Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of Burkitt cell leukemia (FABL3) [1] in a patient 7 years after successful treatment of Hodgkin's disease (HD) by combined modality (chemotherapy and radiotherapy) therapy is described. The B-cell nature of the leukemic blasts is shown by immunologic surface marker studies. While L3 leukemia is very rarely seen following therapy for HD, diffuse lymphoma of small noncleaved cells (LSNC)--resembling the Burkitt tumor--is more common in this setting.
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PMID:Burkitt cell leukemia following treatment of Hodgkin's disease: report of a case and review of the literature. 633 65

14 patients developed acute nonlymphocytic leukemia and 1 patient developed Burkitt's leukemia following longterm chemotherapy and/or radiotherapy for other disorders. The main primary disorders included multiple myeloma, Hodgkin's disease, non-Hodgkin's lymphoma and breast carcinoma. Acute leukemia developed earlier in patients treated by chemotherapy with or without radiotherapy than in patients treated by radiotherapy alone (63 months, range 24-132 months; 201 months, range 48 months to 30 years, respectively). 13 patients presented without organomegaly and 8 were pancytopenic. Abnormalities of myeloid and erythroid cell lines were observed in the majority of the patients. A high rate of acute erythroleukemia (5 out of 14) was found. Increased reticulin fibers were found in 3 patients. The leukemia was invariably refractory to treatment with a median survival of 4 months. The possible role of preexisting abnormal marrow structure in the development of therapy-related leukemia is discussed.
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PMID:Acute leukemia following chemotherapy and radiation therapy--a report of 15 cases. 658 10

NALM-6-M1 is an acute lymphoblastic leukemia cell line previously shown in our laboratory to express the pre-B lymphocyte phenotype, i.e., cytoplasmic IgM+, surface immunoglobulin-. Hybridomas were produced against this cell line by fusing spleen cells from hyperimmunized mice with NS-1 mouse myeloma cells. One monoclonal antibody derived from this fusion, designated BA-1, reacted with peripheral blood B lymphocytes, chronic lymphocytic leukemias, pre-B-ALL, most non-Hodgkin's lymphomas, and most non-T, non-B-ALL. BA-1 showed weak reactivity with B lymphoblastoid cell lines and failed to react with multiple myeloma and pokeweed mitogen-induced plasma cells. BA-1 also reacted with peripheral blood granulocytes and the erythroleukemia cell line K-562. No reactivity was seen with cells of T lymphocyte origin, platelets, red cells, monocytes, or acute myelocytic leukemias. Evidence is presented indicating that the determinant recognized by BA-1 is not surface immunoglobulin, HLA-DR, or receptors for C3 or Fc. We conclude that monoclonal antibody BA-1 may be useful in the study of early stages of human B lymphocyte development.
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PMID:A monoclonal antibody (BA-1) reactive with cells of human B lymphocyte lineage. 696 48

Two adults with advanced Hodgkin disease-one treated with combination chemotherapy, and one with chemotherapy and radiation therapy-developed Burkitt cell leukemia four and seven years after diagnosis, proved by cytochemical and ultrastructural study. Acute lymphocytic leukemia must be considered in the evaluation of therapy-related leukemias.
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PMID:Burkitt cell leukemia following therapy for Hodgkin disease. 706 86

Recently G alpha 16, a new guanosine triphosphate (GTP) binding protein alpha subunit has been described to be specifically expressed in human hematopoietic cells. Expression of G alpha 16 was observed in human cell lines of myelomonocytic and T-lymphocytic origin, but not in human B-cell lines Raji and IM9. We studied the expression of G alpha 16 in human B cells corresponding to different stages of B-cell differentiation by means of reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. The human Burkitt's lymphoma cell lines Raji, Ramos, BJAB, the lymphoblastoid cell line SKW6.4, and the plasmocytoma cell line U266 were devoid of G alpha 16. In contrast, G alpha 16 was detected in the human progenitor B cell lines Reh and Nalm-6. Using the mu+, k- cell line BLIN-1 (pre-B cell phenotype) and its derived subclone 1E8 (surface mu+, k+; B-cell phenotype) G alpha 16 expression was found to disappear on transition from pre-B to B-cell differentiation stage. The analysis of a broad panel of human neoplastic B lymphocytes ranging from progenitor B-acute lymphatic leukemia (pre-pre-B-ALL), common acute leukemias (cALL), pre-B-ALL, mature B-ALL to low grade B-cell lymphoma (chronic lymphocytic leukemia of B-cell type, leukemic centrocytic non-Hodgkins lymphoma [NHL], hairy cell leukemia) showed that G alpha 16 expression is limited to progenitor and pre-B-ALL cells. Therefore, we conclude that within B-cell differentiation, G alpha 16 is expressed solely during early B cell ontogeny and downregulated during differentiation. Thus, G alpha 16 might be an important regulator involved in signaling processes in progenitor B cells.
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PMID:G protein subunit G alpha 16 expression is restricted to progenitor B cells during human B-cell differentiation. 770 90

Using fluorescence in situ hybridization (FISH), we studied chromosome 8 abnormalities in 30 children with mature B-cell acute lymphoblastic leukemia (B-ALL) or B-cell non-Hodgkin lymphoma (B-NHL). FISH was performed on metaphase spreads and interphase nuclei with a whole chromosome 8 painting probe. Fifteen patients were studied retrospectively after metaphases from the malignant cell specimen had already been G-banded. When interphase nuclei were examined, FISH was able to confirm t(8;14)(q24;q32) in all nine patients positive by previous G-banding. FISH, however, was positive in metaphase spreads from only seven patients. Another 15 patients were included in a prospective study. In six of them (40%), a translocation involving chromosome 8 was shown by a split small segment (8q24-8qter) on interphase nuclei. Analysis of metaphase spreads showed only three positive cases each by FISH or G-banding, respectively, with corresponding results in two patients. By interphase FISH, trisomy of chromosome 8 also was detectable. In three patients shown by G-banding to have trisomy, interphase FISH study showed high scores of three chromosome 8 signal positive cells. There was no cross-hybridization to other chromosomes interfering with FISH analysis. FISH analysis on interphase nuclei using a whole chromosome 8 hybridization probe will supplement and can be more sensitive than metaphase cytogenetic techniques for detection of chromosome 8 rearrangements in B-ALL/NHL.
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PMID:Characterization of chromosome 8 abnormalities by fluorescence in situ hybridization in childhood B-acute lymphoblastic leukemia/non-Hodgkin lymphoma. 785 Jul 58

We reviewed all reported cases of Burkitt's lymphoma and/or Burkitt's leukemia (BLL) occurring following therapy for Hodgkin's disease. In addition to the case described in this report, a total of 19 patients have been previously reported. The male/female ratio was 3.75. Treatment for Hodgkin's disease included chemotherapy combined with radiation therapy in 15 patients, chemotherapy in 3 patients, and radiation therapy alone in 1 patient. Median interval between Hodgkin's disease and the diagnosis of BLL was 97 months. Patient characteristics are similar to those with de novo BLL. Bone marrow, abdomen, central nervous system, as well as extranodal organs were commonly involved. Typical cytogenetic translocations seen in patients with primary BLL were found in 6 patients, but 5 of these patients had additional cytogenetic abnormalities. Only 2 patients achieved complete remission after chemotherapy. The mechanism for the development of BLL after treatment for Hodgkin's disease is unknown. Although the majority of cases have been seen in patients treated with combined-modality therapy, the role of previous therapy in causing this complication cannot be assessed in this study.
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PMID:Burkitt's lymphoma-leukemia in patients treated for Hodgkin's disease. 895 57

The product of the protooncogene c-kit is the receptor for the hematopoietic cytokine stem cell factor (SCF). C-kit is expressed on leukemic cells of the erythroid, myeloid, and mast-cell lineage and SCF has a proliferative effect on some of these cells. The role of SCF and c-kit in lymphoid malignancies is much less clear. Here we review the role of c-kit in normal lymphopoiesis and summarize its role in lymphoid malignancies. C-kit is expressed in normal lymphopoiesis and its ligand SCF synergizes with IL-7 to enhance the proliferation of B- and T-cell progenitors. In malignant lymphopoiesis, c-kit can also be expressed in B and T-lymphoblastic cells from children with non Hodgkin's lymphoma (NHL) or acute lymphoblastic leukemia (ALL) when analyzed by the highly sensitive reverse transcriptase polymerase chain reaction (RT-PCR). While c-kit receptors were detected by flow cytometric (FCM) analysis on about 40% of fresh T-lymphoblastic biopsy tumor cell preparations or T-lymphoblastic cell lines, no receptors were detected on B-lymphoblastic fresh cells or cell lines from children with B-ALL or Burkitt's lymphoma (BL). Almost all of the lymphoblastic cells expressing c-kit protein responded to recombinant human (rh)SCF with a downregulation of c-kit receptors. A proliferative response was detected only in a minority of these cells. B-ALL or BL cell lines showed no response to rhSCF. Upregulation of c-kit in T-lymphoblastic cells could be demonstrated by the addition of IL-1 beta, TNF-alpha, TGF-beta or A23187, and downregulation by rhSCF or phorbol myristate acetate (PMA). Despite upregulation of c-kit mRNA, protein remained undetectable on B-ALL or BL cells in the presence of A23187. The metabolic state of the cells seemed to influence c-kit expression, since c-kit was upregulated in T-lymphoblastic cells by the addition of new medium. C-kit appears to play a role in the growth of some malignant T-lymphoblastic but not B-lymphoblastic cells.
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PMID:C-kit receptors in childhood malignant lymphoblastic cells. 916 31

The pediatric Non-Hodgkin's lymphomas are a heterogeneous group of malignancies of B- or T-cell origin. Approximately half of them are characterized as Burkitt's lymphomas. Typically, one of the reciprocal translocations t(8;14)(q24;q32), t(2;8)(p11;q24) or t(8;22)(q24;q11) is seen in the tumor cell, each involving the protooncogene c-myc on chromosome 8. Characteristically, in most patients the translocation occurs between the distal end of the long arm on chromosome 8 (c-myc) and chromosome 14 (immunoglobulin heavy chain locus, IgH). The breakpoint regions are distributed over a wide range of more than 10 Kb on chr. 8 and over several hundred Kb on chr. 14. With standard-PCR, fragments can only be amplified to a size of about 2 Kb. The development of PCR-applications to generate long products up to 20 Kb now allows a detection of these breakpoints. Several primer pairs from different regions of the IgH-gene and the c-myc-gene were tested in each patient. Until now, 20 patients with Burkitt's Lymphoma or B-ALL characterized by L3 morphology were examined. All patients were treated according the protocols of the NHL-BFM '90 or '95 study. In 11/20 patients, recombinations between chromosomes 8 and 14 could be detected with our primer pairs. In serial dilutions of DNA from malignant cells in DNA from healthy controls, sensitivities of one malignant cell in 2 x 10(4) normal cells could be obtained. This method will now allow us to characterize the involved breakpoints more exactly and to analyze patient samples (blood, bone marrow, aphereses products and residual tumors) during or after therapy for the existence of minimal residual tumor cells.
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PMID:[Detection of translocation t(8;14)(q24;132) in pediatric Burkitt's lymphomas using "long distance" polymerase chain reaction: a new method for diagnosis of Burkitt's lymphomas]. 934 Apr 26

CD66c is a surface (and intracellular) molecule bound to the membrane by a glycosyl-phosphatidylinositol anchor. While its expression on peripheral granulocytes is well recognized, less is known about its distribution in early steps of normal and neoplastic hematopoiesis. We analyzed by flow cytometry cell surface expression of CD66c on bone marrow cells from 4 healthy subjects and on bone marrow or peripheral blood cells from 127 patients with newly diagnosed hematologic malignancies: 70 de novo acute myeloid leukemias (AML), 6 refractory anemias with excess of blasts in transformation, 3 myeloid and 3 lymphoid blastic phases of chronic myelogenous leukemia, 33 B-lineage and 6 T-lineage acute lymphoblastic leukemias (B- and T-ALL), and 3 B-cell and 3 T-cell non-Hodgkin's lymphomas in the leukemic phase. We found that in normal bone marrow CD66c expression was myeloid restricted, reaching its highest level on promyelocytes. As for de novo AML, slight expression of CD66c was found on 6/25 (24%) AML-M4 and only occasionally in other subgroups. In 9 out of 10 cases of acute promyelocytic leukemia, CD66c was totally absent, but antigen expression was easily detectable following in vitro exposure to all-trans retinoic acid. Among lymphoid malignancies, CD10+ early-B-ALL consistently expressed the molecule (20/23 cases, or 87%) whereas both CD10- early-B ALL and SmIg+ B-ALL completely lacked it. Finally, dual staining with CD66c and CD10 proved to be a suitable tool for distinguishing even low percentages of residual leukemic cells (CD10+/CD66c+) from normal regenerating early-B cells (CD10+/CD66c ) in CD10+ early-B-ALL induced into remission.
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PMID:CD66c antigen expression is myeloid restricted in normal bone marrow but is a common feature of CD10+ early-B-cell malignancies. 971 68


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