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)

There is evidence for defective DNA repair in xeroderma pigmentosum, Cockayne's syndrome, and trichothiodystrophy, but for increased cancer risk only in xeroderma pigmentosum. Natural and adaptive immune surveillance and mutant frequency to 6-thioguanine resistance in circulating T-lymphocytes were studied in five patients with xeroderma pigmentosum, two with Cockayne's syndrome, and one with trichothiodystrophy. Forty-eight-hour cutaneous hypersensitivity responses to recall antigens excluded anergy and circulating CD3+, CD4+, CD8+, and CD16+ cell numbers were within normal limits in all patients tested, as were proliferative lymphocyte responses to PHA, except in the trichothiodystrophy patient. Proliferative responses to recall antigens (PPD, SKSD, and Candida) showed that all patients responded to one or more antigens. Direct natural killer cytotoxicity measured against the human erythromyeloid leukaemia cell line K562 using a 4-h 51Cr release assay was significantly reduced in xeroderma pigmentosum (specific cytotoxicity less than mean +/- SD greater than 17.4 +/- 9.4 per cent, with effector:target cell ratio of 50:1) compared to normal controls (45.8 +/- 17.8), but normal in Cockayne's syndrome and trichothiodystrophy. Generation of lymphokine activated killer cell activity was normal in the two xeroderma pigmentosum lines tested. The mutant frequency in the xeroderma pigmentosum donors was significantly increased (p less than 0.01) and was elevated in the two Cockayne's syndrome donors, taking age into account. No mutants were observed from the single trichothiodystrophy donor. These findings suggest that reduced natural killer cell activity may contribute to the greatly increased susceptibility to skin cancer in xeroderma pigmentosum.
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PMID:Immune function, mutant frequency, and cancer risk in the DNA repair defective genodermatoses xeroderma pigmentosum, Cockayne's syndrome, and trichothiodystrophy. 238 95

Tumor cells were cultured in RPMI1640 medium with 16% fetal calf serum and 5% conditioned medium of PHA-stimulated murine spleen cells. After cloning, the tumor cells were reinoculated into normal susceptible mouse. When tumor developed, they grew easily in subsequent cultures in vitro, thus establishing tumor cell lines. By this method, 5 leukemia cell lines and 2 tumor cell lines have been established.
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PMID:[An efficient method for establishing murine tumor cell lines]. 236 77

The effect of erythropoietin (Epo) on colony formation by blast progenitors in acute myeloblastic leukaemia other than erythroleukaemia was studied using a blast colony assay. Epo alone did not induce colony formation, but when it was used together with phytohaemagglutinin-stimulated leucocyte-conditioned medium (PHA-LCM) the number of leukaemic colonies significantly increased in nine out of 12 cases studies. Preincubation of Epo with anti-Epo antibody completely abolished this enhancement, indicating that the increase in colony numbers was caused by Epo itself. Cell surface phenotype analysis of colonies produced by Epo plus PHA-LCM showed no increase in percentages of erythroid and megakaryocyte lineages. The addition of Epo also increased the self-renewal capacity of leukaemic blast cells. Fresh leukaemic cells did not express Epo receptors, but they were induced after incubation with PHA-LCM. The present study thus showed that the proliferative response to Epo is not restricted only to the erythroid lineage, but also extends to AML blast cells other than those in erythroleukaemia in the presence of colony stimulating factors.
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PMID:Enhanced growth of clonogenic cells from acute myeloblastic leukaemia by erythropoietin. 237 25

Murine splenocytes immune to influenza virus-activated human T-cells were fused with SP2/0 cells, selected in chemically defined HAT media, and subcloned to yield a monoclonal antibody (MAb) termed 7G7/B6. 7G7/B6 binds to lectin- and antigen-activated T-cells, but not resting T-cells or B-lymphoblastoid lines from the same donor. 7G7/B6 immunoprecipitates a 50-55 kD band from cell surface iodinated PHA-activated T-cells or the T-cell leukemia line HUT 102B2, as shown on SDS-PAGE. Cross-clearing studies demonstrate that 7G7/B6 binds the same cell surface molecule(s) as anti-Tac, a MAb which has been shown previously to recognize the human receptor for IL-2. 35S-methionine pulse chase experiments in HUT 102B2 cells reveal that 7G7/B6 binds to an early (less than 30 min) 35-37 kD and late (greater than 4 h) 50 kD protein. Sequential immunoprecipitations demonstrate that these are identical to the molecules identified by anti-Tac under similar conditions. However, only anti-Tac coprecipitates a higher molecular band at 110 kD. 7G7/B6 and anti-Tac do not competitively inhibit the binding of each other to PHA-activated T-cells. Functional studies reveal that in contrast to anti-Tac, 7G7/B6 has almost no inhibitory effect in vitro on IL-2-driven proliferation of IL-2-dependent T-cell lines, or alloimmune cytotoxic T-cell generation (however, once generated, these cytotoxic T-cells were both 7G7/B6 and anti-Tac positive). Finally, IL-2 does not inhibit the binding of 7G7/B6 to activated T-cells under conditions which result in up to 75% inhibition of anti-Tac binding. Therefore, 7G7/B6 is another MAb recognizing the human IL-2 receptor, but binding to an epitope distinct from that recognized by either IL-2 or anti-Tac.
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PMID:A monoclonal antibody 7G7/B6, binds to an epitope on the human interleukin-2 (IL-2) receptor that is distinct from that recognized by IL-2 or anti-Tac. 240 92

The activity of nucleolar organizer regions (NOR) in chromosomes and interphase nuclei of bone marrow cells from 11 adult patients with acute lymphoblastic leukemia (ALL), 35 patients with acute nonlymphoblastic leukemia (ANLL), and eight healthy donors has been studied with silver nitrate staining. PHA-stimulated lymphocytes of the same individuals were used as standards of the maximum silver-staining patterns for each person. In 90% of patients with acute leukemia the average number of Ag+NOR in metaphases was lower when compared with that of PHA-stimulated lymphocytes. A variable expression of NOR was observed within the cell population and between individual patients. The populations tested showed high heterogeneity in relation to the content of Ag-negative mitoses. Ag+NOR per metaphase and the content of Ag-negative mitoses in bone marrow did not differ between patients with ALL and ANLL. Differences in the staining pattern in leukemic cells are discussed.
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PMID:The activity of nucleolar organizer regions of human bone marrow cells studied with silver staining. II. Acute leukemia. 243 24

Prostaglandins have been implicated as possible modulators of the proliferation and differentiation of neoplastic cells. The aim of this work was to determine 6-keto-PGF1 alpha and TXB2 concentrations in the blood plasma and in the supernatant of 96 hour PHA stimulated and unstimulated leukaemic cell cultures of chronic lymphocytic leukaemia patients. 62 patients with CLL classified to the 1st or 4th stage according to RAI, and 23 healthy individuals were investigated. The blastogenic transformation was measured by the standard tritiated thymidine method. The quantity of 6-keto-PGF1 alpha and TXB2 was estimated by the isotopic method using a RIA-kit. In the 4th stage of CLL a low value of blastogenic transformation was observed, whereas in the 1st stage, the values were similar to those of the control group. It was shown that in the 4th stage of the disease an increase in the 6-keto-PGF1 alpha concentrations occurs in the blood plasma and the culture supernatant together with a significant decrease in TXB2 in the culture supernatant, whereas in the 1st stage a significant decrease in the 6-keto-PGF1 alpha as compared with those of the control group is noted. These results may indicate on antagonistic action of PGI2 and TXB2 in leukaemia cell proliferation.
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PMID:The behaviour of 6-keto PGF1 alpha and TXB2 concentrations in the culture supernatant of chronic lymphocytic leukaemia cells. 243 11

ICO-1 Mab were obtained following BALB/c mouse immunization with 24-week human fetal thymocytes. Cloning for two times by the method of limited dilutions led to a hybridoma with a stable production of G3 isotype Mab. ICO-1 Mab have immunoprecipitated an antigen consisting of two polypeptide chains with molecular weight 29 and 34 kDal. The antigen expression was enhanced following PHA or alloantigen activation of blood mononuclear cells. ICO-1 Mab inhibited the alloantigenic response of blood mononuclear cells. Mab detected 29% of antigen-positive cells in the peripheral blood of healthy adults. When the reaction of ICO-1 Mab was compared with that of Mab against monomorphic Ia-like antigens OKLa, anti-Ia-BRL, BMA-021 and HLA-Dr on blood cells from healthy donors and patients with leukemia proved to be identical.
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PMID:[Standardization of ICO-1 monoclonal antibodies against monomorphic Ia-like (Dr) antigens]. 244 25

The oncogene kit has been shown genetically to map in the W locus of the mouse. This locus is known to have an important role in the regulation of normal hemopoietic stem cell growth. The blast cells of acute myeloblastic leukemia may be considered to arise in predeterministic stem cells. Accordingly, we sought evidence that kit was involved in the regulation of AML blast growth, using a cDNA probe to the external domain of c-kit. With this probe the gene was found to be in germline configuration in blast cells from AML, ALL, and continuous myeloblastic cell lines. However, expression could be detected by Northern analysis or RNA dot blots only in fresh AML blast cells. Fresh cells from ALL patients, normal bone marrow, PHA-stimulated lymphocytes, and four myeloblastic continuous cell lines were expression negative by the same techniques.
Leukemia 1989 Oct
PMID:The expression of the proto-oncogene C-kit in the blast cells of acute myeloblastic leukemia. 247 40

A study was made of the expression of the cellular oncogens c--myc, c--sis and c--abl in mononuclears from normal donors and patients with different patterns of leukemia and hemopoietic dysplasia using spot hybridization on nitrocellulose filters with virus homologs of the given oncogens. Altogether 43 persons were examined. No specific expression of the oncogens indicated was established whatever the pattern of leukemia. The relationship between the expression of these oncogens and the efficacy of the treatment of acute myeloblastic leukemia was demonstrated. However, in the given investigations, no differences were identified in the expression of oncogens in the leukemic and normal cells stimulated with PHA and phorbolic ether. Enhanced expression of cellular oncogens myc, sis and abl occurred in acute leukemia.
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PMID:[Human oncogene expression in the normal state and in various blood system diseases]. 247 91

We have determined the organization and nucleotide sequence of the gene encoding the human T cell surface glycoprotein CD8 alpha. This gene spans approximately 8 kb and is organized into six exons which encode separate functional domains of the protein. Exon 1 encodes the 5' untranslated region and leader peptide, exon II the Ig V-like region, exon III the hinge-like region, exon IV the transmembrane domain, and exons V and VI the cytoplasmic tail. Alternative splicing that excludes nucleotide sequences from exon IV results in a transcript which encodes a secreted form of the protein. This transcript accounts for approximately 15% of the total CD8 alpha mRNA in human T cell leukemia lines and in normal human tissues. Secreted CD8 alpha protein can be detected in culture supernatants of T cell leukemia lines and PHA-stimulated PBMC by immunoprecipitation with the anti-CD8 alpha mAb OKT8 or with a polyclonal rabbit antiserum specific for the 28 amino acid cytoplasmic domain of CD8 alpha. The secreted CD8 alpha protein forms homodimers; when analyzed by SDS-PAGE, the protein migrates with an apparent molecular mass of 27 or 54 kDa under reducing or non-reducing conditions, respectively. Human secreted CD8 alpha may serve an immunoregulatory role for the interactions of T cells with their targets in vivo.
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PMID:Alternatively spliced mRNA encodes a secreted form of human CD8 alpha. Characterization of the human CD8 alpha gene. 249 67


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