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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the arrangement of the alpha, beta and gamma T cell receptor (TCR) genes in 27 patients with T cell lymphoproliferative disorders. Nine patients had acute lymphoblastic leukaemia (T-ALL), nine patients had prolymphocytic leukaemia (PLL), six patients presented with a T-CLL/T-lymphocytosis syndrome, two patients had Sezary syndrome (SS) and one patient had HTLV-I positive T-cell leukaemia/lymphoma (ATLL). alpha TCR gene rearrangement could be demonstrated by the use of three available probes in only one case. By contrast, both beta and gamma TCR gene rearrangement could be demonstrated by Southern blot analysis of DNA samples digested with appropriate restriction enzymes in the majority of cases. In general, when rearrangements were present they involved both alleles. The proportion of rearranged chromosomes was lower in T-ALL than in other forms of T-cell leukaemia and it was lower in cases with the CD4-/CD8+ phenotype than in those with a CD4+/CD8- phenotype. In three out of 34 cases of B-cell leukaemia the TCR beta-gene but not the TCR gamma-gene was rearranged, just as in two out of 26 cases of T-cell leukaemia the immunoglobulin (Ig) heavy chain but not the light chain genes were rearranged. These data suggest that development of the machinery required for gene rearrangement may precede commitment to B or T cell lineage. The use of this technique is especially useful for the classification of cases of ALL in which the cells are negative with respect to most current phenotypic markers and in cases of T cell lymphocytosis in which the finding of a gene rearrangement identifies a monoclonal cell population.
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PMID:Alpha, beta and gamma T-cell receptor genes: rearrangements correlate with haematological phenotype in T cell leukaemias. 296 64

The state of T-cell receptor beta-chain gene rearrangement in human T-cell leukaemias has been analysed. All forms of leukaemia tested (T-CLL, ALL, PLL, Sezary syndrome and ATL) exhibit rearrangements of C beta genes confirming the clonality of these neoplasias. However we find no evidence for common gene rearrangements nor for restricted rearrangement patterns within this type of neoplasia. We find evidence of T-cells with C beta 1 and C beta 2 rearrangements, sometimes associated with Igh JH rearrangements, but several cases of T-cell leukaemia with a marker inversion of chromosome 14 (q11;q32) do not have Igh JH rearrangements. The results suggest that TCR beta gene rearrangement occurs early in T-cell ontogeny but that this rearrangement is most often irrelevant to leukaemogenesis.
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PMID:Heterogeneity of T-cell beta-chain gene rearrangements in human leukaemias and lymphomas. 300 Jul 64

Human T-lymphotropic type I (HTLV-I) proviral sequences were detected in leukemic cells of a patient living in Marseilles (south of France) and suffering from Sezary syndrome. He did not have any travel history outside France and did not receive blood transfusion or hepatitis B vaccination. This case of HTLV-I positive Sezary syndrome is the first one described outside the known endemic regions for HTLV-I. Moreover, this patient was found to be negative for viral antibodies. This observation should therefore stimulate new and thorough analysis of the association of this human retrovirus with leukemia and lymphoma in the Mediterranean region, both by seroepidemiological and molecular biology techniques.
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PMID:Detection of HTLV-I (human T-cell lymphotropic virus, type I) proviral DNA in leukemic cells from a French patient with Sezary syndrome. 300 72

Recent advances in analysis of leukemic cell phenotypes using cell surface markers have provided important insights into leukocyte differentiation and the cellular origin of leukemia. In addition to the traditional cell surface markers, i.e., surface membrane immunoglobulin and receptors for sheep erythrocytes that define B and T lymphocytes, highly specific monoclonal antibodies have been developed that discriminate various stages of human lymphocyte and granulocyte differentiation. Explorations of the detailed phenotypes of leukemic cells in relation to normal hemopoietic differentiation reveal that consistent, composite phenotypes of different subclasses of lymphoid malignancies closely mimic those of corresponding normal cells at equivalent levels of maturation. This is exemplified in lymphoma cells (chronic lymphocytic leukemia of B or T type, Sezary Syndrome, immunocytoma) that resemble mature and immunocompetent T and B cells, in T cell acute lymphoblastic leukemia (T-ALL) (equivalent to thymus cells) and in non-T ALL (corresponding to lymphoid progenitor cells in the bone marrow). The major phenotypes documented in different leukemias represent the level of maturation arrest imposed on the dominant subclone; this is determined by, but not necessarily synonymous with, the target cell and associated clonogenic cell population in the leukemia. The clinical significance of immunodiagnosis of leukemia cell types becomes best evidenced in acute leukemias. Besides the improvement of diagnosis by using objective criteria, clinically useful subclassifications became evident: five major subtypes of ALL are now recognized, including unclassified or null ALL, common ALL, pre-B-ALL, B-ALL and pre-T/T-ALL. In addition to disclosing that ALL is an heterogeneous disease, such classifications have proved to be prognostically significant. This is exemplified in 248 children and 145 adults with ALL which were analysed for cell type and clinical data. In addition to their utility in leukemia classification, monoclonal antibodies that identify leukemia associated antigens are becoming used therapeutically, e.g., to lyse residual leukemia cells from remission bone marrows removed from leukemia patients before reinfusion. New approaches to the treatment of leukemia in which the objective is to encourage maturation of leukemia cells rather than to achieve leukemia eradication, can be monitored by phenotyping the alterations of the cell surface, and cell markers may hopefully be useful in identifying cell types that can be induced to differentiate.
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PMID:Cell surface markers in leukemia: biological and clinical correlations. 301 41

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

Oncogenes, in the context of retroviruses, are a common cause of leukemia in animals. Recently, activation of cellular oncogenes has been shown to be associated with leukemia in humans. Relatively few studies of oncogene activation in chronic lymphocytic leukemia (CLL) have been reported. In most instances, rearrangement of oncogenes has not been detected. Exceptions include the bcl-1 oncogene in B-cell prolymphocytic leukemia, the tcl-1 oncogene in T-cell CLL, the Hu-ets-1 and Hu-ets-2 oncogenes in small cell lymphocytic lymphoma and c-myc in a Sezary cell leukemia cell/line. Overall, it appears that oncogene abnormalities are less common in CLL than in other leukemias. The reason for it is uncertain and may relate to the relatively few cases evaluated. Alternatively, novel mechanisms of oncogene involvement or gene other than oncogenes may be important in the etiology or pathogenesis of CLL.
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PMID:Oncogenes in chronic lymphocytic leukemia. 328 28

1255 cases of leukemia-lymphoma were tested between 1972 and 1984 by multiple marker analysis. Routine leukemia phenotyping was performed using standard morphological and cytochemical techniques in combination with clinical and histo-pathological information; the main emphasis was put on immunological surface marker analysis using erythrocyte rosette assays, TdT and a large panel of poly- and monoclonal antibody tests. The 1255 cases were divided into these major types and subtypes: 349 cases of ALL and related immature T- and Burkitt-lymphomas (cALL, pre B-ALL, B-ALL and Burkitt-lymphomas, T-ALL and immature, mostly leukemic T-lymphomas, Null-ALL), 454 cases of mature T- and B-cell malignancies (T-CLL, mycosis fungoides, Sezary-syndrome, T-lymphomas, B-CLL, hairy cell leukemia, multiple myeloma, B-lymphomas), 263 cases of acute myeloid leukemias (AML, AMMoL/AMoL), 182 cases of chronic myeloid leukemias (CML in chronic phase, CMoL, CML in blast crisis), 6 cases of erythroleukemia and 1 case of megakaryoblastic leukemia. A simplified classification scheme which has been used in our laboratories is presented. Phenotyping is of diagnostic, prognostic and therapeutic relevance, most evidently for patients with ALL. Routine leukemia phenotyping should be performed with highly standardized techniques and reagents and by combining information from several fields in the multiple marker analysis. New areas of leukemia research might become very useful for the routine procedure of phenotyping.
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PMID:Phenotyping of malignant hematopoietic cells. Analysis of 1200 cases of leukemia-lymphoma. 348 82

The morphology of the cells from 29 cases of T-prolymphocytic leukaemia (T-PLL) was studied by light (LM) and transmission electron microscopy (TEM) and was compared with that of 33 B-cell PLL. The membrane phenotype of T-PLL cells was T4+, T8- in two-thirds of the cases, others being T4- T8+ or T4+ T8+. Two morphological types of T-PLL were defined according to the nuclear features: regular (55% of cases) and irregular (45% of cases). T-PLL cells with a regular, round or oval, nuclear outline resembled B-PLL cells but had less abundant cytoplasm and a higher nucleo-cytoplasmic ratio. Irregular T-prolymphocytes displayed a distinct convoluted nucleus. A 'small-cell' variant of T-PLL was recognized by TEM in six cases in which the diagnosis was uncertain by LM. A characteristic of all types of T-prolymphocytes by LM was the presence of a deep basophilic cytoplasm which by TEM corresponded to clusters of ribosomes and endoplasmic reticulum. No differences in clinico-haematological features or membrane markers were apparent between the morphological types of T-PLL, although it was noted that the three T4- T8+ cases had irregular cells and four of the small cell variant were T3- T4+. TEM permits a more precise assessment of the cytoplasmic organelles and nucleolus than LM analysis and facilitates the distinction between T-PLL and other leukaemias with a mature T-cell phenotype, namely adult T-cell leukaemia/lymphoma. Sezary syndrome and T-chronic lymphocytic leukaemia.
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PMID:The morphological spectrum of T-prolymphocytic leukaemia. 348 82

Diagnosis and therapy of malignant lymphoma of the skin were reviewed. Cutaneous T-cell lymphoma (CTCL), which is a new name for mycosis fungoides and Sezary syndrome, is one of the peripheral T-cell malignancies. It is generally confined to the skin for a long period of time, distinct from other malignant lymphomas, and may then progress to involve the lymph nodes and internal organs with a fatal outcome. Thus, diagnosis and therapy of CTCL may be different from those of other malignant lymphomas. Diagnostic characteristics of clinical, histopathological, haematological and immunological findings of CTCL were described. Differentiation between CTCL and adult T-cell leukemia-lymphoma (ATL) were discussed. As for the therapy for CTCL, there are five therapeutic modalities; local chemotherapy, PUVA therapy, electron beam irradiation therapy, systemic chemotherapy and combined modality. However, the most appropriate therapy for each stage of CTCL has not yet been determined. The advantages and dis-advantages of each therapeutical modality were discussed.
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PMID:[Malignant lymphoma of the skin]. 387 74

The rat monoclonal antibody CAMPATH-1 recognizes a hitherto undefined antigen present on virtually all normal lymphocytes and monocytes. Its reactivity with 105 samples of fresh leukaemic cells and 13 cell lines was measured by indirect fluorescence and peroxidase staining to define in more detail which stages of differentiation it recognizes. It was found to bind to cells from virtually all cases of lymphoid leukaemia (B cell CLL, T cell ALL, cALL and the few examples of HCL, PLL, Sezary syndrome and CGL in lymphoid blast crisis). The single case of cALL in relapse and four of six cases of null ALL were negative. Binding to non-lymphoid leukaemia cells (AML, AMML, AMoL, APL, AEL and CGL in blast crisis) was weaker or undetectable. Binding to established lymphoid cell lines was generally weak compared with fresh cells but some lines (MOLT4, DAUDI and X308) expressed adequate amounts of antigen to be lysed by CAMPATH-1 with human complement. Because CAMPATH-1 is very effective at killing lymphocytes in the presence of human complement, it has been used for removal of T cells in allogeneic transplants. The present results suggest that it might also have a role in purging bone marrow of leukaemia cells prior to autologous transplantation for acute lymphocytic leukaemia.
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PMID:Reactivity of rat monoclonal antibody CAMPATH-1 with human leukaemia cells and its possible application for autologous bone marrow transplantation. 389 Sep 29


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