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

Rearrangements of oncogenes c-myc and c-abl were detected by non-radioactive hybridisation in a case of Burkitt's lymphoma/leukaemia. The surface phenotype of Burkitt's cells were positive for CD19, CD20, HLA-DR, CD14, CD33 and surface immunoglobulin markers. Although cytogenetic analysis was not performed, the c-myc and heavy immunoglobulin genes had the same 14.2 kilobase EcoRI molecular size fragment, suggesting a possible t(8;14) translocation which is a common marker of this malignancy. The c-abl oncogene was also rearranged in DNA digested BamHI and EcoRI. The physiopathological implications of the rearranged c-abl gene are unknown, this being the first case, as for as is known, of Burkitt's lymphoma/leukaemia with a rearranged c-abl gene.
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PMID:Rearrangements of c-myc and c-abl genes in tumour cells in Burkitt's lymphoma. 840 11

The recombination activating gene-1 (RAG-1), which is required for immunoglobulin (Ig) gene rearrangement, is expressed in murine B-lymphoid precursors but not in mature B lymphocytes. In order to characterize the temporal relationship of RAG-1 expression to other markers of human B-lymphoid differentiation [cell surface antigens, terminal deoxynucleotidyl transferase (TdT), Ig gene rearrangements], RAG-1 expression was studied in a group of B lineage childhood acute lymphoblastic leukemia (ALL). ALL cells from 21 patients were grouped into three developmentally related phenotypes based on the expression of the differentiation antigens CD19, CD10, and CD20. All 21 leukemias were surface Ig (slg) negative. There were leukemias representing each developmental stage of Ig gene rearrangement. RAG-1 was expressed in 20 of 21 B-lineage ALL, including leukemic cells from each stage of differentiation, as defined by immunophenotype and IgH and IgL gene rearrangement status. RAG-1 was expressed in slg- ALL, regardless of the Ig heavy chain (IgH) or Ig light chain (IgL) gene configuration. RAG-1 was not expressed in two Burkitt lymphomas and Burkitt lymphoma cell lines with slg+ mature B-lymphocyte phenotype. In two cases, RAG-1 was expressed in TdT-negative ALL; conversely TdT was expressed in the one RAG-1 negative ALL. These results suggest that RAG-1 in B-lineage ALL is expressed at all phenotypic and genotypic developmental stages preceding surface immunoglobulin expression, and that TdT and RAG-1 may be regulated by different mechanisms.
Leukemia 1993 Mar
PMID:Recombination activating gene-1 (RAG-1) expression in all differentiation stages of B-lineage precursor acute lymphoblastic leukemia. 844 48

The immunophenotype of 304 adult lymphoblastic leukemias (> 18 years) diagnosed on the basis of the FAB criteria was determined at the time of diagnosis using a panel of monoclonal antibodies. The series comprised cases diagnosed and immunophenotyped in 43 Italian centers (GIMEMA Cooperative Group) between April 1988 and June 1991. The immunophenotypic characterization consisted of two consecutive steps. The initial screening was based on the reactivity for TdT, HLA-Dr, CD7, CD10, CD13, CD19, CD24, CD33 and CD41. According to the results obtained, the second level of investigation assessed the positivity for intra cytoplasmic (Cy) Ig, CD1a, CD2, CD3, CD4, CD5, CD8 and CD20. Based on the hierarchical expression of the different B- and T-cell related antigens, each case was assigned to a given differentiation stage. B-lineage ALL were classified in five subgroups (B0-B4) and T-lineage ALL in four subgroups (T0-T3). Cases in which the blasts were lymphoid according to the FAB criteria, but expressed myeloid antigens in association with B- and T-lymphoid markers were defined as hybrid leukemias. As expected, CD10+ cases (B2-B3) were the most frequent within the B-lineage ALL (83.2% of cases). CyIg+ (B3) accounted for about 20% of CD10+ ALL. Twenty eight cases (13.4%) were at a pre-cALL stage (B0-B1) and of these, 8 (3.8% of the total series) were positive only for TdT and HLA-Dr (B0). Intermediate and mature thymic phenotypes (T2-T3) were predominant within the T-ALL (67.2%) groups. Five cases, were positive only for TdT and CD7 (CD5+), and classified as T0. 9.2% of cases fulfilled the definition of hybrid leukemia, largely in view of the co-expression of B-lymphoid and myeloid markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunophenotype of acute lymphoblastic leukemia cells: the experience of the Italian Cooperative Group (Gimema). 847 81

We report here a case of "splenic lymphoma with villous lymphocytes" (SLVL) which exhibited both B- and T-cell phenotypes and genotypes. The patient was a 73-year-old man. Physical examination revealed splenomegaly and lymphadenopathy. The white blood cell count was 55.2 x 10(9)/L with 70.5% atypical lymphocytes, having cytoplasmic villi, characteristic of SLVL. The atypical cells infiltrated both the red and white pulps. Immunological analysis of the peripheral leukocytes showed both B- and T-cell phenotypes (CD5,CD11c,CD19,CD20,HLA-DR, SmIgM and lambda positive). DNA analysis revealed a dual rearrangement of the immunoglobulin heavy chain gene and T-cell receptor beta gene. SLVL has been identified as a B-cell leukemia with a relatively benign clinical course. This case had both B- and T-cell pheno- and genotypes with a progressive course. To the best of our knowledge, no case of SLVL with dual genotypes has ever been reported.
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PMID:Dual rearrangement of immunoglobulin and T-cell receptor genes in a case of splenic lymphoma with villous lymphocytes. 853 6

Cell line NKL was established from the the peripheral blood of a patient with CD3-CD16+CD56+ large granular lymphocyte (LGL) leukemia. The neoplastic LGL of this patient mediated natural killing and antibody-dependent cellular cytotoxicity (ADCC) and exhibited proliferative responses similar to normal CD16+CD56dim natural killer (NK) cells. The Morphology of NKL cells resembles that of normal activated NK cells. The karyotype of NKL is 47, XY, add (1) (q42), +6 del (6) (q15 q23), del (17) (p11). NKL cells express CD2, CD6, CD11a, CD26, CD27, CD29, CD38, CD43, CD58, CD81, CD94, CD95, class II MHC, and the C1.7.1 antigen, but do not express detectable levels of CD3, CD4, CD5, CD8, CD14, CD19, CD20, CD28, alpha/beta or gamma/delta T cell receptors on the cell surface. The density of the CD16, CD56, and CD57 antigens declined markedly on NKL cells during prolonged im vitro culture. Nevertheless, NKL cells can mediate ADCC as well as natural killing. NKL cells are strictly dependent on interleukin-2 (IL-2) for sustained growth and die if deprived of IL-2 for more than 7 days. NKL cells proliferate in response to concentrations of IL-2 as low as 1 pM, but an optimal proliferative response requires approximately 100 pM IL-2. NKL cells growing in the presence of IL-2 express abundant IL-2R alpha with little or no detectable IL-2 beta or gamma chain on the cell surface; NKL cells deprived of IL-2 express high levels of both IL-2R alpha and beta. IL-4, IL-7, and IL-12, unlike IL-2, do not maintain the viability of NKL cells. Furthermore, IL-1, IL-4, IL-6, IL-7, IL-12, tumor necrosis factor-alpha (TNF-alpha), interferon-alpha (IFN-alpha) and IFN-gamma do not support the growth of NKL cells. The NKL cell line may prove useful for studies of human NK cell biology.
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PMID:Characterization of a cell line, NKL, derived from an aggressive human natural killer cell leukemia. 859 69

Activation of CD20, a cross-membrane ion channel, induces cell cycle progression from G0 to G1 in B lymphocytes. Subsequent activation of CD40, a membrane receptor of the nerve growth factor receptor superfamily, transits the B cells to the S phase. CD40 may also act synergistically in combination with IL-4 (B lymphocytes) or IL-3/IL-7 (B-cell precursors). We investigated the proliferative responses of B-lineage acute lymphoblastic leukaemia (ALL) cells to CD20/CD40 activation. In 18/56 ALL cases, CD20 activation resulted in significant increases in DNA synthesis. Similar, although more moderate, effects were seen of activation of CD40 in 10/44 cases. Responses to CD20 or CD40 activation were independent of co-stimulation with IL-3, IL-4 or IL-7, and various cocktails of the different growth stimuli did not act synergistically.
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PMID:CD20 and CD40 mediated mitogenic responses in B-lineage acute lymphoblastic leukaemia. 861 44

In this study we describe a fast and sensitive method using three-colour immunofluorescence for the detection of cells with phenotypes that are rare in normal bone marrow (BM) but occur frequently in children with precursor B acute lymphoblastic leukaemia. We show that, in the first year after initiation of therapy, in 17/18 patients (10 patients were analysed after first diagnosis and nine patients after first BM relapse; one patient was analysed on both occasions) the percentage of CD10+ CD19+ cells and CD20- CD22+ cells in the CD34+ cell population indicated the likelihood of relapse. A suppression of cells expressing these phenotypes after initiation of therapy was followed by an outgrowth of normal precursor B cells after 12 months. Therefore this early test for impending relapse (which occurred 10-28 months after starting chemotherapy) was only applicable in the first year after beginning the treatment. However, despite this predictive value, comparison of fluorescence data with PCR results obtained from the same BM sample indicated that only a subpopulation of the CD34+ CD10+ CD19+ and CD34+ CD20- CD22+ cells above the determined threshold value represented malignant cells. A large prospective study to confirm the predictive value of this three-colour immunofluorescence assay is warranted.
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PMID:Triple immunofluorescence staining for prediction of relapse in childhood precursor B acute lymphoblastic leukaemia. 861 86

Leukemic cells frequently persist in the bone marrow of patients treated for acute lymphoblastic leukemia (ALL), and may regrow to produce relapse. We have used a long-term co-culture system to analyze the interaction of ALL blasts with components of the marrow microenvironment. Blast cells from 10 cases of precursor-B ALL were cultured on allogeneic human bone marrow stromal layers at 37 degrees C in microtiter wells, and replated when stroma showed evidence of deterioration. Leukemic cells from seven of 10 cases showed evidence of survival and proliferation beyond 30 days in culture, while in three cases there was a progressive decline in the number of viable leukemic cells by 7-21 days. Two cases continued to proliferate for 149 to 332+ days, while five underwent senescence after 34-52 days. In the two cases with long-term proliferation, the leukemic identity of the cells was confirmed by immunophenotyping, cytogenetics, and demonstration of clonal immunoglobulin gene rearrangements. Evidence of selection of leukemic subclones was seen in two cases, with immumophenotypic evidence of loss of CD10 and CD34 antigens, and acquisition of CD20 and surface mu chain. The leukemic cells in these cases grew either in clumps attached to the surface of the stroma, or as'cobblestone areas' beneath the stromal cells. Survival and growth of two evaluable cases was dependent on the continuing presence of stromal cells in the culture system. In one case, direct contact with stroma was shown to be necessary to main- tain viability, while blast cells from the other case survived equally well when separated from the stroma by a 0.4-micron pore size microporous membrane. These results indicate that leu- kemic cells from the majority of cases of precursor-B ALL are able to persist and undergo proliferation in vitro in the presence of normal marrow stroma. This process appears dependent on either direct cell-cell contact, or on diffusible factors derived from the stroma. The availability of ALL cells capable of indefinite proliferation under these conditions will allow further analysis of the mechanisms mediating leukemic cell proliferation.
Leukemia 1996 May
PMID:Long-term survival and proliferation of precursor-B acute lymphoblastic leukemia cells on human bone marrow stroma. 865 76

The expression of lymphoid-associated antigens (LAA) on blasts in acute myeloid leukemia (AML) and myeloproliferative disorders in myeloid blast crisis (MPD/MBC) has often been used to establish a diagnosis of acute mixed lineage leukemia (AMLL). The purpose of this study was to determine the incidence of LAA expression in AML and MPD/MBC (Ly + AML); to assess lymphoid differentiation at the genomic level in Ly + AML; and to compare features of Ly + AML with AML and MPD/MBC lacking these antigens (Ly-AML). Seventy-four consecutive cases of AML and MPD/MBC were reviewed for blast morphology, TdT reactivity, and cytochemistry results. Blast immunophenotyping was performed by multiparameter flow cytometry. Acute myeloid leukemia was subtyped according to the FAB classification. Acute myeloid leukemia and MPD/MBC cases expressing one or more of the following antigens, CD2, CD3, CD5, CD7, CD19, or CD20, were considered to be Ly + AML. Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangement studies were performed by Southern blot analysis using probes for JH, Jkappa, and JBI/BII. Sixteen of the 74 cases (22%) were identified as Ly + AML. Of these, the T-cell-associated markers CD7, CD2, and CD5 were expressed on 7(44%), 6(38%), and 4(25%) Ly + AML cases, respectively. The B-cell-associated markers CD19 and CD20 were expressed on two cases (13%) and one (6%) case, respectively. The FAB subtypes were similarly represented among Ly + AML and Ly-AML. Expression of LAA did not correlate with TdT positivity. In nine cases of Ly + AML (7 expressing T-cell-associated antigens and two expressing B-cell-associated antigens), Southern blot analysis revealed no Ig or TCR gene rearrangements. These results suggest that expression of CD2, CD5, and CD7 in otherwise straightforward AML should not be taken as evidence of lymphoid lineage commitment and does not warrant a diagnosis of AMLL.
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PMID:Lymphoid-associated antigen expression by acute myeloid leukemia. 871 71

A 16-year-old boy was operated upon for synovial sarcoma of the right thigh and underwent chemotherapy consisted of adriamycin (320 mg), cisplatin (780 mg), etoposide (4,200 mg) and ifosfamide (30,000 mg). He developed secondary leukemia 18 months after the chemotherapy. Acute lymphoblastic leukemia (L3) was initially diagnosed because of poor staining of alpha-naphtyl butylate esterase and induction chemotherapy with the LVP regimen (L-asparaginase 5,000 U/m2 day 8-21, vincristine 1.5 mg/ m2 day 1, 6, 11, 16, 21, 26, prednisolone 40 mg/m2 day 1-28) was performed. After the therapy was initiated, the leukemia was finally diagnosed as acute momocytic leukemia (M5a) because of the following data; blasts were positive for CD33 and HLA-DR and negative for CD10, CD19 and CD20; serum lysozyme was 104.0 micrograms/ml; re-evaluation revealed that blasts were strongly positive for alpha naphtyl butyrate esterase in a small part of the slides; 95% of the bone marrow cells showed t (9; 11) chromosomal aberration; gene rearrangement was positive for MLL and negative for JH, JK and TCR C beta 1. Nevertheless, complete remission was obtained after 1 course of LVP therapy. He received bone marrow transplantation from an unrelated volunteer donor after 3 courses of consolidation therapy. He has remained in complete remission for 16 months.
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PMID:[Complete remission achieved by L-asparaginase, vincristine and prednisolone (LVP) therapy in secondary leukemia (M5a type) with an MLL gene rearrangement]. 905 68


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