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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)

The 9-year-old boy was admitted to Shizuoka Children's Hospital because of cervical lymphoadenopathy. Complete blood count showed normal RBC and platelet counts. WBC was 2700/microliters with no tumor cells. Bone marrow aspirate showed normocellularity with 34% tumor cells. Lymph node biopsy from his right neck was performed and the patient was diagnosed as non-Hodgkin's lymphoma (lymphoblastic type). Surface marker analysis disclosed that the tumor cells were positive for CD5, CD7, CD19, CD38, CD71, and Ia antigen. Chromosomal analysis of the cervical lymph node revealed 46, XY, t(7;14) (p15;q32). Molecular investigation with appropriate probe showed germ-line configurations of IgH gene, TcR beta gene, and TcR gamma gene, and one rearranged band of TcR delta gene. Monoclonality of tumor cells was demonstrated from chromosomal analysis and molecular study. CD7 and CD19 are not lineage specific antigens because CD7 is expressed on immature AML cells and CD19 is expressed on T ALL cells or AML cells. Moreover, TcR delta rearrangement is considered to occur at early phase of hematolymphoid cells. Based on these data, tumor cells of this patient is considered to originate from immature lymphoid cell, so-called lymphoid stem cell.
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PMID:[CD5+, CD7+, and CD19+ non-Hodgkin's lymphoma in a child]. 170 16

From 1983 to 1989 we performed a prospective trial of 70 consecutive, in vitro purged autologous bone marrow transplants (BMT) for patients with progressive non-Hodgkin's lymphoma. Forty-nine patients had responsive disease at the time of transplantation while 21 others had refractory high risk lymphoma. Forty-two patients with B-lineage lymphoma received autologous marrow purged in vitro with monoclonal antibody (anti CD9, CD10, CD24) plus complement, 12 with T-lineage lymphoma received monoclonal antibody immunotoxins (anti CD5, CD7-ricin conjugates) along with 4-hydroperoxycyclophosphamide purging and 16 received unpurged marrow. All received cyclophosphamide, 57 with fractionated total body irradiation, and 13 with BCNU and cytarabine. Hematologic engraftment was prompt and unaffected by phenotype (B vs. T) or by in vitro purging used (B vs. T vs. none) although nine of 16 non-relapse deaths were related to poor graft function. Fifty-one patients (73%) were alive in complete remission (CR) 1 month following transplantation while 15 patients (12 with initially refractory disease) had persistent disease. Subsequently, 41 +/- 18% (by Kaplan-Meier estimate; +/- 95% confidence limits) of those who achieved CR remained relapse free 1-6.4 (median 3) years post-BMT. Neither risk group, purging, nor immunophenotype predicted subsequent post-transplant relapse. Among those 51 who achieved CR, 13 of 43 (27 +/- 14%) with responsive disease survive disease free while three of eight (38 +/- 34%) refractory patients survive disease free (p = 0.96). Overall, 24 patients survive, 16 in continuous complete remission 1-6.5 years following transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autologous bone marrow transplantation for progressive non-Hodgkin's lymphoma: clinical impact of immunophenotype and in vitro purging. 193 55

We report the characterization of a novel human T-cell line, HPB-MLp-W, which was established from blastic cells of a lymph node specimen from a patient with non-Hodgkin's lymphoma. They demonstrated the T-cell association antigens, CD2 and CD4, but no CD3, CD8, CD1, CD5, CD7 nor T-cell antigen receptor on their cell surfaces. They were also positive for Ia and Ki-1 antigen, and negative for CD25 (Tac-1). The cell line HPB-MLp-W had the same pattern of antigen expression as the patient's cells. Southern-blot analysis of DNA showed a rearrangement of the T-cell receptor-alpha and beta genes. To our knowledge, this is a novel cell line with unique T-lineage marker, to be established from a case of non-Hodgkin's lymphoma.
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PMID:Establishment of a novel cell line with T-lineage phenotype (HPB-MLp-W) from a non-Hodgkin's lymphoma patient. 204 90

We analyzed the rearrangement of T-cell receptor (TcR) delta chain gene in 88 cases of lymphoproliferative disorders; 31 acute lymphoblastic leukemias/lymphoblastic lymphomas (ALL/LBL); 27 adult T-cell leukemias/lymphomas, 9 angioimmunoblastic lymphoadenopathies (AILD); 10 T-cell lymphomas (non-Hodgkin's lymphoma); and 11 Hodgkin's disease. All of 9 T-ALL/LBL cases, of which 4 cases have neither beta nor gamma gene rearrangement, had a new rearranged band of TcR delta locus. Ten of 16 B-lineage ALL/LBL had rearranged band(s) or deletion of TcR delta locus. The rearranged bands were recognized in 2 cases of AILD and 1 case of T-cell lymphoma. All cases of adult T-cell leukemias/lymphomas, 4 of AILD, 4 of T-cell lymphoma, and 8 of Hodgkin's disease had deleted TcR delta locus. Heterogeneous findings of TcR delta locus analysis were observed in AILD, T-cell lymphoma, and Hodgkin's disease. In 16 cases with TcR delta rearrangement, the J delta 1 region was frequently used and the J delta 2 region was rearranged in one AILD. It is suspected that J delta 3 was used in one T-ALL/LBL. There was no correlation between the phenotypic pattern of CD3, CD4, CD8 in T-cell disorders and the rearrangement of the TcR delta gene. These findings suggest that the newly identified TcR delta chain gene rearranges at a very early stage of T-cell ontogeny; prior to the other TcR genes and perhaps at almost the same stage with CD7 expression. The TcR delta gene is useful in assessing clonality for the most immature T-cell neoplasms not showing rearrangement of the other TcR genes. This gene is not lineage specific; however, when used in conjunction with immunoglobulin heavy chain gene, it may be a useful tool to distinguish lymphoid lineage of ALL/LBL.
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PMID:Rearrangement of T-cell receptor delta chain gene as a marker of lineage and clonality in T-cell lymphoproliferative disorders. 250 Oct 27

A case of chemotherapy-resistant non-Hodgkin's lymphoma simultaneously expressing T cell (CD7)-, B cell (CD19)- and myeloid (CD13, CD33)-associated surface antigens is presented. Cytochemical analysis revealed that the lymphoma cells were positive for terminal deoxynucleotidyl transferase, but negative for myeloperoxidase and esterase. Rearrangements of both the T cell receptor beta chain and gamma chain genes were observed, but the immunoglobulin genes showed a germ line configuration. The rearrangement was not detected within the breakpoint cluster region on chromosome 22. These findings are considered to represent aberrant expressions of the B cell- and myeloid-associated antigens in early-stage T cell lineage lymphoma cells.
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PMID:Multiphenotypic lymphoma with rearrangements of the T cell receptor beta chain and gamma chain genes. 254 Jun 3

A 16 year-old boy of non-Hodgkin's lymphoma (NHL) was reported. Although Hodgkin's disease was suspected by the presence of Reed-Sternberg-like cells and lacunar cells histologically, a diagnosis of NHL was made because of atypism and monoclonality of the background's cells as well as the morphology of invasive cells in the bone marrow. The tumor cells expressed, CD2, CD3, CD4, CD5 and CD7 antigens, which corresponded to the phenotype of helper-inducer T-lymphocytes. In the analysis of their karyotypes, 16 out of 24 cells revealed normal karyotype, while all the rest showed near-triploidy. Common abnormality was identified as trisomies of No. 1, 3, 5, 16, 21 chromosomes, tetrasomies of No. 10, 19, 20 chromosomes, and 4q+, 7q+, 14p+. Multimodal chemotherapy was successful to induce the patient promptly into complete remission. He has been free from the disease for approximately 12 months. Thus far, triploid clones in hematopoietic malignancies have rarely been described. More importantly, the appearance of them in pediatric lymphoid neoplasms has not yet been reported.
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PMID:[A T-cell type non-Hodgkin's lymphoma with a near-triploid karyotype]. 262 6

Important insights into leukocyte differentiation and the cellular origins of leukemia and lymphoma have been gained through the use of monoclonal antibodies that define cell surface antigens and molecular probes that identify immunoglobulin and T-cell receptor genes. Results of these studies have been combined with markers such as surface membrane and cytoplasmic immunoglobulin on B lymphocytes, sheep erythrocyte receptors on T lymphocytes, and cytochemical stains. After using all of the aforementioned markers, it is now clear that acute lymphoblastic leukemia (ALL) is heterogeneous. Furthermore, monoclonal antibodies that identify B cells, such as the anti-CD20 and anti-CD19 antibodies in combination with studies of immunoglobulin gene rearrangement, have demonstrated that virtually all cases of non-T-ALL are malignancies of B-cell origin. At least six distinct subgroups of non-T-ALL can now be identified. T-ALL is subdivided by the anti-CD7, anti-CD5, and antibodies that separate T lymphocytes subsets into three primary subgroups. Monoclonal antibodies are also useful in the subclassification of non-Hodgkin's lymphoma, and certain distinct markers can be correlated with morphological classification. Although monoclonal antibodies are useful in distinguishing acute myeloid from acute lymphoid leukemias, they have less certain utility in the subclassification of acute myelogenous leukemia (AML). Attempts to subclassify AML by differentiation-associated antigens rather than by the French-American-British (FAB) classification are underway in order to document the potential prognostic utility of surface markers. Therapeutic trials using monoclonal antibodies in leukemia and lymphoma have been reported. Intravenous infusion of unlabeled antibodies is the most widely used method; transient responses have been demonstrated. Antibodies conjugated to radionuclides have been quite successful in localizing tumors of less than 1 cm in some studies. Therapy trials with antibodies conjugated to isotopes, toxins, and drugs have shown promise. Purging of autologous bone marrow with monoclonal antibodies and complement in vitro has been used in ALL and non-Hodgkin's lymphoma; preliminary data suggest that this approach may be an effective therapy and may circumvent many of the obstacles and toxicities associated with in vivo monoclonal antibody infusion.
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PMID:Laboratory and clinical applications of monoclonal antibodies for leukemias and non-Hodgkin's lymphomas. 265 57

Nine children with mediastinal non-Hodgkin's lymphoma (NHL) were treated according to our new regimen which is characterized by intensified therapy with high-dose cytosine arabinoside (HDCA). After induction therapy with a combination of five drugs, such as vincristine, doxorubicin, cyclophosphamide, 1-asparaginase, and prednisolone, intermediate dosages of methotrexate (MTX) (1 g/m2) and HDCA (1.5 g/m2 x 12 doses) were administered. All but one patient (88.9%) achieved complete remission and then received this intensified therapy. With a median follow-up period of 25.5 months, five patients are still in complete remission, but three patients have relapsed. From the phenotypic point of view, these relapsed patients showed only very immature T-cell differentiation antigens such as CD2 and CD7 (or CD5). These results suggest that HDCA as intensified therapy for children with mediastinal NHL seems to be effective. However, for patients with an immature phenotype of T-lineage cells, more sophisticated regimens should be prepared.
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PMID:Poor prognosis of mediastinal non-Hodgkin's lymphoma with an immature phenotype of CD2+, CD7 (or CD5)+, CD3-, CD4-, and CD8-. 278 59

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

The establishment of Clusters of Differentiation for T- and B-lymphoid cells during International Workshops on Human Leukocyte Differentiation Antigens prompted the authors to evaluate the immunophenotypes in 160 cases of non-Hodgkin's lymphoma (NHL). In this group, 130 were of B-lymphocyte lineage (117 by monotypic immunoglobulin expression), and 30 of T-cell lineage. In the B-NHL series the expression of immunoglobulin isotypes, B-cell maturation/differentiation antigens of CD9, CD10, CD19-24, CD37, and CD38 (OKT10), HLA-DR and peanut agglutinin binding showed no significant relationship with histopathologic diagnosis as defined by the Kiel classification. Of the T-cell markers, CD5, CD6, and CD7 showed lineage promiscuity by their presence on some B-NHL. Conversely, the authors grouped the cases according to phenotypes (either CD antigens or immunoglobulin isotypes) which occur in distinct stages of (physiologic) B-cell maturation/differentiation. Eighty-six of the 130 cases could be fitted according to CD phenotype expression. This approach did not yield a significant relationship between phenotype and individual histopathologic categories either. The staging by CD phenotype and by immunoglobulin isotype yielded different results in this respect. Most B-NHL had an intermediate stage of B-cell maturation/differentiation. In the T-NHL series most cases showed a phenotype (CD1-CD8, CD38, TdT, and peanut agglutinin binding capacity) compatible with mature T-lymphocyte characteristics. The exceptions were lymphoblastic convoluted lymphomas, which exhibited an immature immunophenotype. It is concluded that NHL in distinct histopathologic categories are heterogeneous in immunologic phenotypes, and that the immunophenotype of lymphoma cells has no evident association with that of their presumed counterparts in physiologic cell maturation/differentiation.
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PMID:Immunophenotyping of non-Hodgkin's lymphoma. Lack of correlation between immunophenotype and cell morphology. 331 Jun 50


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