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)

In mantle cell lymphoma (MCL), minimal residual disease (MRD) is an indicator of the disease outcome. Quantitative methods used so far do not provide a suitable molecular marker in 30-70% patients with MCL (depending on the technique used). We tested cyclin D1 as a marker for quantitative MRD monitoring. The real-time PCR of cyclin D1 mRNA was performed in 144 bone marrow (BM) specimens including 95 BMs from MCL patients, 39 BMs from patients with other B-cell non-Hodgkin's lymphomas and 10 BMs from healthy volunteer donors. In 73 BMs obtained from 20 MCL patients we examined the cyclin D1 level during the treatment and follow-up period. We detected a cyclin D1 overexpression exclusively in BMs infiltrated with MCL, including minimal residual infiltration. Dynamics of cyclin D1 correlated with the patient's clinical status in 69/73 BMs. Individual monitoring of patients during the disease course showed cyclin D1 quantitative changes accompanying either the disease relapse or a successful treatment response or the disease-free survival (remission) and it showed a predictive significance. Cyclin D1 detection is a promising approach for the quantitative MRD monitoring in MCL patients, and the individual monitoring of the cyclin D1 dynamics represents a suitable indicator of the disease course.
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PMID:Quantitative monitoring of cyclin D1 expression: a molecular marker for minimal residual disease monitoring and a predictor of the disease outcome in patients with mantle cell lymphoma. 1879 51

T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) are considered the same disease, differing by the extent of bone marrow infiltration. According to recent gene expression profiling data, T-ALL and T-LBL can be separated by prediction analysis of microarrays showing an overexpression of MML1 in T-LBL and CD47 in T-ALL. Immunophenotypes of T-LBL and T-ALL are identical but differ in frequency, with a higher rate of cortical or mature immunophenotypes in T-LBL, which is probably related to the higher rate (> 90%) of mediastinal tumors. Treatment approaches in T-LBL changed from conventional non-Hodgkin lymphoma (NHL) protocols to intensive NHL protocols but recently to ALL-designed protocols. T-ALL remission rates are 90%, and overall survival (OS) has improved to 60%-70%. Mediastinal tumors resolve in most cases of T-ALL with chemotherapy only, whereas in T-LBL additional mediastinal irradiation seems to be beneficial. Strategies for stem cell transplantation (SCT) in T-LBL and T-ALL differ. Autologous SCT in complete remission (CR) in T-LBL gives a 70% survival rate, which is similar to chemotherapy alone. In T-ALL, the subtypes of early and mature T-ALL have a poor outcome with chemotherapy alone (< 30%) and might profit from an allogeneic transplantation in first CR (OS > 50%). There seems to be no need for transplantation in thymic T-ALL in first CR. Prognostic factors are published for T-ALL but not for T-LBL. MRD may guide further treatment strategies in T-ALL and probably also in T-LBL as indications for a SCT or for the evaluation of novel, particularly T-cell-specific, drugs.
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PMID:T-cell lymphoblastic lymphoma and T-cell acute lymphoblastic leukemia: a separate entity? 1977 44

Presence of normal plasma cells (PCs), hemodilution of bone marrow aspirate, and changes in the immunophenotype are important considerations in minimal residual disease (MRD) assessment in multiple myeloma (MM). We evaluated 124 subjects-107 with MM, 11 with Hodgkin lymphoma, and 6 allogeneic stem cell transplantation donors-for the immunophenotype of neoplastic, reactive, and normal PCs respectively. Of the patients with MM, 36 were evaluated for MRD and 23 for a change in immunophenotype after chemotherapy. The immunophenotype of normal and reactive PCs was similar and differed from that of neoplastic PCs with respect to CD19, CD45, CD56, CD52, CD20, and CD117. At least 2 antigens were aberrantly expressed in all cases and 3 in 90.7% of MM cases. A change in the immunoprofile of PCs was observed in 18 (78%) of 23 cases. By using flow cytometry, we detected MRD in all samples, and a neoplastic PC index (percentage of neoplastic PCs/total bone marrow PCs) of less than 30 could differentiate immunofixation (IFx)- from IFx+ samples (complete and partial responders, respectively).
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PMID:Flow cytometric immunophenotyping and minimal residual disease analysis in multiple myeloma. 1984 14

B-cell maturation from hematogones to mature B cells in bone marrow exhibits a consistent, complex spectrum of sequential antigen expression. CD5 expression, however, has not been characterized. We studied the dynamics of CD5 expression on developing B cells by 4-color flow cytometry in 32 patients, aged 9 months to 63 years, with hematogone hyperplasia (>3.5% of total events). The mean percentage of hematogones was 8.1%. We demonstrate consistent CD5 expression on normal, polytypic B cells in a continuum, predominantly at later stages of maturation, specifically on stage 3 hematogones and mature B cells. Awareness of this normal pattern of CD5 expression on B-cell subsets has implications in the analysis of minimal residual disease of CD5+ B-lineage non-Hodgkin lymphomas.
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PMID:Significant CD5 expression on normal stage 3 hematogones and mature B Lymphocytes in bone marrow. 1984 15

Assessing molecular persistent or minimal residual disease (PD/MRD) in childhood Burkitt lymphoma (BL) is challenging because access to original tumor is usually needed to design patient-specific primers (PSPs). Because BL is characterized by rearranged immunoglobulin heavy chain (IgV(H)) genes, IgV(H) primer pools from IgV(H1)-IgV(H7) regions were tested to detect PD/MRD, thus eliminating the need for original tumor. The focus of the current study was to assess the feasibility of using IgV(H) primer pools to detect disease in clinical specimens. Fourteen children diagnosed with B-NHL had follow-up repository specimens available to assess PD/MRD. Of the 14 patients, 12 were PD/MRD negative after 2 months of therapy and remained in remission at the end of therapy; 2/14 patients were PD/MRD positive at 2-3 months and later relapsed. PSP-based assays from these 14 patients showed 100% concordance with the current assay. This feasibility study warrants further investigation to assess PD/MRD using IgV(H) primer pools, which could have clinical significance as a real-time assessment tool to monitor pediatric BL and possibly other B-cell non-Hodgkin lymphoma therapy.
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PMID:Screening for residual disease in pediatric burkitt lymphoma using consensus primer pools. 1989 Apr 67

BACKGROUND: The mechanisms responsible for resistant or recurrent disease in childhood non-Hodgkin lymphoma (NHL) are not yet fully understood. A unique mechanism suggesting the role of the mitochondria as the key energy source responsible for residual cells has been assessed in the clinical setting on specimens from patients on therapy were found to have increased copies of mitochondrial DNA (mtDNA) associated with positive minimal residual disease and/or persistent disease (MRD/PD) status. The potential role of mtDNA in MRD/PD emphasizes queries into the contributions of relevant enzymatic pathways responsible for MRD/PD. This study hypothesized that in an in-vitro model, recovering or residual cells from chemotoxicity will exhibit an increase in both citrate synthase and isocitrate dehydrogenase expression and decrease in succinate dehydrogenase expression. PROCEDURE: Ramos cells (Burkitt lymphoma cell line) were exposed to varying concentrations of doxorubicin and vincristine for 1 hr; and allowing for recovery in culture over a 7-day period. cDNA was extracted on days 1 and 7 of the cell culture period to assess the relative expression of the aforementioned genes. RESULTS: Increase citrate synthase, increase isocitrate dehydrogenase and decrease succinate dehydrogenase expressions were found in recovering Ramos cells. CONCLUSION: Recovering lymphoma cells appear to compensate by regulating enzymatic levels of appropriate genes in the Krebs Cycle suggesting an important role of the mitochondria in the presence of residual cells.
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PMID:Possible Mitochondria-Associated Enzymatic Role in Non-Hodgkin Lymphoma Residual Disease. 1993 79

Mantle cell lymphoma (MCL) is a rare non-Hodgkin lymphoma (NHL) entity. The translocation between chromosomes 11 and 14 is the cytogenetics hallmark of MCL. This translocation leads to the dysregulation of the CCDN1 gene, and overexpression of cyclin D1 which promotes cell cycling. Despite a classical phenotype (CD19+, CD20+, CD5+, CCND1+, CD10-, CD23-, Bcl-2+, Ig at the membrane, mainly IgM), MCL is not a homogeneous disease and several cytological, phenotypic, cytogenetic and clinical variants have been described. MCL represents 5 % of NHLs with its incidence constantly increasing over the last years. Median age at diagnosis is 68 years. Stage III-IV disease is observed in more than 80 % of patients at presentation, with intestinal and bone marrow being the most frequently involved organs, while the spleen is enlarged in half of cases. Intensive strategies including high-dose chemotherapy, followed by autologous stem cell transplantation have significantly improved the outcome of MCL patients. Median overall survival rate increased from 3 to 5 years during the last decade. At present, induction chemotherapy followed by high-dose chemotherapy and autologous stem cell transplantation is the standard regimen in younger patients. However, most of MCL patients will experience relapse. Thus, close monitoring of minimal residual disease (currently under evaluation) may represent a valuable tool for assessment of disease response during follow-up. Future innovative therapies that are being presently investigated in prospective trials include transduction pathways inhibitors, proteasome inhibitors, pro-apoptotic molecules, immunotherapy and/or radiolabeled immunotherapy, and will likely open a new era for targeted therapies in MCL.
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PMID:[Mantle cell lymphoma: an overview from diagnosis to future therapies]. 2048 92

High-dose chemotherapy followed by autologous stem cell transplant (ASCT) leads to durable remissions in approximately half of patients with chemosensitive relapsed or refractory aggressive lymphomas; however, many will relapse despite ASCT secondary to persistent minimal residual disease (MRD) or malignant graft contamination. Post-transplant rituximab may eradicate MRD. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2) might enhance the efficacy of rituximab by augmenting antibody-dependent cellular cytotoxicity (ADCC). We hypothesized that given together, rituximab, GM-CSF, and IL-2 might eradicate MRD and improve event-free survival following ASCT. Forty-six patients with relapsed non-Hodgkin lymphoma (NHL) or Hodgkin lymphoma (HL) were enrolled. Stem cells were mobilized with G-CSF and GM-CSF following chemotherapy. Following BEAM conditioning, patients received GM-CSF until neutrophil engraftment. Between days + 30 and + 120, patients received one dose of rituximab 375 mg/m(2) (cycle 1), followed by three cycles of GM-CSF 250 microg/m(2)/day SQ days 1-5, IL-2 1.5 x 10(6) IU/m(2)/day SQ days 6-12, and rituximab 375 mg/m(2) IV day 9, repeated every 21 days. Thirty-eight patients were eligible for post-ASCT immunotherapy. Nine patients completed 1-2 cycles and 21 completed 3-4 cycles; eight patients did not receive post-ASCT immunotherapy. Grade 3-4 neutropenia and grade 3 thrombocytopenia were observed. With a median follow-up of 30 months, the estimated 5-year OS and EFS for all patients eligible for immunotherapy are 65% and 45%, respectively. Post-ASCT immunomodulation with rituximab, IL-2, and GM-CSF was feasible and safe, but not all patients were able to continue on to post-ASCT immunotherapy.
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PMID:Phase II study of immunomodulation with granulocyte-macrophage colony-stimulating factor, interleukin-2, and rituximab following autologous stem cell transplant in patients with relapsed or refractory lymphomas. 2049 94

Flow cytometric immunophenotyping (FCM) of multiple myeloma (MM) is commonly accepted in academic centers as providing clinically significant information and is becoming increasingly utilized in the private setting. FCM has established clinical relevance in the following: (1) differential diagnosis of MM from other plasma cell dyscrasias; (2) differentiating MM from lymphoplasmacytic lymphoma (LPL) and other non-Hodgkin lymphomas; (3) diagnosis of unusual cases of myeloma (eg, to confirm the diagnosis of rare cases of IgM MM); (4) determining the risk of progression of monoclonal gammopathy of uncertain significance (MGUS) and smoldering MM; (5) prognostication in MM; and (6) minimal residual disease detection (MRD) post therapy. FCM may have an emerging role in the enumeration of abnormal plasma cells in diagnosis of MM, but further studies are needed. We review the clinical value of FCM in evaluation of peripheral blood and bone marrow in early myeloma.
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PMID:Role of flow cytometry of peripheral blood and bone marrow aspirates in early myeloma. 2123 56

The monoclonal chimeric anti-CD20 antibody, rituximab, has considerably improved therapeutic outcome in B-cell chronic lymphocytic leukemia. Rituximab has limited clinical activity when used as a single agent. The combination of the monoclonal antibody with fludarabine-based regimens clearly demonstrated, in Phase II and randomized trials, an increase in clinical efficacy in previously untreated and pretreated patients. Furthermore the addition of rituximab enabled the eradication of minimal residual disease, which is correlated with the prognosis in a high proportion of patients. Although the combination of rituximab with fludarabine-based regimens increased myelosuppression and immunosuppression, incidence of infections did not increase. The benefit of adding rituximab to other purine analogs or other chemotherapeutic combination regimens has also been explored. Moreover there could be a role for achieving better quality of responses with the combination of different monoclonal antibodies, considering that they target different antigens and exert different mechanism of action. Although the role of rituximab as maintenance therapy in low grade non-Hodgkin's lymphomas has been determined, the benefit and optimal schedule in chronic lymphocytic leukemia are still under investigation. This review brings together knowledge of the pharmacokinetics, mechanism of action and clinical use of rituximab in chronic lymphocytic leukemia.
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PMID:The spectrum of use of rituximab in chronic lymphocytic leukemia. 2128 58


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