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)

Over the last three decades, there has been a wide range of options in the management of follicular lymphoma, including observation (watching and waiting), single-agent or combination (e.g., alkylating agents, anthracyclines or purine nucleoside analogs) radiation therapy, immunotherapy alone or in combination with chemotherapy, and interferon. A number of trials studying the treatment of follicular lymphoma patients have investigated the benefit of adding rituximab either concurrently or sequentially to chemotherapy. In the current review, these studies were selected based on the fact that they were randomized Phase III studies with two arms comparing chemotherapy alone with rituximab-based chemo-immunotherapy regimens. In September 2006, the US FDA approved the use of rituximab (Rituxan) as front-line treatment of patients with follicular lymphoma in combination with cyclophosphamide, vincristine and prednisone (R-CVP) as well as for the treatment of patients with low-grade non-Hodgkin's Lymphoma who achieve stable disease or better following first-line treatment with the same chemotherapy regimen (CVP --> R). The European Medicines Agency also approved the use of rituximab (MabThera) as front-line treatment of patients with stage III-IV disease in combination with CVP chemotherapy. In conclusion, although the clinical studies discussed in this article provide evidence for a progression-free survival benefit, overall survival advantage was clearly shown for the first time in a recent update of the initial study in patients with follicular lymphoma.
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PMID:Update on front-line therapy for follicular lymphoma: chemo-immunotherapy with rituximab and survival. 1762 54

Non-Hodgkin lymphomas (NHLs) comprise a diverse group of lymphatic malignancies of primarily B-cell origin, which are steadily increasing in prevalence worldwide. Approximately 63,190 new cases of NHL are expected to be diagnosed in the United States in 2007, representing 4% of all cancers. Further, the annual incidence rate of NHL in 2000-2004, estimated from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute, was 19.3 cases per 100,000 persons. Of these, the indolent NHLs, although initially responsive to a variety of therapeutic regimens, have a continuous relapsing nature and are essentially incurable. Over the past decade, the availability of monoclonal antibodies has revolutionized the treatment of patients with various types of NHL. To date, the most noteworthy agent of this type has been rituximab, an antibody directed against the CD20 antigen found on the majority of B-cell lymphomas. Rituximab is associated with improved and durable responses as a single agent and in combination with chemotherapy for patients with newly diagnosed or relapsed/refractory NHL. Recent data suggest an improvement in survival in recently diagnosed patients who have had access to rituximab therapy and provide new insights into the use of rituximab in frontline combination chemotherapy and as maintenance therapy. Other emerging therapeutics include new chemotherapeutics, small-molecule and monoclonal antibodies, radioimmunotherapy, apoptosis-inducing agents, and immunomodulators.
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PMID:Emerging treatments for indolent lymphoma. 1763 94

Rituximab is a chimeric human-mouse anti-CD20 monoclonal antibody, which is used in the treatment of both B-cell lymphomas and rheumatic diseases. We describe a case of a previously healthy 57-year-old man developing arthritis while being treated with rituximab-CHOP chemotherapy (R-CHOP) for a non-Hodgkin lymphoma. The remittant arthritis developed at successively shorter time-intervals after R-CHOP administration and only improved after rituximab was removed from the chemotherapy schedule, suggesting a rituximab-related phenomenon, as extensive diagnostic testing ruled out any other diagnosis.
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PMID:A 57-year-old man who developed arthritis during R-CHOP chemotherapy for non-Hodgkin lymphoma. 1766 Sep 34

In industrialized nations people infected with HIV remain at increased risk for malignancies despite highly active antiretroviral therapy. In these countries, lymphoma is the most common HIV-associated malignancy. This review summarizes progress from January 2005 to February 2007. The majority of investigation has been in diffuse large B cell lymphoma, with infusional therapy remaining promising but cumbersome. Rituximab likely improves complete response rates, and, possibly overall survival, but is likely associated with increased infections in a subset of patients with very low CD4 counts. Biologic insights have been attained in the spectrum of HIV-associated non-Hodgkin's lymphoma, Hodgkin's lymphoma, and virologic coinfections. Overall, the outcome for non-Hodgkin's lymphoma and Hodgkin's lymphoma in the setting of HIV continues to improve as insights into the pathophysiology and treatment advance.
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PMID:Update on HIV lymphoma. 1770 67

Recombinant human rhApo2L/TRAIL selectively stimulates apoptosis in various cancer cells through its receptors DR4 and DR5, and is currently in clinical trials. Preclinical studies have established antitumor activity of rhApo2L/TRAIL in models of epithelial cancers; however, efficacy in non-Hodgkin lymphoma (NHL) models is not well studied. Of 7 NHL cell lines tested in vitro, rhApo2L/TRAIL stimulated apoptosis in BJAB, Ramos RA1, and DoHH-2 cells. Rituximab, a CD20 antibody used to treat certain types of NHL, augmented rhApo2L/TRAIL-induced caspase activation in Ramos RA1 and DoHH2 but not BJAB or SC-1 cells, through modulation of intrinsic rather than extrinsic apoptosis signaling. In vivo, rhApo2L/TRAIL and rituximab cooperated to attenuate or reverse growth of tumor xenografts of all 4 of these cell lines. Depletion of natural killer (NK) cells or serum complement substantially reduced combined efficacy against Ramos RA1 tumors, suggesting involvement of antibody-dependent cell- and complement-mediated cytotoxicity. Both agents exhibited greater activity against disseminated than subcutaneous BJAB xenografts, and worked together to inhibit or abolish disseminated tumors and increase survival. Moreover, rhApo2L/TRAIL helped circumvent acquired rituximab resistance of a Ramos variant. These findings provide a strong rationale for clinical investigation of rhApo2L/TRAIL in combination with rituximab as a novel strategy for NHL therapy.
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PMID:Cooperation of the proapoptotic receptor agonist rhApo2L/TRAIL with the CD20 antibody rituximab against non-Hodgkin lymphoma xenografts. 1772 41

Rituximab is a humanized monoclonal antibody directed against CD20-positive B cells and originally developed for the treatment of non-Hodgkins lymphoma. We report a case of severe mucous membrane pemphigoid responsive to rituximab infusions. The clinical presentation, etiology, and management options for mucous membrane pemphigoid are also discussed.
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PMID:Successful adjuvant treatment of recalcitrant mucous membrane pemphigoid with anti-CD20 antibody rituximab. 1776 98

Advanced stage follicular lymphoma is incurable by conventional treatment. Important progress has been observed with the development of new therapies based on monoclonal antibodies and on the use of radioimmunotherapy (RIT) in the treatment of non-Hodgkin lymphomas (NHL). Rituximab in combination with chemotherapy in the upfront setting significantly improved treatment outcome as compared with chemotherapy alone. Different studies also indicate that RIT has an important role in the management of NHL and could be beneficial in combination with chemotherapy. These two new treatment options have clearly distinctive mechanisms of action, rituximab being an exclusively biological treatment and RIT adding targeted systemic radiation therapy. Both RIT and the unlabeled antibody treatments might be further improved by different strategies including repetition of RIT or combination of different antibodies. We present here our experience with RIT using 131I-tositumomab (Bexxar) and discuss different topics regarding RIT, like the use of different antibodies, the best choice of the radioisotope or the place of radio-imaging. From the therapeutic point of view, we argue that the debate should not be as to which one among antibody immunotherapy or RIT should be best added to chemotherapy, but that all three treatments might be optimally combined with the aim to get the highest chance of cure for advanced stage follicular lymphoma.
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PMID:[Radioimmunotherapy of follicular lymphoma: a step towards cure?]. 1787

The year 2007 marks the 10th anniversary of approval by the U.S. Food and Drug Adminstration of the first monoclonal antibody for the treatment of cancer. Rituximab, an anti-CD20 chimeric monoclonal antibody, was approved for the treatment of patients with relapsed/refractory low-grade B-cell non-Hodgkin lymphomas. From an immunologic perspective, this therapeutic indication provided the long-elusive validation of immunotherapy as the fourth modality of treatment for patients with cancer. From a clinical perspective, it was hard to imagine then that this nonchemotherapeutic approach would dramatically impact the management of patients with almost every type of B-cell malignancy and that it would even find a place as a therapeutic option for patients with non-malignant disorders. Although thousands of patients have been treated worldwide with rituximab, there is still debate regarding its mechanism(s) of action. The demonstration that a number of patients do not benefit with this treatment and that no cures have been achieved with single-agent rituximab prompted several investigators to identify those barriers limiting the efficacy of this monoclonal antibody. Here, we summarize what we have learned in the past 10 years about rituximab efficacy and its mechanisms of action and resistance. We also discuss the new generation of monoclonal antibodies, the development of which has been spurred by the widespread success of anti-CD20 MAb therapy.
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PMID:Monoclonal antibodies for B-cell lymphomas: rituximab and beyond. 1802 35

A 63 year old woman with non-Hodgkin lymphoma presented with unilateral pleural effusion, which when aspirated revealed CD19 and CD20 positive malignant cells. Prior to this, the patient had received several lines of chemotherapy (CHOP, VAD, FED) with no effect on pleural effusion. Repeated percutaneous drainage procedures were unable to control the effusion either. Rituximab was therefore instilled in a dose escalating manner via repeated pleurocenteses. Fifty days after the application of rituximab, pleural effusion was still present but reduced in size. Flow cytometry and immunocytochemistry performed on the same day showed CD19 positive cells which were lacking CD20 epitope, which could be explained by either engagement or destruction of the CD20 epitope upon interaction with rituximab making the detection of the CD20 molecule impossible by routine flow cytometry. What is especially interesting is the fact that even 50 days after the application of rituximab intrapleurally no new CD20 positive cells could be found in the pleural effusion by immunochemistry or flow cytometry, opening an interesting issue concerning the length of rituximab's activity when applied locally. Although our patient had no adverse effects, further analysis of rituximab's activity and safety when applied intrapleurally is warranted.
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PMID:[The disappearance of CD20 positive lymphocytes in the pleural effusion after intrapleural application of rituximab]. 1804 81

In an attempt to define mechanisms by which B-cell non-Hodgkin lymphoma (NHL) may escape rituximab immunotherapy, we developed several rituximab-resistant cell lines (RRCL) generated from the rituximab-sensitive cell lines (RSCL) Raji and RL. Rituximab resistance was associated with CD20 downregulation and upregulation of CD52 and the complement inhibitory proteins (CIPs) CD55 and CD59. No significant alemtuzumab-associated complement-mediated cell lysis (CMC) or antibody-dependent cellular cytotoxicity (ADCC) was demonstrated in RSCL. In contrast, in vitro exposure of RRCL to alemtuzumab resulted in a significant degree of CMC and ADCC. Of note, in vitro blocking of CD52 with anti-CD52 F(ab')(2) fractions in RRCL improved rituximab-associated CMC as compared to unblocked RRCL. Our current data provides a basis for further evaluation of alemtuzumab-based clinical trials for patients with rituximab-resistant NHL.
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PMID:CD52 over-expression affects rituximab-associated complement-mediated cytotoxicity but not antibody-dependent cellular cytotoxicity: preclinical evidence that targeting CD52 with alemtuzumab may reverse acquired resistance to rituximab in non-Hodgkin lymphoma. 1806 19


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