Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three permanent human leukaemia cell lines, designated EW2, LG3 and MS6, were established from bone marrow aspirates of a patient with acute myelomonocytic leukaemia (EW2), acute monocytic leukaemia (LG3) and acute myeloblastic leukaemia (MS 6). In vitro all lines exhibited a myelomonocytoid marker profile in terms of classical staining reactions and cell-surface antigen structure. In supernatants and extracts of EW2 and MS 6 cells immunoreactive human calcitonin was found in raised levels. No significant levels of immunoreactive human calcitonin were found in supernatants of LG3 cells, while extracts of LG3 cells and the patients sera at diagnosis contained high levels, suggesting the in vitro selection of a non-secreting clone of leukaemic cells. Gel-chromatography showed several peaks of ihCT with higher molecular weight than normal human calcitonin, suggesting the production of precursor molecules. In addition to ihCT raised levels of immunoreactive calcitonin gene related peptide (ICGRP) was found in supernatants of EW2. These data support the concept of ectopic immunoreactive human calcitonin production by leukaemic cells.
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PMID:Establishment of three permanent human leukaemia cell lines producing immunoreactive calcitonin. 347 87

The expression of the DNA excision repair enzyme uracil-DNA glycosylase was investigated in bone marrow and peripheral samples from seven patients with acute lymphoblastic leukemia (ALL), from 17 patients with acute non-lymphocytic leukemia (ANLL), and from one patient with chronic granulocytic leukemia (CGL) in blast crisis. In addition, uracil-DNA glycosylase activities were determined in nine human leukemia/lymphoma cell lines. There was a clear correlation between the percentage of blast cells and the enzyme activity when mononuclear cell fractions from patient samples were analysed. The following uracil-DNA glycosylase activities were recorded (mean +/- S.D., number of samples): ALL = 45.6 +/- 14.8 U/mg of protein, N = 10; ANLL = 41.1 +/- 13.8 U/mg of protein, N = 22; CGL (blast crisis) = 44.7 U/mg of protein. The uracil-DNA glycosylase activity in nine human leukemia/lymphoma cell lines ranged from 35.2 to 66.0 U/mg of protein, and no striking differences were observed between the T-ALL, B-ALL, null cell ALL or myeloid lines. Similarly, the various biological features, such as the common ALL surface antigen, the terminal deoxynucleotidyl transferase enzyme, the sub-type of leukemia, chromosomal aberrations, or previous chemotherapy, did not apparently affect the expression of uracil-DNA glycosylase. We propose that the integrity of the genetic information is well protected by uracil-DNA glycosylase in different forms of leukemia, including cases with a low proportion of S-phase blasts, as assessed by flow cytometry in the present work. When compared to the activities in benign hematopoietic progenitor cells, studied previously in this laboratory, no big differences between the benign and malignant hematopoiesis were demonstrated. Hence, it is unlikely that selectivity of chemotherapy towards malignant vs benign hematopoietic growth could be based on the enzyme uracil-DNA glycosylase.
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PMID:Uracil-DNA glycosylase activity in human acute leukemia. 347 82

The antigenic characteristics of the leukaemic cell population in 31 patients with acute myeloid leukaemia (AML) and 5 patients with acute undifferentiated leukaemia (AUL) was investigated using a panel of 15 monoclonal antibodies (Mc Abs). We chose 14 Mc Abs that react with lineage--and stage related myeloid antigens and L243 Mc Ab that reacts with HLA-DR antigen. In AML cases we correlated the antigenic phenotype with morphological FAB classification. The study indicates a substantial antigenic heterogeneity of the surface antigen expression on leukaemia cells particularly in M1, M2 and M4 AML cases. The morphological subtype of these leukaemias tended to correlate with the immunologic phenotype, particularly in more differentiated AML cases such as M3 or M5. The most immature cell phenotype characterised "undifferentiated" AML, which was expressed by the reactivity or L243, BI3C5, MY9, VIM-2 and S3-13 Mc Abs with the majority of the patients. The analysis shows that although there is a tendency for the morphology to correlate with the surface antigen phenotype each morphological group contains patients having different surface antigen phenotype.
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PMID:Antigenic phenotype of the myeloid leukaemic cells defined by monoclonal antibodies. 347 33

CD2 (T11, sheep erythrocyte receptor) is a surface antigen of the human T-lymphocyte lineage. cDNA clones encoding CD2 have been isolated by using the purified, denatured CD2 to raise a rat antiserum. Positive clones were recognized in a phage lambda gt11 expression library prepared from the human leukemia T-cell line J6. The DNA sequence contained an open reading frame encoding 360 amino acids. The N-terminal 24 amino acids were characteristic of a signal peptide and were followed by a region that matched all 25 residues of the CD2 N terminus previously determined by amino acid sequencing. The predicted amino acid sequence is consistent with that of a transmembrane glycoprotein containing three potential N-glycosylation sites on the N-terminal side of a 26-amino acid hydrophobic segment. There is a large cytoplasmic domain of 125 amino acids that is rich in proline and in basic residues. RNA blot-hybridization analysis demonstrated hybridization only in those T cells that were positive for surface CD2 antigen. There are limited regions of sequence similarity to members of the immunoglobulin supergene family.
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PMID:Molecular cloning of the human T-lymphocyte surface CD2 (T11) antigen. 349 Jun 70

The structure and the expression of 11 cellular oncogenes (protooncogenes) were analyzed in primary cells from 20 acute lymphocytic (ALL) and 31 acute myelogenous (AML) leukemia patients. Neoplastic cells, obtained prior to initiation of therapy, were purified and classified, on the basis of both surface antigen pattern and morphology, into pre-B, B, and T ALL and M1-M5 AML. RNA was extracted and analyzed for expression of cellular oncogenes coding for nuclear proteins (c-myc, c-myb, c-fos), the beta-chain of platelet-derived growth factor (c-sis), growth factor receptors or related proteins (c-src, c-abl, c-fes, c-erbB), or putative intermediate transducers of mitogenic signals (c-Ha-ras, c-Ki-ras, c-N-ras). Quantitative analysis of total RNA was carried out by dot blot hybridization to specific cDNA or genomic probes. Number and size of transcripts were evaluated by blot hybridization of electrophoretically fractionated poly(A)+ RNA. Expression of c-myc and c-myb was detected in all leukemic cells at variable levels and was characterized by well-defined patterns within ALL subtypes. Conversely, significant levels of c-fos transcripts were detected only in myelomonocytic (M4) and monocytic (M5) leukemias. Among the "src-family," c-fes was expressed more in AML than ALL, and c-abl was expressed at variable but not elevated levels in all leukemia types. c-Ha-ras was uniformly expressed at low levels, as in non-neoplastic cells. c-Ki-ras transcription was detected only in T ALL; N-ras expression was barely demonstrable. The structure of these protooncogenes was not grossly modified, as evaluated by Southern analysis, except for c-myc rearrangement in B ALL. These studies indicate that cellular oncogene expression in specific subtypes of leukemic cells may relate to either the proliferative activity (c-myc, c-myb) or the differentiation state (c-fos) of the cells, or possibly to expression of receptors for putative hemopoiesis-related growth factors (c-fes, c-abl). Our data provide a basis for in-depth analysis of protooncogene expression in normal and neoplastic hemopoiesis.
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PMID:Expression of cellular oncogenes in primary cells from human acute leukemias. 352 May 70

The tumor-associated surface antigen on L1210 leukemia cells was studied by immunofluorescence staining and immunoprecipitation. Anti-L1210 serum was prepared in BALB/c X DBA/2 F1 mice by priming with a hybrid of L1210 and human Lesch-Nyhan fibroblast cells and hyperimmunizing with L1210 leukemia cells. This hyperimmune serum was able to demonstrate specific surface fluorescence on L1210 cells, while the antiserum did not react with various mouse tumor cell lines, normal lymphoid tissues, or mitogen-activated lymphoid cells. The anti-L1210 serum immunoprecipitated a single polypeptide with a molecular weight of 90,000 from 125I-labeled L1210 cells. The expression of this antigen was enhanced by tumor-promoting agent and heat shock treatment. The biological significance of the L1210-specific cell surface antigen is discussed.
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PMID:Identification and characterization of a unique tumor-associated surface antigen on L1210 leukemia cells recognized by semisyngeneic antisera. 354 98

This report describes the qualitative acid phosphatase (acP) isoenzyme profiles detected in permanent human hematopoietic cell lines. The acP activity was separated into its isoenzymes by isoelectric focusing on horizontal thin-layer polyacrylamide gels. The pattern of acP isoenzyme was investigated in a total of 86 cell lines. These cell lines were classified into five groups on the basis of their phenotypes characterized in the multiple marker analysis: 74 leukemia-lymphoma cell lines (26 T-, 34 B-, 6 myelomonocytic, 8 Non-T, Non-B cell lines) and 12 so-called 'normal' Epstein-Barr virus transformed B-lymphoblastoid cell lines. Their immunological features had been analysed in detail by use of a large panel of poly- and monoclonal antibodies which led to a further subclassification into stages of differentiation. A progressive increase in number and staining intensity of the isoenzymes which paralleled the expression of surface markers at different stages of differentiation along their developmental pathway was seen in the T- and B-leukemia-lymphoma cell lines. Some cell lines whose isoenzyme profiles did not correspond to the stage of differentiation as evidenced by surface antigen analysis might represent good examples of deranged gene expression in otherwise normally programmed malignant cells, i.e. in our study a mismatch between the isoenzymatic and immunological phenotypes. The tartrate-resistant isoenzyme was detected in 9 out of 74 leukemia-lymphoma cell lines (4 T-, 2 B-, 1 myelomonocytic, 2 Non-T, Non-B cell lines) and in 10 out of 12 normal B-lymphoblastoid cell lines; the only one studied hairy cell leukemia cell line did not express this isoenzyme. The relative specificity of the tartrate-resistant acP is discussed in detail. No leukemia-lymphoma specific isoenzyme or an additional isoenzyme which was not seen in normal hematopoietic cells could be observed. Nor did we find an isoenzyme or isoenzyme pattern characteristic for a certain cell lineage. This underlines the necessity of a combined analysis using markers from different disciplines in the 'multiple marker analysis' in order to accurately characterize normal and malignant blood cells. Furthermore, our results support the concept of maturation arrest at particular stages of differentiation together with the theory of normal gene expression in leukemic cells equivalent to that in their normal counterparts.
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PMID:Isoenzyme studies in human leukemia-lymphoma cells lines--II. Acid phosphatase. 387 27

The gag membrane protein gP85gag, encoded by Moloney murine leukemia virus (M-MLV), was identified as a target molecule recognized by Moloney murine sarcoma virus--M-MLV (M-MSV--M-MLV)-specific cytolytic T lymphocyte (CTL) clones. Target cells infected with Ab-X-MLV, an M-MLV-derived mutant virus not encoding gP85gag, were not lysed by the CTL clones. The same CTL clones were shown previously to induce the destruction of M-MLV-induced tumor cells in the peritoneal cavity. We have now characterized CTL-resistant antigen-loss tumor cell variants that have lost the surface antigen, but which retain transcriptionally silent M-MLV genomes. A cloned antigen-loss variant that reverted in vitro to the CTL-susceptible phenotype reexpressed M-MLV genomes that had undergone an insertion event in the region of the viral DNA coding for the gag membrane protein. Intravenous injection of virus-specific CTL clones inhibited tumor formation in mice injected subcutaneously with M-MSV--M-MLV.
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PMID:Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo. 389 2

A novel cell-surface antigen (L25) expressed on human B cells was identified using a B cell-reactive monoclonal antibody (TB1-4D5). This L25 antigen was expressed on most B-lineage cells but not other cell types including thymocytes, T cells, granulocytes and monocytes. Thus, L25 existed on the majority of normal B cells present in the blood and lymphoid tissues, on cultured cell lines derived from normal and malignant B cells, and on neoplastic cells isolated from patients with B cell-derived malignancies. Though L25 was persistently expressed on B cells until 7 days after their activation with pokeweed mitogen (PWM), neither normal nor neoplastic plasma cells expressed L25. Moreover, L25 was present on cultured as well as freshly isolated leukaemic cells with common acute lymphatic leukaemia (CALL) antigen, which have been thought to correspond to the early B-cell ontogeny. Besides pan-B cell reactivity of TB1-4D5 antibody, it apparently cross-reacted with so-called dendritic or interdigitating cells located in the thymic-dependent areas of peripheral lymphoid organs, which have been presumably ascribed to those associated with accessory-cell function. Functional studies showed that anti-L25 (TB1-4D5) antibody had inhibitory effect on induction of immunoglobulin synthesis by PWM-stimulated B cells.
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PMID:A novel human B-lymphocyte antigen shared with lymphoid dendritic cells: characterization by monoclonal antibody. 390 5

The C-type particles produced by the A9 and A9HT sublines of mouse L cells were shown to infect C3H (N type), but not C57BL (B type), mouse embryo fibroblasts. Infection was indicated by distinct single giant cell formation in the XC monolayer used to overlay the mouse embryo fibroblasts. On the basis of these results it was concluded that the L cell virus is N tropic. A9 and A9HT cells were fused to various mouse cells derived from tumors and normal tissues. The ability to produce the Moloney-type surface antigen and to release infectious virus was introduced by the A9 component into the hybrid cell. Virus production, measured by antigen induction on JLS-V9 cells, was suppressed in those hybrids in which the partner cell had a genotype determining low infectibility with that particular virus (B-type cell). It thus appears that the major genetic locus affecting resistance to infection with leukemia viruses, the Fv-1 locus, regulates infectious virus production in somatic cell hybrids also. The same genetic locus did not seem to govern the expression of all virus-related functions, for the virus-determined membrane antigen was demonstrated in many of the N x B-type hybrids in which production of infectious virus was suppressed.
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PMID:The influence of the partner cell on the production of L virus and the expression of viral surface antigen in hybrid cells. 434 52


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