PubMed Health⌕ Search

Biomedical subjects

A Tabilio

Publications and source records attributed to A Tabilio.

At least 91 records · Page 5Linked to original sources
PubMed1988

5q- syndrome terminating in acute myeloid leukemia. Karyotype evolution and immunologic characterization of blast cells.

We report a case of 5q- syndrome that progressed to acute nonlymphocytic leukemia after 9 years of clinically and morphologically stable disease. The transition from the chronic to the leukemic phase was characterized by the appearance of an additional cytogenetic anomaly [inv(2)] in the cell carrying the 5q-, together with the expansion of a clone showing an apparently normal karyotype.

Anemia, Refractory↗
PubMed1988

Immunophenotype of leukemic blasts with small peroxidase-positive granules detected by electron microscopy.

Forty-three cases of undifferentiated leukemias by light microscopy examination were diagnosed as acute myeloblastic leukemias by ultrastructural revelation of peroxidase and were subsequently studied by immunological markers. In 41 of these cases, blasts were labeled by at least one of the antimyeloid MoAbs (My 7, My 9, and 80H5). An antimyeloperoxidase polyclonal antibody was used in 23 cases and was clearly positive in 11 of them, while cytochemistry by light microscopy was negative. These myeloblasts were frequently mixed with a minority of blasts from other lineages especially promegakaryoblasts. It is noteworthy that in 6 cases myeloid and lymphoid markers (E rosette receptor, common acute lymphoblastic leukemia antigen (cALLA), CD 9, CD 19 antigens (anti-B4 MoAb] were detected on a fraction of blast cells, suggesting a bilineage leukemia. However, in double labeling experiments, blasts with myeloperoxidase coexpressed lymphoid and myeloid markers including cALLA and CD 19 antigen. In one case, blasts had a typical non-B, non-T acute lymphoblastic leukemia phenotype (HLA-DR, CD 9, CD 19, cALLA positive) without staining by any of the antimyeloid MoAbs. However, 70% of the blasts were labeled by the antimyeloperoxidase antibody and expressed peroxidase-positive granules at ultrastructural level. In conclusion, most of the AML undiagnosed by optical cytochemistry are identified by antimyeloid antibodies. Some of these cases are also stained by some antilymphoid MoAbs. Use of antibodies against myeloperoxidase may improve the diagnosis of difficult cases of acute myeloblastic leukemia.

Antibodies, Monoclonal↗
PubMed1987

Establishment and characterization of a human IgA-kappa-secreting plasma cell line (MT3).

We have established a new human plasma cell line from the peripheral blood of a patient with an IgA-kappa plasma-cell leukemia. Morphological, immunological, cytogenetic and molecular studies confirm that the cultured cells are derived from the same clone of leukemic plasma cell in vivo. The established cell line (MT3) grows in suspension, secretes high amounts of IgA kappa and exhibits morphological and ultrastructural characteristics of plasma cells. Surface marker analysis shows that both primary and cultured cells express the plasma-cell-associated antigens PCA-1 and T10, while specific B- and T-cell determinants and EBV nuclear antigen are undetectable. In the established cell line a few cells express Ia-like and CALLA antigens. Cytogenetic analysis of MT3 cells reveals a prevalent hypertriploid karyotype with constant chromosomal aberrations consisting of 14q+, 22q- and marker chromosomes.

Antigens, Surface↗
PubMed1987

High frequency of clonal immunoglobulin or T cell receptor gene rearrangements in acute myelogenous leukemia expressing terminal deoxyribonucleotidyltransferase.

Ig and T cell receptor rearrangements have been used as irreversible markers of lineage and clonality in the study of B- and T-lymphoid populations. We have addressed the issue of lymphoid lineage specificity of these rearrangements by analyzing a panel of 25 TdT- acute myelogenous leukemias, 13 TdT+ AMLs, and 4 TdT+ undifferentiated leukemias. We report that while gene rearrangements represent extremely rare events in classical TdT- AML (less than 8%), rearrangements of either the Ig or T beta locus or both were detectable in the majority of the TdT+ AMLs (greater than 60%), and rearrangements of both loci were detectable in all of the TdT+ undifferentiated leukemias. These data demonstrate a significant association between TdT expression and Ig or T beta gene rearrangements even outside the lymphoid lineage, further supporting a role for TdT in Ig and T cell receptor gene assembly. These data also indicate that a coordinated program of lymphoid gene expression involving TdT-CD7-expression and Ig/T beta rearrangements can be activated before myeloid commitment. Whether the activation of this program represents a normal, albeit rare, event in early myelopoiesis or a transformation-related event present only in leukemic cells remains to be determined.

Cell Differentiation↗
PubMed1986

Expression of a particular beta-N-acetylglucosaminidase isoenzyme in human haematopoietic leukemic cell-lines.

N-acetyl-beta-D-glucosaminidase (NAG) activity and isoenzyme profiles were studied in myeloid, histiocytic, B-lymphoid, T-lymphoid and lymphoblastoid continuous cell lines in order to determine if N-acetyl-beta-D-glucosaminidase isoenzyme expression may help to distinguish among various types of leukemic proliferation. Total NAG activity in myeloid, histiocytic, erythroleukemic cell lines were higher than Burkitt's lymphoma derived cell lines (B-lymphoid), T- or lymphoblastoid cell lines. On chromatofocusing by PBE 94 coupled with an automated enzyme assay an intermediate (I) beta-N-acetyl-glucosaminidase form, eluting between forms B and A, was found in all leukemic and in Epstein-Barr virus infected lymphoblastoid cell lines analysed. The different profiles recorded, the expression of the I form and the different I/B ratios may be useful as markers of tumour proliferation.

Acetylglucosaminidase↗
PubMed1986

t(4;21) (p16;q22) in blastic crisis of a chronic myeloid leukemia with variant Philadelphia translocation.

A chronic myeloid leukemia (CML) patient who had presented a t(2;9;22) translocation during the chronic phase developed an unusual t(4;21) (p16;q22) translocation during the M2 type FAB classification blastic crisis. The role of these two recombinant chromosomes in the genesis of the terminal phase is discussed, particularly as the breakpoint on chromosome 21 near to the ets-2 oncogene locus, seems to be the same as that described in the t(8;21) (q22;q22) translocation specific of type M2 AML.

Aged↗
PubMed1985

Megakaryoblastic micromegakaryocytic crisis in chronic myeloid leukemia.

Atypical megakaryoblasts (MKB) or megakaryocytes (MK) are occasionally present in the peripheral blood during the terminal development of chronic myeloid leukemia (CML). We report on a 49-year-old female suffering from Ph1 chromosome-positive CML with typical megakaryoblastic transformation in the peripheral blood and in the bone marrow. The small "blasts" were at the most only slightly larger and were occasionally even smaller than lymphocytes but showed megakaryoblastic or atypical megakaryocytic differentiation. The cytoplasmic cytochemical pattern of the atypical megakaryocytic cells was identical to that of large atypical thrombocytes. Platelet peroxidase was detected upon electron-microscopic (EM) examination. Immunologic characterization disclosed the presence of MK-specific antigens. When cultured in vitro on agar, the blasts transformed spontaneously into large mature MK, exhibiting characteristic cytochemical and immunological patterns. Cytogenetic examination of peripheral blood showed severe abnormalities. The patient did not respond to therapy and died 3 months after manifestation of the blast crisis.

Bone Marrow Cells↗
PubMed1985

Variant Philadelphia translocation in an immunologically and clinically typical case of chronic myeloid leukaemia.

Cytogenetic analysis of bone marrow from a chronic myeloid leukemia patient in chronic phase revealed a classical Philadelphia chromosome from a complex translocation t(2;9;22). The break points on 9 and 22 were, apparently, the same as for the standard translocation (9;22). However, whereas the terminal band of 9 (9q34) was translocated in the usual site, that is on 22q-, the tract deleted from 22 was present on band p13 of chromosome 2. The finding of this rare 22 translocation in classical CML would seem to support the hypothesis that the crucial event in the pathogenesis of CML is the translocation of band 9q34, that contains the c-abl oncogene, onto the Ph' chromosome, rather than the translocation of the tract deleted from 22 to some other chromosome site.

Aged↗
PubMed1985

Human mononuclear phagocyte differentiation: a study of the U-937 cell line by ultrastructural cytochemistry and surface antigen analysis.

U-937 represents a well-established permanent human haematopoietic cell line, which exhibits characteristics of the monocyte/macrophage series. U-937 cells were investigated by peroxidase ultrastructural cytochemistry in order to determine the normal developmental stage to which they correspond. This study was performed in non- and TPA-stimulated cells, in conjunction with surface analysis by monoclonal antibodies. It is concluded: (1) peroxidase-positive U-937 cells are monoblasts and promonocytes involved in myeloperoxidase synthesis; (2) TPA-stimulation caricatures transformation of these cells into monocytes but not into resident macrophages, as far as peroxidase cytochemistry is concerned; (3) the reactivity of myeloperoxidase present in the endoplasmic reticulum of synthesizing cells is inhibited by glutaraldehyde fixation.

Antigens, Surface↗
PubMed1985

Presence of the Tn antigen on hematopoietic progenitors from patients with the Tn syndrome.

The Tn syndrome is an acquired clonal disorder characterized by the exposure of a normally hidden determinant, the Tn antigen, on the surface of human erythrocytes, platelets, granulocytes, and lymphocytes. Two distinct populations, Tn positive (Tn+) and Tn negative (Tn-), of mature hemopoietic cells are present in Tn patients. To determine whether the Tn antigen is already expressed on erythroid, myeloid, and pluripotent progenitors, light-density mononuclear blood cells from two patients with this syndrome were separated by fluorescent-activated cell sorting and by affinity chromatography into Tn+ and Tn- fractions, using their binding properties to Helix pomatia agglutinin (HPA). Burst-forming-unit erythroid (BFU-E), colony-forming-unit granulocyte/macrophage (CFU-GM), cells were assayed in plasma clot cultures. After 12-14 d of culture, colonies were studied by a double fluorescent labeling procedure. First, a fluorescein-conjugated HPA permitted evaluation of the presence or absence of the Tn antigen at the surface of the cells composing each colony, and second, the binding of a murine monoclonal antibody against either glycophorin A (LICR-LON-R10) or against a myeloid antigen (80H5), revealed by an indirect fluorescent procedure, was used to establish the erythroid or myeloid origin of each cell. The Tn+ fraction obtained by cell sorting gave rise to nearly 100% Tn+ colonies composed exclusively of cells bearing this antigen. The reverse was observed for the Tn- cell fraction. These results demonstrate that in the Tn syndrome, BFU-E, CFU-GM, and CFU-GEMM of the Tn+ clone express the Tn antigen at this early stage of differentiation.

Antigens, Neoplasm↗
PubMed1985

Expression of vimentin intermediate filament cytoskeleton in acute nonlymphoblastic leukemias.

Since vimentin intermediate filament (IF) expression in hemopoietic cells varies with the cell lineage as well as the state of differentiation of the cells, we studied the vimentin cytoskeleton by direct immunofluorescence and electron microscopy in 50 cases of acute nonlymphocytic leukemias. We found that malignant cells tend to reproduce the vimentin organization characteristic of their normal cellular counterpart. Thus, in M2 and M3 leukemias (French-American-British classification), vimentin was often reduced to a juxtanuclear bundle of filaments contrasting with the rich filamentous network expressed by M4 or M5 leukemias. In erythroblastic leukemias (M6) and megakaryoblastic leukemias, both identified by the expression of lineage-specific antigens, the absence of vimentin IFs could be correlated with the level of differentiation reached by the blasts. M1 leukemias displayed an abnormal pattern of vimentin organization with aggregated filaments giving a ring-like structure. However, no abnormality of the vimentin polypeptide could be detected by two-dimensional electrophoresis. These results show that the expression of the vimentin IF cytoskeleton may be a useful marker of differentiation in the study of leukemic cells.

Acute Disease↗
PubMed1984

Therapy-related leukemia associated with myelofibrosis. Blast cell characterization in six cases.

Six patients exhibiting severe pancytopenia or overt leukemia associated with myelofibrosis after chemotherapy for malignant disease have been investigated by immunologic techniques and ultrastructural cytochemistry. Initially, five patients displayed severe thrombocytopenia contrasting with mild neutropenia and anemia. Bone marrow biopsies showed a clear megakaryocytic proliferation and an excess of immature mononuclear cells. The demonstration of peroxidase activities at the ultrastructural level and immunofluorescence labeling with a panel of monoclonal antibodies, including an antiplatelet glycoprotein Ib and an antiglycoprotein IIb-IIIa complex, on blood or marrow cells, permitted identification of otherwise unidentifiable promegakaryoblastic proliferation. In two patients, the use of an immunoperoxidase technique with an antifactor VIII-R-Ag antibody has allowed direct confirmation of this diagnosis on bone marrow sections. This megakaryoblastic proliferation was not pure and was variably associated with blasts of other cell lines (erythroblasts or myeloblasts). Changes in the population of blasts were observed during evolution in two patients. The sixth patient had a mild thrombocytopenia associated with severe neutropenia and anemia. Bone marrow biopsy displayed a myelofibrosis and immature cells, without megakaryocytic proliferation. Ultrastructural study revealed a pure basophil-mast cell proliferation. In conclusion, in five of six patients with secondary acute leukemia associated with myelofibrosis, a proliferation of promegakaryoblasts was demonstrated using both immunofluorescent and ultrastructural cytochemical techniques.

Aged↗
PubMed1984

Expression of platelet membrane glycoproteins and alpha-granule proteins by a human erythroleukemia cell line (HEL).

We demonstrate that HEL, a human erythroleukemic cell line, has numerous megakaryocytic markers which were markedly enhanced following the addition of the inducers dimethyl sulfoxide or 12-O-tetradecanoylphorbol-13-acetate to the culture medium. Ultrastructural and cytochemical studies showed: (i) the presence of organelles morphologically resembling the platelet alpha-granules; and (ii) a peroxidase activity with the same characteristics as that specifically found in platelets. The platelet alpha-granule proteins (von Willebrand factor, platelet factor-4 and beta-thromboglobulin) were immunologically detected in the HEL cell cytoplasm and their amounts increased after induction. Of particular interest was the presence of platelet membrane proteins. A monoclonal antibody specific for glycoprotein Ib bound to HEL cells. Platelet membrane glycoproteins IIb and IIIa were identified on intact cells using specific antibodies in a binding assay or in cell lysates using either crossed immunoelectrophoresis or an immunoblotting procedure following SDS-polyacrylamide gel electrophoresis. Most HEL cells also expressed the platelet alloantigen PIA1. All of the platelet membrane proteins were present in higher amounts after induction. Glycophorin A, specific for the erythroid lineage, was also detected on HEL cells. Thus, while confirming the presence of erythroid markers, our studies provide evidence that the HEL cell line also expresses platelet antigens. As such, HEL cells represent a unique system with which to study the biosynthesis of platelet-specific proteins and glycoproteins.

Beta-Globulins↗
PubMed1984

A mature thymocyte-like phenotypic pattern on human cord circulating T-lymphoid cells.

Cord blood samples from healthy full-term newborns were tested with antimature and antiimmature lymphoid-cell monoclonal antibodies, as well as more traditional markers, in order to identify the phenotype of circulating precursor cells. The results demonstrated that human cord blood contains a lower number of OKT3+, E-rosetting mature T cells than adult blood, very high levels of OKT10+ cells, and few OKT9+, OKT8+ OKT3-, and OKT4+ OKT3- cells. Although the finding of OKT9+ and OKT10+ cord circulating cells could be indicative of cell activation, double marker studies in newborn blood pointed to phenotypically immature lymphoid subsets at different stages of maturation, according to Reinherz's hypothesis. In addition, the absence of nuclear Tdt-positive and hot-rosetting cells, together with the fact that most of these are OKT3+, OKT10+, OKT4+, or OKT8+ cells, suggests that the surface phenotype of newborn lymphocytes is similar to that of mature thymocytes.

Antibodies, Monoclonal↗
PubMed1984

K562 cells induced to differentiate by phorbol ester tumor promotors resist NK lysis.

The effect of various phorbols and phorbol diesters on the NK sensitivity of the human leukemic K562 cells was studied. A marked decrease in K562 cell susceptibility was achieved by culture in the presence of either 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or beta-phorbol-dibutyrate. The maximum protection against NK lysis was achieved when K562 cells were cultured in the presence of 160 nM TPA for 48 hr (mean percentage inhibition: 61% of specific lysis). As for untreated targets, the residual killing of K562 cells after TPA treatment was mediated through large granular lymphocytes (LGL). The experimental procedures required to achieve maximal NK protection with TPA resulted simultaneously in marked phenotypical changes in K562 cells: erythroid and early myeloid markers decreased, whereas the expression of megakaryocytic markers was increased as shown by staining with antiplatelet monoclonal antibodies and assessment of platelet peroxidase activity. Chemical phorbol analogs which were unable to induce K562 cell differentiation did not affect K562 cell sensitivity to NK lysis. De novo protein synthesis is involved in the TPA-induced NK resistance, since this effect was abolished by pretreatment of K562 cells with actinomycin D or cycloheximide. TPA has been previously demonstrated to reduce NK effector activity. In our data however, the observed TPA effects were not due to release of TPA acting on effector cells during the NK assay since TPA-treated K562 cell supernatants were unable to inhibit NK activity in control assays. Thus, TPA appears to decrease NK killing of malignant cells, both by depressing NK effector cells functions and by reducing the susceptibility to NK lysis of the target cells. In single-cell agarose assays, TPA-treated K562 cells demonstrated reduced NK-binding capacity and reduced sensitivity to lysis after binding. These defects could not be reversed by activation of the NK effector cells with interferon. The results here reported extend the previously suggested relations between the expression of NK-target structures and the differentiation stage of malignant cells.

Cell Differentiation↗
PubMed1984

Inhibition of transferring binding and iron uptake of hematopoietic cell lines by phorbol esters.

Phorbol esters inhibit cell growth and the binding of transferrin to receptors on K 562, HL 60 and U 937 human leukemic cell lines. Exposure of these cells to 12-0-tetradecanoyl phorbol-13-acetate (TPA) at 37 degrees C results in a 40% reduction of the specific binding of 125I-transferrin, which is apparent within 15 min. Half-maximal inhibition occurs at about 1 nM. Other tumor promoting phorbol esters also inhibit 125I-transferrin binding in a dose-dependent manner which parallels their known promoting activity in vivo. TPA reduces the number of transferrin receptors, and does not alter the degradation or the internalization of transferrin. In addition, TPA inhibits iron uptake by these cell lines. These effects are specific, since phorbol esters do not affect either cell growth or the binding of transferrin to Friend erythroleukemia cells and Raji cell line. On the basis of these findings it is suggested that the inhibition of transferrin binding may represent one of the mechanisms by which phorbol esters affect the growth and the differentiation of hematopoietic cell lines.

Biological Transport↗
PubMed1984

Immunological characterization of the leukemic megakaryocytic line at light and electron microscopic levels.

Twenty cases of leukemia involving platelet precursors have been identified by a panel of monoclonal and polyclonal antiplatelet antibodies and by the ultrastructural demonstration of platelet peroxidase (PPO). The two techniques were in close agreement both for identification and for the quantitation of the blast cells except in three cases where PPO was present in the absence of the immunological markers. The immunological appearance of the leukemic megakaryocytic precursors was identical to that of their normal counterparts; the cells were positive with J 15 (anti GP IIb-IIIa complex), C 17 (anti GP IIIa), J 2 (anti GP 26,000) AN 51 (anti GP Ib). A diffuse cytoplasmic labelling was observed with anti factor VIII vwF and anti platelet factor 4 (PF 4). In addition, the leukemic maturation was quite similar to normal megakaryocyte differentiation since in micromegakaryocytes the expression of Gp Ib was strong and an intense granular pattern of labelling with anti factor VIII vwF and anti PF 4 was observed. In no case was the leukemic megakaryocytic series labelled by anti-erythroid antibodies, anti myeloid antibodies or J 5, B 1, OKT 11 antibodies. Using ultrastructural immunoferritin with J 15 it was possible to demonstrate that labelling with this antibody only occurred on PPO-positive cells. Immunogold or peroxidase labelling with AN 51 at the EM level in cases of mixed leukemia showed that Gp Ib was absent from proerythroblasts and myeloblasts. Therefore, in no case were specific platelet markers expressed in the leukemias of other cell lineages.

Antibodies, Monoclonal↗