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)

A retrospective study was conducted to determine whether exposure to murine mammary tumor virus (MuMTV) induced MuMTV-specific serologic responses among intramural laboratory personnel. Results obtained with a panel of five purified structural proteins of the RIII mouse strain milk-derived MuMTV (gp55, gp34, p28, p18, and p12), by means of the enzyme-linked immunosorbent assay to assess antibody binding, established that MuMTV exposure resulted in highly significant increases in serologic responses to these test antigens as compared to age- and gender-matched controls without overt contact with MuMTV. Furthermore, immunoreactions to gp55 and gp34 were found not to be directed to the carbohydrate moieties of these glycoproteins. Similar results were obtained by assays of human immunoglobulin binding to Western blots of MuMTV proteins. These increased MuMTV-specific immunoreactivities, in general, were found to be related to degree and length of exposure to this virus. These results with MuMTV suggest the possibility of important human immune response differences between exposure to type B (MuMTV) and animal type C (leukemia-sarcoma) RNA tumor viruses, perhaps reflective of sensitivity to antibody dependence of complement-induced virolysis.
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PMID:Serologic responses to murine mammary tumor virus (MuMTV) in MuMTV-exposed laboratory personnel. 300 44

An effective subunit vaccine against feline leukemia virus infection and related diseases has been developed. The source of the vaccine immunogen is feline retrovirus persistently infected cells that continuously synthesize and shed virus polypeptides. Western blot analysis identifies FeLV-gp70, p27, p15, p12, and p10 in the subunit vaccine preparation. Cats immunized with the vaccine developed antibodies to a 70,000 MW protein of the vaccine that seems to be distinct from, but related to the FeLV-gp70 polypeptide.
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PMID:Feline leukemia vaccine: efficacy, contents and probable mechanism. 300 10

The organization of the transforming protein encoded by Abelson murine leukemia virus (A-MuLV) in transformed lymphoid and fibroblast cells was examined using immunofluorescent analysis. Antibodies specific for v-abl were capable of detecting cytoplasmic Abelson protein molecules in fixed cells, but none were able to stain the surface of live A-MuLV transformed cells. However, a series of monoclonal antibodies selected for the ability to bind to the surface of A-MuLV-transformed cells did stain live cells. These antibodies were shown to react with a determinant within the helper virus-derived p15 sequences that are present at the amino terminus of the Abelson protein, indicating that gag-derived determinants are exposed on the surface of transformed cells. The inability of a p12-specific monoclonal antibody to stain live cells indicates that only a small portion of the amino terminal sequences are exposed. Examination of the ability of these antibodies to react with Abelson protein encoded by a series of gag deletion mutants suggests that the determinant recognized by these antibodies lies between amino acids 38 and 114 of p15.
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PMID:Gag-derived but not abl-derived determinants are exposed on the surface of Abelson virus-transformed cells. 302 Jul 82

An unusual case of 'pseudo-lymphoid' leukaemia is described. The leukaemic cells resembled small, mature lymphocytes but lacked B- and T-cell membrane markers as well as immunoglobulin (Ig) and T-cell receptor gene rearrangements. They showed, instead, features of early myeloid cells since they expressed 2 myeloid antigens, CDW13 and My9, and displayed peroxidase activity demonstrable by electron microscopy (EM) on unfixed cells. Cytogenetic studies showed monosomy 5, t(4;17) (p12;p11), t(2;3)(p23;q14) and an abnormal chromosome 12. Abnormalities of chromosomes 4 and 5 have been previously associated with 'pseudo-lymphoid' leukaemias. This case illustrates the value of sensitive methods for the characterization of blast cells and for the precise diagnosis of leukaemias with apparent 'lymphoid' morphology.
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PMID:'Pseudo-lymphoid' leukaemia with unusual features: ultrastructural, immunological, cytogenetic and molecular studies. 303 99

Fragile site studies were performed on a total of 126 patients with leukemia and other hematologic disorders including myelodysplastic syndrome (MDS) and polycythemia vera (PV). Compared with an incidence (6.0%) of heritable rare fragile sites in the healthy population, the frequency was not higher in the patient group (3.2%), as a whole. However, two cases of fra(17)(p12) in MDS appeared fourfold larger than expected for this group of patients. In one case, a homozygous carrier of fra(17)(p12) in PV was also very rarely expected from its population incidence. These findings suggested a possible role of rare fragile sites, at least in the etiology of these preleukemic or myeloproliferative disorders.
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PMID:Heritable rare fragile sites in patients with leukemia and other hematologic disorders. 316 95

Clinical, hematological, and cytogenetic data of 32 patients with loss of part of the short arm of chromosome 9 (9p-) are reviewed. There were 20 acute lymphoblastic leukemia (ALL), seven non-Hodgkin lymphoma (NHL), three acute myeloid leukemia, one refractory anemia with excess blasts in transformation, and one chronic myeloid leukemia (CML) in blast crisis. The cytogenetic findings were heterogeneous: 13 cases of del(9)(p21), among them four as sole karyotypic change; five cases of del(9)(p12), three of them as sole karyotypic change; four patients with i(9q), three with unbalanced translocations involving 9p12; and seven with unbalanced translocations involving 9p21. In addition, 10 patients showed known specific translocations for determined subgroups of ALL, NHL, and CML. The immunological phenotypes in the 20 ALL patients were common ALL (35%), pre-B-ALL (35%), B-ALL (5%), T-ALL (15%), and null ALL (10%). Three NHL were of T cell origin and the others of B cell origin. No specific association between the karyotypic change, immunophenotype, and clinical presentation could be ascertained for patients with ALL, acute myeloid leukemia, CML in blast crisis, and B-NHL. In T-NHL, three children with deletion of 9p, T immunoblastic lymphoma originating from common thymocyte and presenting with a mediastinal mass and pleural effusion may constitute a definite subgroup with good prognosis. All other cases had a poor outcome. Previously suggested association of 9p- with T-ALL and "lymphomatous features" was not confirmed.
Leukemia 1987 Jul
PMID:Abnormalities of the short arm of chromosome 9 with partial loss of material in hematological disorders. 331 44

We detected phosphorylation of the major Moloney murine leukemia virus (M-MuLV) capsid polypeptide, p30, by using 32Pi-labeled virions. This was observed both on two-dimensional polyacrylamide gels directly or on one-dimensional gels of viral lysates that had been immunoprecipitated with monospecific goat anti-p30 serum. The phosphorylation event had been difficult to detect because pp12 the major virion phosphoprotein incorporates almost all of the 32P label added to infected cells (Y. Yoshinaka and R. B. Luftig, Virology 116:181-195, 1982). When immunoprecipitates from M-MuLV lysates labeled with 32Pi were compared with those labeled with [35S]methionine, it was calculated that the degree of phosphorylation at the p30 domain of Pr65gag was only 0.22 to 0.54% relative to phosphorylation at the p12 domain. Two-dimensional gel electrophoresis of the 32P-labeled p30 immunoprecipitates showed that there were three phosphorylated p30 forms with isoelectric points (pIs) of 5.7, 5.8, and 6.0. These forms were generally more acidic than the [35S]methionine-labeled p30 forms, which had pIs of 6.0, 6.1, 6.3 (the major constituent with greater than 80% of the label), and 6.6. The predominant phosphoamino acid of the major phosphorylated p30 form (pI 5.8) was phosphoserine. Further, tryptic peptide analysis of this p30 form showed that only one peptide was predominantly phosphorylated. Based on a comparison of specific labeling of p30 tryptic peptides with [14C]serine, [35S]methionine, and 32Pi, we tentatively assigned the phosphorylation site to a 2.4-kilodalton NH2-terminal peptide containing triple tandem serines spanning the region from amino acids 4 to 24.
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PMID:Detection of phosphorylated forms of Moloney murine leukemia virus major capsid protein p30 by immunoprecipitation and two-dimensional gel electrophoresis. 333 49

Two sequential lymph node biopsies taken from a non-Hodgkin lymphoma patient revealed two karyotype abnormalities peculiar to B cell neoplasias: trisomy 12 and t(2;8)(p12;q24) translocation. The first was documented in all cells analyzed, while the second was present in 20% of the metaphases from the first biopsy and in 100% from the second. This suggests that the t(2;8) translocation arose as a secondary karyotypic change. In addition, although immunological characterization of the neoplastic cells disclosed a monoclonal B cell population that expressed immunoglobulin kappa light chains, as usually found in Burkitt's lymphoma with t(2;8) translocation, Southern blot analysis provided evidence of rearrangement in only one kappa chain allele.
Leukemia 1988 Jan
PMID:Immunological and molecular studies in a case of follicular lymphoma with an extra chromosome 12 and t(2;8) translocation. 333 3

To determine the baseline frequency of autosomal rare fragile sites in cancer patients, we conducted a population cytogenetic study of 370 patients with leukemias, solid tumors, and other neoplastic disorders. Twenty carriers of rare fragile sites were detected in this patient group. The rare autosomal fragile sites were at fra(8)(q24), fra(11)(p15), fra(16)(p12.1), fra(16)(q22), and fra(17)(p12). All of these fragile sites were found to be distamycin A inducible. Compared with a population incidence in healthy subjects (44 of 845, 5.21%), the overall incidence of distamycin A-inducible fragile sites was not higher in the patient group (20 of 370, 5.41%). Analysis of these individual fragile sites and particular diseases, however, suggests that the distamycin A-inducible fragile sites may play a role in the etiology of leukemia, myeloproliferative disorders, and benign tumors.
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PMID:Distamycin A-inducible fragile sites and cancer proneness. 340

Congenital monoblastic leukemia cutis is a rare disorder. We report an infant who developed infiltrative skin lesions by 2 weeks of age, which, when biopsied at 4 1/2 months of age revealed a monoblastic infiltrate. Blasts in the peripheral blood were not seen until 1 week before her death at 8 months of age. Chromosomal analyses of her bone marrow showed an abnormal clone of cells with a 46,XX,del(10)(p12) karyotype. Although chromosome 10 is rarely involved in hematologic malignancies, abnormalities of this chromosome within the region 10p11-10p13 have now been shown in four of 10 reported cases of congenital monoblastic leukemia.
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PMID:Congenital monoblastic leukemia cutis. A case report with chromosomal abnormality: del (10p). 346 18


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