Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 73-year-old man was admitted to our hospital with nasal hemorrhage and high grade fever on Aug, 1992. Physical examination revealed a tumor in the nasopharyngeal cavity, generalized skin eruptions and three tumors on different subcutaneous lesions, splenomegaly 2 cm below the costal margin, and the enlargement of the right cervical and axillary lymph nodes. Biopsy of the nasopharyngeal and cutaneous tumor disclosed non-Hodgkin's lymphoma (WF: Diffuse small cleaved). Peripheral blood examination showed a WBC of 4,800/microliters with 10% blastoid cells. Bone marrow examination showed 60% blastoid cells which frequently appeared a hand mirror configuration had no azurophilic granules in the cytoplasm. Flow cytometic analysis of these cells in the bone marrow showed that they expressed CD56 (NKH-1) and Ia but not expressed T-cell antigens as well as B-cell antigens and myeloid cell antigens. Phenotype of subcutaneous tumor biopsy cells was similar to that of blastoid cells in the bone marrow. T-cell receptor gene (TCR beta and gamma) rearrangements in blastoid cells were not found. The patient was treated with local radiotherapy to nasopharyngeal and skin tumors, followed by chemotherapy. The patient died of complication with pulmonary bleeding due to DIC. These results suggested that this nasopharyngeal lymphoma derived from NK cell.
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PMID:[Primary nasopharyngeal lymphoma with CD3- and CD56+ phenotype]. 753 74

In this study, specimens from 59 cases of non-Hodgkin's lymphoma (NHL) were immunophenotyped with L26 and UCHL-I McAb, then investigated for gene rearrangement by PCR technique. The results showed that the rates of positive amplification of clonal IgH and TCR beta gene rearrangement were 71.4% (10/14) and 83.3% (10/12) respectively in the fresh tissues, and the IgH (semi-nested PCR technique) and TCR beta were 80% (12/15) and 73.3% (11/15) respectively in paraffin embedded tissues. Definitive diagnosis was made for the 6 cases which could not be diagnosed by routine and immunohistochemical methods, and all 6 exhibited IgH or TCR beta single band. No cases with pseudopositive amplification were discovered. This study suggested that the PCR technique was the most specific, sensitive and rapid detection method for clonal gene rearrangement in NHL.
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PMID:[The application of PCR technique in genetic diagnosis of non-Hodgkin's lymphoma]. 780 47

The present study demonstrates differential regulation of three members of the TNF family, lymphotoxin (LT), LT-beta, and TNF-alpha, by activated murine T cell clones. We report for the first time that murine T cells transcribe LT-beta mRNA in the absence of any activating signal. Activation through the TCR by anti-CD3 did not increase the accumulation of LT-beta mRNA but did increase the accumulation of two species of TNF-alpha mRNA and three species of LT mRNA. We determined that anti-CD3-activated T cells differ in their regulation of LT, LT-beta, and TNF-alpha at the transcriptional and post-transcriptional levels. Anti-CD3 activation resulted in substantial increases in the extent of transcription of the TNF-alpha and LT genes, although with different rates. LT mRNA accumulation was also post-transcriptionally regulated by anti-CD3. In anti-CD3-activated T cells, the t1/2 of LT mRNA was three to four times longer than that of TNF-alpha mRNA. LT-beta mRNA decayed at a rate similar to that of LT mRNA. We also noted a dramatic difference in the cycloheximide sensitivity of LT, LT-beta, and TNF-alpha mRNAs. Cycloheximide superinduced the accumulation of LT mRNA, but not that of TNF-alpha and LT-beta mRNA, post-transcriptionally. Thus, this study demonstrates dramatic differences in the molecular mechanisms of regulation of LT, LT-beta, and TNF-alpha. It also indicates that LT production is probably the rate-limiting step in the formation of the LT-LT-beta complex. These differences suggest that the reason for the redundancy of LT, LT-beta, and TNF-alpha is their differential regulation rather than their functions.
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PMID:Differential regulation of lymphotoxin (LT), lymphotoxin-beta (LT-beta), and TNF-alpha in murine T cell clones activated through the TCR. 815 57

Twenty-seven patients with non-Hodgkin's lymphoma (NHL) have undergone peripheral blood stem cell (PBSC) harvesting for autologous transplantation (Tx). A molecular marker was found at presentation in 23/27 patients. Immunoglobulin heavy chain (IgH) or T cell receptor beta (TCR beta) rearrangements were detected by Southern blotting or the polymerase chain reaction (PCR) in 13 patients; PCR detected the bcl-2/JH fusion in 10 patients. Fifteen autologous PBSC transplants have been performed in 11 patients. In 5/11 patients, the marker was present in at least one PBSC collection (in four patients, every PBSC collection was positive). Survival data are available for nine patients (two early deaths); three patients relapsed and died (221 - 930 d), one is alive and in relapse (354 + d) and five are alive and in complete remission (330 - 1290 + d). These findings suggest that tumour cell contamination of PBSC harvests is not uncommon. Whether these cells are clonogenic and contribute to disease relapse remains to be elucidated. The presence of residual disease at the time of transplantation and the reappearance (or persistence) of marker positive cells post-transplantation both appear to be poor prognostic factors for disease-free survival.
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PMID:Molecular detection of residual lymphoma cells in peripheral blood stem cell harvests and following autologous transplantation. 838 94

Two cases of regressing atypical histiocytosis (RAH) are presented. Both patients followed a typical regressing/relapsing course for several years before progression to high-grade neoplasia. In both cases these high-grade tumors were diagnosed as T-cell non-Hodgkin's lymphoma on histopathologic and immunophenotypic grounds, and demonstrated T-cell receptor beta chain (TCR beta) gene rearrangement on Southern blotting. The original cases of RAH were considered to be indolent neoplasms of histiocytic lineage. A single case of a patient with RAH demonstrating TCR beta and gamma gene rearrangements has been described. Our cases lend further weight to the proposition that RAH is a neoplasm of T-cell lineage, and ultimately of aggressive potential. This description accords with current thinking that many of the conditions previously classified as malignant histiocytosis would be better classified as T-cell non-Hodgkin's lymphoma.
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PMID:Regressing atypical histiocytosis: report of two cases with progression to high grade T-cell non-Hodgkin's lymphoma. 838 60

Nineteen patients with Hodgkin's disease (HD), representing 4 different subtypes, were examined for immunophenotype and immunogenotype. Quantitative immunophenotypic analysis of 13 cases revealed a predominance of Leu1 and Leu3 T cells in all subtypes, except in the case of HD lymphocytic-depression (HDLD). The positive rate of LeuM1 and Ki1 in Reed-Sternberg (RS) cells was 65% (11/17) and 73% (11/15), respectively. In DNA hybridization analysis, 5 of the 19 cases of HD were found to have gene rearrangements--immunoglobulin (Ig) gene rearrangements in 3 cases and T cell receptor beta chain (TCR beta) gene rearrangements in 2 cases. Epstein-Barr (EBV) DNA genomes were detected in 8 cases, including 2 of 5 cases which previously had been shown to contain clonal Ig and TCR beta gene rearrangements. By contrast, there were no detectable cytomegalovirus (CMV) DNA sequences in 19 cases of HD or 30 cases of non-Hodgkin's lymphoma (NHL). Although our findings differed somewhat from those obtained on Westerners, they suggest the presence of a monoclonal lymphoid population in HD patients and that the EBV is related to the etiology of HD.
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PMID:Immunoglobulin and T cell receptor beta chain gene rearrangements and Epstein-Barr viral DNA in tissues of Hodgkin's disease in Taiwan. 839 9

CD30 is found on Reed-Sternberg cells of Hodgkin's disease and on a variety of non-Hodgkin's lymphoma cells and is up-regulated on cells after Epstein-Barr virus, human T cell leukemia virus, and HIV infections. We report here that the thymus in CD30-deficient mice contains elevated numbers of thymocytes. Activation-induced death of thymocytes after CD3 cross-linking is impaired both in vitro and in vivo. Breeding the CD30 mutation separately into alpha beta TCR-or gamma delta TCR-transgenic mice revealed a gross defect in negative but not positive selection. Thus, like TNF-receptors and Fas/Apo-1, the CD30 receptor is involved in cell death signaling. It is also an important coreceptor that participates in thymic deletion.
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PMID:Impaired negative selection of T cells in Hodgkin's disease antigen CD30-deficient mice. 859 42

A 77 year-old woman was admitted to the hospital because of nasal obstraction on March 1994. Tumorectomy of the nasopharyngeal tumor disclosed non-Hodgkin's lymphoma (LSG : diffuse, medium sized). The patient was treated with local radiotherapy to nasopharyngeal region and combined chemotherapy (2 courses of CHOP) to reduce residual tumor. On July, the pericardial effusion appeared and the large granular lymphocyte (LGL) like lymphoma cells were observed in the effusion. Flow cytometic analysis of these cells showed that they expressed CD 2, CD 7, CD 56 and HLA-DR, but did not express CD 3. T-cell receptor gene (TCR beta) rearrangement was not observed and natural killer activity was detected in these lymphoma cells. The patient was treated with ProMACE and the pericardial infusion of methotrexate, carboplatin and prednisolone, but the patient died of heart failure. Monoclonarity of lymphoma cells in the pericardial effusion was determined by southernblot analysis, using the terminal repeat of Epstein-Barr virus (EBV) for probe. It was suggested that EBV participated in tumorgenesis in this case.
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PMID:[Nasopharyngeal natural killer cell lymphoma with pericardial infiltration]. 870 91

A clonal-specific polymerase chain reaction technique to detect T-cell receptor delta gene rearrangement in acute lymphoblastic leukaemia (ALL) and non-Hodgkin's lymphoma (NHL) was evaluated. It was applied to detect minimal residual disease. A sensitive and specific technique to detect minimal residual disease for T-cell malignancies was explored. Southern analysis and polymerase chain reaction (PCR) were used to detect the rearranged V-D-J segment of T-cell receptor delta (TCR delta) gene from malignant cell specimens of patients with leukemia and lymphoma of T-cell lineage. The PCR product was sequenced and from the DNA sequences of the V-D-J region, a 3' anti-sense primer was designed and synthesized for clonal specific PCR (CS-PCR). T-cell receptor delta (TCR-delta) gene rearrangement was studied in 40 cases of acute leukaemia and lymphoma of T-cell lineage at diagnosis. Using Southern analysis, the positive rates were 28 and 32% for the 18 T-lymphoma and 22 T-ALL, respectively. A one stage Polymerase Chain Reaction (PCR) technique was used to detect the rearrangement in Southern positive cases and the PCR positive rates were 80 and 86%, respectively. The PCR technique had a sensitivity of 0.1%. Serial follow-up marrow specimens were available from 4 T-ALL patients following chemotherapy for monitoring of minimal residual disease. Their PCR products were DNA sequenced. A 3' primer was designed for each case for a clonal specific (CS) PCR. The technique had a sensitivity of 0.003%. It was applied to detect minimal residual disease in serial follow-up marrow samples. The first patient had persistent negative CS-PCR results and enjoyed continuous remission for more than 3 years. The second patient with negative one stage PCR but positive CS-PCR results had eventual relapse of leukaemia. The other two patients never achieved a morphological remission. These preliminary results appeared to support the usefulness of these PCR techniques in detecting minimal residual disease and predicting relapses for ALL. However, further clinical correlation in larger populations of patients is necessary.
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PMID:Detection of T-cell receptor delta gene rearrangement in T-cell malignancies by clonal specific polymerase chain reaction and its application to detect minimal residual disease. 875 82

We report a 65-year-old woman with non-Hodgkin's lymphoma (NHL) carrying a t(3;14)(q27;q11) and BCL6 rearrangement in the affected cells. She had generalized lymphadenopathy and the bone marrow was infiltrated by lymphoma cells at presentation. Histological diagnosis was "malignant lymphoma, diffuse, large cell" type according to an International Working Formulation. Chromosome analysis revealed a t(3;14)(q27;q11), which is a new variant translocation of t(3;14) (q27;q32). Southern blot analysis showed rearrangement of BCL6, JH, and TCR beta but not of TCR delta. Cosmid probe of BCL6 hybridized to 14q11 and 3q27 by fluorescence in situ hybridization (FISH). Although the band 14q11 is a locus of T-cell receptor alpha- and delta-chains (TCR alpha/delta), lymphoma cells expressed B-cell, IgGk phenotype. The findings suggest that a novel proto-oncogene in the vicinity of TCR alpha/delta is involved in this translocation.
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PMID:Translocation (3;14)(q27;q11): a new variant translocation in a patient with non-Hodgkin's lymphoma of B-cell type with BCL6 rearrangement. 878 Jul 47


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