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)

Bispecific antibodies (BsAb) can be used to retarget T cells irrespective of their specificity to certain target cells inducing target cell lysis. We have tested the efficacy of the BsAb SHR-1, directed against the T cell antigen CD3 and the B cell antigen CD19 to induce (malignant) B cell kill by T cells as measured in a 51Cr-release assay. Two cytotoxic T cell clones (CTL), expressing TCR alpha beta or TCR gamma delta, were effective in killing CD19 expressing B cell lines at different stages of differentiation in the presence, but not in the absence, of the BsAb. CD19- target cells were not killed. Fresh CD19+ leukaemia/lymphoma cells were also efficiently killed by SHR-1 preincubated CTL clones. In addition, phytohaemagglutinin (PHA) or CD3-activated IL-2 expanded peripheral blood mononuclear cells (PBMC) of normal donors did so after 2 weeks of stimulation. A concentration of 100 ng/ml of the BsAb was sufficient to obtain optimal lysis of all target cells tested. These results show that fresh human leukaemia/lymphoma cells, freshly derived from active lymphoblastic leukaemia (ALL) as well as non-Hodgkin's lymphoma (NHL) patients, can be effectively killed in the presence of this BsAb by activated T cells.
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PMID:Killing of human leukaemia/lymphoma B cells by activated cytotoxic T lymphocytes in the presence of a bispecific monoclonal antibody (alpha CD3/alpha CD19). 128 Oct 55

Subsets of non-Hodgkin's lymphoma in humans have been shown to involve activation of protooncogenes such as MYC and BCL2 resulting from chromosome translocation involving the IGH and TCR genes. Malignant lymphomas in the canine present histologic and clinical subsets similar to those in humans. To study the genetic nature of these lymphomas, we undertook this study to determine, by Southern blotting analysis, the extent of homology between the human and canine genes MYC, BCL2, IGH, and TCRB using human gene probes. Our results, presented here, show that the organization of these genes in the two species is very similar.
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PMID:Detection of canine homologs of human MYC, BCL2, IGH, and TCRB genes by Southern blot analysis. 138 33

A-31-year-old man with right cervical and supraclavicular lymphadenopathy was admitted in March, 1991. He was diagnosed as having muscular sarcoidosis at the age 8 year, and was treated with corticosteroids. Since age 18, his skin was erythematous and ulcerous, and later his skin became gradually atrophic. Lymph node biopsy revealed diffused large cell non-Hodgkin's lymphoma. Lymphoma cells showed TCR-beta gene rearrangement by Southern blot hybridization. His lymphoma was refractory to CHOP and CHOP-Bleo regimens. Complete remission was achieved with cisplatin and etoposide. However, early relapse occurred, and he died of pulmonary hemorrhage 4 months after the diagnosis of non-Hodgkin's T-cell lymphoma. The so called "sarcoidosis-lymphoma syndrome" is uncommon in Japan. In 9 of 10 cases previously reported, malignant lymphoma occurred during the course of sarcoidosis. Most of the sarcoidosis cases were chronic active type, and required systemic administration of corticosteroids. Hodgkin's disease coexistent with sarcoidosis as reported in other countries, was not found in Japan. These findings suggest that the low incidence of sarcoidosis-lymphoma syndrome in our country is due to the relative rareness of Hodgkin's disease. The sarcoidosis-lymphoma syndrome possibly appears as a consequence of immunological abnormalities observed in sarcoidosis.
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PMID:[Non-Hodgkin's lymphoma in a patient with sarcoidosis (the sarcoidosis-lymphoma syndrome)]. 140 63

Using Southern-blot analysis, we studied samples of bone marrow (BM) cells from 73 patients with non-Hodgkin's lymphoma (NHL) in various clinical status. The frequency of gene rearrangement was disease-status dependent with a frequency of 65.8% at the diagnostic stage, 81.8% after relapse and 33.3% upon complete remission (CR). BM involvement was evident in a substantial portion of patients with untreated and relapsed lymphoma. The significance of BM involvement by DNA hybridization in relation to conventional clinical staging and histological grade was studied. By Southern-blot analysis, BM involvement was found in 76% of the patients at clinical stages (CS) I-III. The incidence of BM involvement in low, intermediate and high grades of NHL (Working Formulation) was 57%(4/7), 67%(22/33), and 89%(8/9) respectively. A comparative study of conventional BM biopsy vs DNA hybridization in a group of 47 NHL patients showed that all 12 patients (100%) with morphological BM involvement and 25 out of 35 patients (71%) with morphologically normal BM had clonal rearrangements of immunoglobulin (Ig), heavy chain and/or light chain; or T-cell receptor beta chain (TCR beta) genes in BM cells. The false negative rate in conventional BM biopsy was 53%(25/47). Southern-blot analysis on lymph nodes (LN) and BM cells from 37 patients showed that 6 patients (16%) had cross-lineage or different rearranged patterns in the same or different tissues. Southern-blot analysis was found to be highly reliable for the detection of even minimal populations of lymphoma cells in the BM and therefore should be the diagnostic choice for clinical staging of lymphoma.
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PMID:Study of bone marrow cells in non-Hodgkin's lymphoma by DNA analysis. 166 35

We studied peripheral blood mononuclear cells, bone marrow cells and lymph node cells from 30 patients with non-Hodgkin's lymphoma by DNA hybridization. Clonal JH or TCR beta gene rearrangements were detected in peripheral blood or bone marrow mononuclear cells from 15 of 30 (50.0%) patients studied, including 31.8% of those without evidence of tumor cells by morphological method. Four of 9 cases demonstrated identical clonal gene rearrangements at diagnosis and in remission phase in peripheral blood mononuclear cells. The presence of clonal gene rearrangements roughly correlated with the clinical stage of disease. And the proportion of clonal rearrangements was higher in the groups with small & medium sized cell types (64.3%) than in the group with large cell type (33.3%). So, we concluded that Southern blot analysis was more useful than morphological method to detect monoclonality of circulating lymphoma cells and minimal tumor cells.
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PMID:[Detection of minimal tumor cells in peripheral blood patients with non-Hodgkin's lymphoma by Southern blot analysis]. 183 19

To investigate effects of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) on lymphoid cells in vivo, we monitored changes in absolute lymphocyte counts, plasma concentrations of soluble interleukin-2 receptor (sIL-2R) and soluble cytotoxic/suppressor (sCD8) antigens, and phenotypic changes of surface membrane antigens of peripheral mononuclear cells from 14 patients with malignant lymphoma treated with rhGM-CSF. Eight of the 14 patients had relapsed or had refractory non-Hodgkin's lymphoma (NHL) and received rhGM-CSF after intensive chemotherapy with novantrone (NO) and high-dose Ara-C (AC) (NOAC) as salvage regimen. Six other patients with NHL or Hodgkin's disease (HD) were in complete remission and treated with rhGM-CSF to enhance peripheral hematopoietic progenitor cell harvest for autografting. An increase in absolute lymphocyte count at the zenith of leukocyte elevation and a drastic increase in concentration of sIL-2R from a median of 565 U/mL to 6,700 U/mL on rhGM-CSF infusion were found in all patients. There was also a moderate increase in sCD8 levels from a median of 277 U/mL to 470 U/mL. Ten patients were available for serial studies of phenotypic changes in surface membrane antigens. A significant increase in CD25+ (IL-2R+) (P = .0020) and CD4+ (P = .0137) lymphocytes was observed in all patients, but no significant change in CD3+, CD8+, TCR delta 1+, or CD19+ cells. Elevations in absolute lymphocyte counts or in concentrations of sIL-2R or sCD8 were not observed in four other patients during recovery from intensive chemotherapy without rhGM-CSF support. Our results provide evidence that administration of rhGM-CSF might activate lymphocytes in vivo. The impact of this activation on the remission rate and duration, as well as survival in patients with NHL, warrants further investigation.
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PMID:Activation of lymphocytes induced by recombinant human granulocyte-macrophage colony-stimulating factor in patients with malignant lymphoma. 210 62

Expression of six proto-oncogenes (fos, myc, myb, Ki-ras, Ha-ras, and N-ras) in 43 cases of non-Hodgkin's lymphoma was analyzed by means of in situ hybridization. Biotinylated DNA probes of the six oncogenes and those of immunoglobulin H (IgH) gene and T-cell receptor beta (TCR beta) chain gene were used. The results of in situ hybridization performed under blind conditions by IgH gene and TCR beta chain gene probes were compatible with those of typing by cell surface markers. The nuclear protein-related proto-oncogenes, fos, myc, and myb, were expressed in about 70% to 80% of all cases regardless of phenotype, histology, or histologic grade. On the contrary, genes of ras family were expressed in more limited numbers of cases except for the Ki-ras gene, which was more frequently expressed by cases of the T-cell immunophenotype with a high malignancy grade. The results of dot hybridization with RNA extracted from some cases were compatible with those of in situ hybridization, further demonstrating the specificity of in situ hybridization.
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PMID:Histologic typing of non-Hodgkin's lymphomas by in situ hybridization with DNA probes of oncogenes. 252 66

We investigated for rearrangements of the immunoglobulin (Ig) heavy and light chain genes and of the T cell receptor gamma (TCR gamma) and beta (TCR beta) genes 45 biopsy samples from a variety of lymphoproliferative disorders. They were diagnosed histopathologically and immunophenotypically as non-Hodgkin's lymphomas (NHLs) of the B cell type (19 cases), NHLs of the T cell type (3 cases), NHLs of "undetermined" cell type (3 cases), atypical lymphoid proliferation (1 case) and AIDS-related lymphadenopathies with florid polyclonal follicular hyperplasia (19 cases). A monoclonal proliferation of B cells was shown by DNA analysis in all 19 B cell NHLs. In two immunohistologically determined T cell NHLs (both diagnosed as mycosis fungoides) the cells had rearrangements of TCR beta gene, whereas in the third case (lymphoblastic NHL) the cells had rearrangements of Ig heavy chain and TCR gamma and TCR beta genes. None of the B cell NHLs exhibited TCR gamma and TCR beta gene rearrangement bands. All the "undetermined" cell NHLs demonstrated rearrangements of Ig heavy chain gene associated with the germ line TCR gamma and TCR beta genes; in two cases light chain gene rearrangements were also found. The atypical lymphoid proliferation, in which the differential diagnosis was between a reactive or malignant process, and two out of 19 cases of florid polyclonal follicular hyperplasia showed a clonal B cell population by DNA analysis. This study indicates that there was a strong correlation between the rearrangements of specific genes and the immunophenotype of the NHL; moreover, DNA analysis of tissue biopsy specimens from phenotypically "undetermined" cell NHLs and from equivocal lymphoid proliferation using Ig and TCR gene probes yielded an answer in the cases analyzed. The significance of clonal B cell expansions found in two AIDS-related lymphadenopathies should be interpreted with caution.
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PMID:Immunoglobulin and T cell receptor gene rearrangements and in situ immunophenotyping in lymphoproliferative disorders. 253 56

During recent years cloning of the genes encoding the immunoglobulin (Ig) and T-cell (TCR) antigen receptor has made it possible to analyze clonal expansions of B- or T-cells at the molecular level. We here describe the usefulness of the Ig- and TCR-gene rearrangements in selected cases of malignant lymphoma. In contrast to all other cases investigated, one non-Hodgkin's lymphoma (NHL) exhibited the infrequent phenomenon of oligoclonality, i.e. three distinct B-cell clones were discerned by Southern blot analysis. Detection of clonal TCR- and Ig-gene rearrangements unequivocally documented bone marrow involvement in four of eight NHL-patients, where conventional histologic and cytologic examination remained inconclusive. As expected, analysis of bone marrow DNA revealed clonal Ig-gene rearrangements in three cases with clear histologic evidence of bone marrow infiltrations by the NHL. In one case of a patient with acute mixed lymphoid-myeloid lineage leukemia a previously identified clonal Ig-gene rearrangement vanished after successful chemotherapy. Analysis of Ig- and TCR-gene rearrangements promises to be a very useful diagnostic tool in selected cases of lymphoid neoplasia.
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PMID:[Rearrangements of immunoglobulin and T-cell-antigen receptor genes as diagnostic markers in lymphatic neoplasms]. 308 5

We examined 91 specimens (from 87 patients) for the expression of B-cell- and T-cell-associated differentiation antigens and rearrangements of the Ig and beta-chain of the T-cell (beta-TCR) genes. Of these, 74 were representative of various histologic subtypes of non-Hodgkin's lymphoma and related disorders, 11 of Hodgkin's disease, and 6 of reactive lymphoid hyperplasia. An Ig gene clonal rearrangement correlated to a monotypic (kappa/lambda) phenotype in 32 of 33 histologically defined lymphoma samples. The genotypic analysis also confirmed clonality in six of seven malignant diffuse lymphomas that were nonmonotypic but expressed pan-B antigens; in four, more than one clone was detected within individual tumors. A beta-TCR clonal rearrangement was found in 19 of 19 tumor samples considered as malignant T-cell lymphoma on the basis of histopathology and of the CD3-positive phenotype of tumoral cells, and in two cases of CD3-positive lymphomatoid disorders. A loss of pan-T antigens (CD7, CD5, CD2, CD4/CD8) was observed in all but three of these CD3-positive samples. Such an incomplete T-cell phenotype always correlated to the presence of a monoclonal process as revealed by genotypic analysis. DNA analysis was the only way to demonstrate clonality in other samples with either a polymorphous (partial involvement, pseudolymphoma, angioimmunoblastic lymphodenopathy [AILD]) or an undifferentiated (large cell anaplastic) phenotype. It is concluded that although in the majority of cases immunophenotyping alone provides criteria adequate for the diagnosis of lymphoid malignancy, in some, particularly polymorphous or large cell anaplastic processes, genetic probe analysis was additionally discriminative.
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PMID:Comparison of genetic probe with immunophenotype analysis in lymphoproliferative disorders: a study of 87 cases. 319 72


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