis B virus (HBV) reactivation in HBV-carriers with lymphoma. 1508 99

Rituximab (MabThera, Rituxan) is a chimeric IgG1 monoclonal antibody that specifically targets the CD20 surface antigen expressed on normal and neoplastic B-lymphoid cells. Rituximab is currently used in the treatment of both follicular and aggressive B-cell non-Hodgkin lymphomas. Despite its demonstrated clinical effectiveness, its in vivo mechanisms of action remain unknown and could differ by subtype of lymphoma. Rituximab has been shown to induce apoptosis, complement-mediated lysis, and antibody-dependent cellular cytotoxicity in vitro, and some evidence points toward an involvement of these mechanisms in vivo. Rituximab also has a delayed therapeutic effect as well as a potential "vaccinal" effect. Here, we review the current understanding of the mechanism of action of rituximab and discuss approaches that could increase its clinical activity. A better understanding of how rituximab acts in vivo should make it possible to develop new and more effective therapeutic strategies.
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PMID:From the bench to the bedside: ways to improve rituximab efficacy. 1522 77

Rituximab is a monoclonal antibody directed against the CD20 surface antigen present on B lymphocytes. Following its application, B cells are rapidly and specifically depleted. Rituximab has been approved for the treatment of relapsed and therapy-refractory non-Hodgkin lymphoma and has been incorporated into numerous chemotherapy regimes with promising results. Eradication of auto-reactive B cell clones is the rationale for its application in a variety of autoimmune disorders including the pemphigus group where B cells are thought to play a critical role in the pathogenesis. Preliminary reports in autoimmune disorders are encouraging. Adverse effects are generally well controlled and although severe infections have been reported following rituximab, the overall risk does not seem to be significantly increased. In the pemphigus group, rituximab has been successfully employed in refractory cases and a recent study suggests that a single course induces long-term remission in this patient group.
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PMID:Anti-B- cell-directed immunotherapy (rituximab) in the treatment of refractory pemphigus--an update. 1604 47

Rituximab is a genetically engineered chimeric monoclonal immunoglobulin (Ig)G1 antibody. It binds the CD20 trans-membrane surface antigen expressed by mature B cells but not by antibody secreting plasma cells, and removes the cells by activating complement, inducing cell-mediated lysis, and by apoptosis. Mainly used for the treatment of non-Hodgkin's lymphomas, rituximab has recently been tried with favourable responses in rheumatoid arthritis, systemic lupus erythematosus, and other chronic immunological diseases. Wegener's granulomatosis (WG) is a granulomatous vasculitis with high morbidity and mortality. It is thought that anti-neutrophil cytoplasmatic antibodies (ANCA) with specificity for proteinase 3 (PR3) are possibly involved in the pathogenesis of the disease. Conventional therapy with cyclophosphamide and corticosteroids generally succeeds in inducing remission, but relapses frequently follow. Among the biological agents, tumour necrosis factor-alpha (TNF-alpha) inhibitors have been tried with some success. Based on a case report we recently treated three refractory WG patients with rituximab and achieved almost complete but temporary remission. CD20+ cells disappeared rapidly in peripheral blood, only to rise prior to subsequent disease flares occurring at 34, 63, and 54 weeks, respectively (Figure 1). A new flare occurred in one patient at 86 weeks. At the end of the observation periods (54, 102, and 120 weeks), only one patient had proteinuria. Chest radiographs became normal in two patients, while infiltrates remained unchanged in the third. Granulomatous retro-orbital or sinus masses in two patients seemed unresponsive to therapy.
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PMID:Anti-CD20 therapy of treatment-resistant Wegener's granulomatosis: favourable but temporary response. 1613 30

Radioimmunotherapy (RIT) is a new treatment modality that combines the benefits of radiotherapy and immunotherapy. In RIT, a radionuclide is coupled to a monoclonal antibody, directed against an antigen expressed on tumor cells. Recently, RIT has been introduced targeting the CD20 surface antigen, which is expressed on nearly all B-cell non-Hodgkin lymphomas (NHL). Clinical experience with RIT in the treatment of patients with indolent NHL is increasing. To date, two commercially available agents are used: yttrium-90 ((90)Y)-ibritumomab tiuxetan and iodine-131 ((131)I)-tositumomab. In general, there is no organ-specific non-hematologic toxicity when a standard dose of RIT is used. Bone marrow suppression is the dose-limiting RIT toxicity; therefore, bone marrow infiltration by NHL should be investigated before treatment. Treatment-related myelodysplastic syndromes and acute myeloid leukemia after RIT are being investigated but long-term data are needed for final evaluation. Results are quite encouraging with respect to complete remission and overall response, even in pretreated patients with unconjugated monoclonal antibodies. RIT induces high response rates and a significant subgroup of patients has achieved long-term durable responses. RIT is feasible in heavily pretreated patients and does not compromise future treatments in the event of progressive disease. Randomized phase III studies are in progress to evaluate the timing of RIT in the overall management of indolent NHLInvestigations of new emerging therapeutic strategies for patients with indolent NHL are underway, with research into the feasibility of RIT as first-line therapy and in advanced disease, RIT dose escalation and combined modality approaches with autologous stem cell transplantation. The encouraging results of RIT in indolent NHL have initiated studies focusing on its benefit for patients with aggressive NHL.
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PMID:Radioimmunotherapy for indolent B-cell non-Hodgkin lymphoma in relapsed, refractory and transformed disease. 1683 Oct 19

Patients with low grade (LG) non-Hodgkin's lymphomas (NHLs) typically have a median survival of 8-10 years during which they sustain a series of responses and relapses to therapy. More than 95% of B-cell NHLs express the CD20 surface antigen, affording opportunities for CD20-directed therapy of NHL. Since 1990, 5 trials have tested the safety and efficacy of the murine CD20 MAb Tositumomab and Iodine I 131 Tositumomab (Bexxar therapeutic regimen) in 250 patients with relapsed, refractory, or transformed LG NHL. The I-131 irradiates MAb-bound cells and those within the path length of the isotope. Response rates were 56% (overall) and 30% (complete). With a median follow-up of 44.6 months, 30% of the patients achieved a long-term, durable response; median time to progressive disease or death was 5 years. Thus, a single treatment with Bexxar may produce durable responses and partially reverse the natural history of LG NHL.
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PMID:Targeted radio-immunotherapy with Bexxar produces durable remissions in patients with late stage low grade non-Hodgkin's lymphomas. 1706 Sep 72

Radioimmunotherapy (RIT) represents a relatively new antibody-based radiopharmaceutical treatment for patients with various kinds of tumors. Although the field has a long history of preclinical and clinical investigations using many different agents, to date, only 2 of these immunologically targeted radiopharmaceuticals have been cleared for commercial sale. Both of these agents ((90)Y-ibritumomab tiuxetan or "Zevalin" [Biogen-Idec, Boston, MA] and (131)I-tositumomab or "Bexxar" [GlaxoSmithKline Research, Triangle Park, NC]) are directed against the CD20 surface antigen found on normal mature B cells and greater than 95% of B-cell non-Hodgkin lymphoma (NHL). Both compounds produce similar impressive clinical outcomes (approximately 20%-40% complete response rates and 60%-80% overall response rates for patients with indolent B-cell NHL). Current protocol-based investigations of anti-CD20 RIT relate to new clinical uses and new CD20(+) targets.
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PMID:Radioimmunotherapy as a therapeutic option for Non-Hodgkin's lymphoma. 1759 64

Patients who are hepatitis B surface antigen (HBsAg) positive are at risk for hepatitis flare when receiving cytotoxic or immunosuppressive therapy. It has been reported that as high as 50% of HBsAg-positive individuals who undergo chemotherapy develop elevation of liver transaminases. According to current Association for the Study of Liver Diseases guidelines, prophylactic lamivudine should be routinely administered to HBsAg-positive patients with malignancy before chemotherapy. However, occult hepatitis B virus (HBV) infection, defined as HBsAg negative and HBV DNA positive, regardless of HBV core antibody (anti-HBc) status, is not infrequent in HBV endemic areas. Here, we report the case of a B-cell non-Hodgkin lymphoma female patient who was negative for HBsAg, but positive for anti-HBc at the time of chemotherapy. Unfortunately, she developed a fatal HBV reactivation after completing the course of chemotherapy. This case highlights the potential role of lamivudine or other nucleos(t)ide analogue prophylaxis in anti-HBc-positive malignant patient who is about to undergo chemotherapy to provide better coverage for occult HBV infection.
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PMID:Fatal reactivation of hepatitis B virus in a patient who was hepatitis B surface antigen negative and core antibody positive before receiving chemotherapy for non-Hodgkin lymphoma. 1924

Epidemiological studies performed over the last decade have demonstrated a positive association between persistent, hepatitis B surface antigen (HBsAg)-positive hepatitis B virus (HBV) infection and B-cell non-Hodgkin lymphoma (NHL), with HBV-infected patients having a 2-3-fold higher risk to develop NHL than non-infected patients. Moreover, there is evidence that also occult HBV infection (HBsAg-negative, HBV DNA-positive) associates with NHL. An association with HBV infection may exist also for other hematological malignancies, but available evidence is much less persuasive than for NHL. In this review article we will discuss available results on the association between HBsAg-positive HBV infection and NHL, as well as the significance of other serological markers of HBV infection in these subjects. We will also discuss the possible etiopathogenic role of HBV, and propose a multifactorial model for lymphomagenesis. Experimental evidence for multifactorial etiopathogenesis has been obtained in recent years for HBV-associated hepatocellular carcinoma (HCC), and we suggest that a similar model may apply to HBV-associated lymphoma as well. Eventually, we will also address some unresolved questions. Two of these are of particular relevance. First, do HBV-positive NHL patients show regression of their hematologic malignancy upon antiviral therapy? A positive answer would represent a direct demonstration of the necessary etiological role of the virus in the development of NHL, as has been shown previously for HCV-associated lymphomas. Second, if HBV plays a necessary role in lymphomagenesis, then expansion of HBV vaccination is expected to reduce the number of incident NHL cases, even though this effect might become evident only after a long time interval. Studies in those countries which have introduced universal HBV vaccination about two decades ago, like Italy, may soon provide results on this important point.
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PMID:The association of hepatitis B virus infection with B-cell non-Hodgkin lymphoma - a review. 2243 84


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