Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferons produced by recombinant DNA technology began phase I trials little more than a decade ago. Today interferon alfa-2 is a mainstay in the treatment of hairy cell leukemia, and has demonstrated benefit in the more common chronic myelogenous leukemia. Interferon alfa-2 also has activity in other hematologic malignancies, including indolent non-Hodgkin's lymphomas, cutaneous T-cell lymphomas, T-cell lymphoma, and multiple myeloma, and in solid tumors such as disseminated melanoma, renal cell carcinoma, Kaposi's sarcoma, endocrine pancreatic tumors, and malignant carcinoid tumors. Interferon alfa, beta, and gamma remain under investigation to define potential roles in ovarian, breast, bladder, and cervical carcinomas and gliomas. The greatest value of the interferons will be in prolonging the disease-free interval when used in combination with other treatment modalities, including surgery, radiation, chemotherapy, and other biologic agents.
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PMID:Current status of interferons in the treatment of cancer. 128 Jan 53

In this report, we describe a patient with Philadelphia chromosome-negative chronic myelogenous leukemia (CML) with breakpoint cluster region gene rearrangement who developed T-cell lymphoblastic lymphoma. The occurrence of T-cell lymphoblastic lymphoma coincided with the appearance in the bone marrow of the cytogenetic abnormality, trisomy 22q11.2----22qter. This is the first report of high-grade T-cell lymphoma in a patient with documented CML.
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PMID:Occurrence of high-grade T-cell lymphoma in a patient with Philadelphia chromosome-negative chronic myelogenous leukemia with breakpoint cluster region rearrangement: case report and review of the literature. 843 86

A patient is described with chronic myelogenous leukemia (CML) and an unusual karyotype 46XY,t(Y;12) (q11;p12), whose clinical course was complicated by T-cell lymphoma 5 years later. At that time bone marrow cells showed an additional karyotypic abnormality 46XY,t(Y;12) (q11;p12) del(7) (pter-p21), which remained unchanged until blastic transformation of the CML 8 months later. The bone marrow biopsy specimen, which revealed the blastic transformation of the CML, also showed evidence for localization of T-cell lymphoma. This case, added to two previously reported cases of the concurrence of CML and T-cell lymphoma, suggests a relationship between the two diseases, which is discussed.
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PMID:Sequential development of peripheral T-cell lymphoma in the course of chronic myelogenous leukemia. 240 Sep 70

Mouse monoclonal antibodies were produced against MT-2 cell line derived from adult T-cell leukemia or human T-cell leukemia virus-rich fraction therefrom. Two IgG1 antibodies, Ta60a and Ta60b, were found to be reactive not only with cell lines derived from adult T-cell leukemia or cutaneous T-cell lymphomas, but also with activated peripheral blood lymphocytes, suggesting the similarity of Ta60 antigen group to Tac antigen which is present on interleukin 2 receptor. Thus, the relationship among these antigens was studied. Two Ta60 antibodies and Tac antibody immunoprecipitated the molecule with almost identical electrophoretic mobility, approximately a Mr 60,000 antigen from [3H]glucosamine-labeled activated peripheral blood lymphocytes or MT-2, MT-1, or ATN-1 cells from adult T-cell leukemia and a Mr 53,000 antigen from HUT-102 cells derived from cutaneous T-cell lymphomas. Further, Tac antibody was found to immunoprecipitate Ta60b molecule on 125I-labeled MT-2 cells by sequential immunoprecipitation, indicating that these two epitopes are on the same molecule. Antibody binding inhibition assays with either 3H-labeled Ta60a or Ta60b antibody demonstrated that Ta60a and Tac are the same epitope, but different from Ta60b. Thus, at least two epitopes were demonstrated to be present on interleukin 2 receptor molecule. However, Ta60b antibody showed almost no blocking effects on proliferation of an interleukin-2-dependent cell line, whereas Ta60a antibody did. Various hematopoietic tumor cells were typed with these two antibodies, but the results with Ta60b antibody were described, because they showed a similar specificity. Ta60b antibody reacted with all adult T-cell leukemia cases, but did not react with T-cell acute lymphoblastic leukemia, lymphoblastic lymphoma, or mature T-cell lymphoma. Interestingly, 3 of 12 acute myeloblastic leukemia and 2 of 5 chronic myelocytic leukemia in blastic crisis showed positive reactions. One-third of B-cell chronic lymphocytic leukemia and B-cell lymphoma as well as a few B-cell lines were also weakly reactive with this antibody. A part of the results with direct tests was confirmed by the absorption tests. The results obtained demonstrated the presence of Ta60b on a certain fraction of malignant hematopoietic cells of other than T-cell origin.
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PMID:Two mouse monoclonal antibodies detecting two different epitopes of an activated lymphocyte antigen on adult T-cell leukemia cells. 257 77

The first 72 consecutive bone-marrow transplant recipients with haematological malignancies (29 with acute nonlymphoblastic leukaemia, 31 with acute lymphoblastic leukaemia, nine with CML and three with myelofibrosis, IgA myeloma and T-cell lymphoma, respectively) were investigated for the frequency of relapses 1 year or later after bone-marrow transplantation. Seven relapses occurred from 30 to 850 d after transplantation (median 180 d). All relapses occurred in patients with acute leukaemia less than or equal to 18 years of age with a high risk for relapse, i.e. transplanted in second or later remission or with more than 10% blasts in the marrow before transplantation. Among all patients the probability of relapse was increased in patients without cytomegalovirus (CMV) infection (P = 0.001) and in patients without chronic GVHD (P = 0.049). Among leukaemic patients less than or equal to 18 years of age with a high risk of relapse all relapses occurred in patients (n = 11) without CMV infection, whereas no relapses were seen in patients (n = 13) with CMV infection (P = 0.006). Known risk factors for leukaemic relapse were comparable in both groups.
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PMID:Reduced risk of recurrent leukaemia in bone marrow transplant recipients after cytomegalovirus infection. 301 93

The coexistence of a T-cell lymphoma with a myelodysplatic syndrome seems to be exceptional. In the case reported here the diagnostic problems raised by the appearance of cutaneous nodules in a patient with chronic myeloid leukaemia (CML) were solved by histo-immunological examinations. A 70-year old male patient had been presenting since 1976 with a psoriasis-like skin disease. He was first seen at the Argenteuil hospital in 1984. Physical examination showed psoriasiform finger-like erythemato-squamous lesions, infiltrated plaques and an ulcerated tumoral swelling of the right elbow. A diagnosis of mycosis fungoides was made on histological and immunological examination results. At histology, this epidermotropic lymphoma was peculiar in that the atypical infiltrate was clearly centred on vessels. Electron microscopy confirmed that the vascular walls were invaded by the mycosis cells. Additional examinations showed hyperleucocytosis and myelaemia which were rapidly attributed to a chronic myelocytic leukaemia since the Philadelphia chromosome was present and the leucocytes had a low alkaline phosphatase score. Bone marrow biopsy disclosed a myeloproliferative syndrome of the CML type. Biopsy of a right axillary lymph node showed myelocytic infiltration associated with dermopathic lymphadenitis. There were no circulating Sezary cells, and a search for extension proved negative. From May, 1984 to June, 1985 the patient's CML was treated with busulfan which produced blood and bone marrow remission. The skin lesions were treated first with mechlorethamine, then with topical corticosteroids. Superficial electron therapy was applied to the tumoral lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A combination of mycosis fungoides and chronic myeloid leukemia. Apropos of a case]. 326 Jul 64

The percentage of total 125I-labeled insulin specifically bound to lymphoblasts was measured in 46 children with leukemia. Among 35 children with newly diagnosed acute lymphoblastic leukemia (ALL), specific insulin binding ranged from 0.09 to 14.8% per 10(6) blasts. A lower level of insulin binding was correlated with T-cell surface markers (P less than 0.003), higher hemoglobin level (P less than 0.005), presence of a mediastinal mass (P less than 0.01), lower glucocorticoid receptor level (P less than 0.02), higher platelet count (P less than 0.04), age less than 2 or greater than 10 yr (P less than 0.05), white blood cell count greater than or equal to 100 X 10(3)/mm3 (P less than 0.06) and higher labeling index (P less than 0.07). It was not correlated with the presence of central-nervous-system disease, FAB classification, or sex. With a follow-up of 24 to 33 + months, insulin binding was not correlated with treatment outcome. Six patients with relapsed ALL and three with acute nonlymphoblastic leukemia showed insulin binding levels similar to those in newly diagnosed ALL patients. Blasts from one patient with B-cell ALL and one with chronic myelogenous leukemia were characterized by lower insulin binding, while lymphoblasts from a patient with T-cell lymphoma bound insulin at marginally detectable levels. In vitro studies with IM-9, NALM-1 and NALM-16 cell lines showed that changes in insulin binding caused by dexamethasone treatment were not correlated with hormone-induced cell death. Although study of insulin binding by malignant lymphoid cells may be important in understanding the biology of leukemic cells, it does not appear to have any obvious clinical utility.
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PMID:Clinical and biologic correlates of insulin binding by leukemia lymphoblasts. 389 3

The simultaneous occurrence of malignant T-cell lymphoma and chronic myelogenous leukemia is reported. The lymph nodes contained E rosette forming cells. Blood and bone marrow cell morphology were consistent with the diagnosis of chronic myelogenous leukemia. Lymph nodes, bone marrow and blood mitosis showed a t(6;8) (6pter----6q27 ::8p12----8pter;6qter----6q27 ::8p12----8qter) translocation. So far a number of recent reports have shown simultaneous B lymphoid and myeloid proliferations in some malignancies, this is apparently the first reported case of simultaneous T lymphoid and myeloid proliferations.
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PMID:Simultaneous occurrence of a T-cell lymphoma and a chronic myelogenous leukemia with an unusual karyotype. 659 Sep 32

Terminal deoxynucleotidyl transferase (TdT) is an early T-cell differentiation marker in a number of species, including man. We have demonstrated TdT in the nuclei of cortical thymocytes in paraffin-embedded sections of calf, rat, and human thymus by indirect immunoperoxidase techniques. In addition, these techniques have been used to verify and extend enzyme assay results by detecting TdT in blast cells from 10 patients with convoluted T-cell lymphoma/leukemia, 1 patient with acute granulocytic leukemia, 1 patient with chronic granulocytic leukemia in blast crisis, and 1 patient with non-T non-B acute lymphocytic leukemia.
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PMID:Detection of terminal transferase in paraffin sections with the immunoperoxidase technique. 703 7

T-cells are only rarely involved in chronic myeloid leukemia. We report an unusual case of T-lymphoid extramedullary (lymphadenopathic) blast crisis in a 66-year-old patient with Philadelphia positive chronic myeloid leukemia. The lymph node morphological picture resembled that of a peripheral T-cell lymphoma. Immunohistochemical stainings showed most lymph node blasts to have T-phenotype (positivity for CD-2, CD-3 and CD-5). Flow cytometric phenotyping confirmed T-phenotype, with positivity for CD-7, CD-38 and TdT. Cytogenetic analysis of lymph node cells revealed Philadelphia chromosome with an additional chromosomal abnormality (add(6p)). The BCR-gene rearrangement in the lymph node blasts was identical to that in the bone marrow. This case adds to the growing evidence that CML may be a disorder of the common stem cell from which T-, B- and myeloid progenitors originate.
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PMID:T-lymphoid extramedullary (lymphadenopathic) blast crisis in CML. 759 76


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