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J Breton-Gorius

Publications and source records attributed to J Breton-Gorius.

At least 73 records · Page 4Linked to original sources
PubMed1988

Prostaglandin D2 generation in mouse bone marrow-derived mast cells exposed to dexamethasone is associated with endogenous peroxidase activity.

The appearance of fixative-sensitive peroxidase activity in the nuclear envelope and endoplasmic reticulum of bone marrow-derived mast cells (BMMC) cultured in the presence of 1 microM dexamethasone (DM) for up to 14 days and its relationship with immunologic release of prostaglandin D2 (PGD2) by these cells were studied. Endogenous peroxidase activity, previously shown as a marker of arachidonic acid metabolism in various cell types, was visualized by cell incubation in 3,3' diaminobenzidine-containing solution before glutaraldehyde fixation. PGD2 release was induced by passive sensitization of BMMC with an optimal dose of monoclonal IgE and subsequent challenge with specific a antigen. We found that 4-week-old BMMC, used as the starting population of the present study, exhibited immature morphologic features, did not present peroxidase activity when cytochemically processed, and released minute amounts of PGD2 in response to IgE-dependent stimulation. When such BMMC were exposed to DM during 24 hours, they showed aldehyde-inhibited peroxidase activity in the perinuclear envelope and a few endoplasmic reticulum segments. As compared with untreated cells, 24-hour DM-exposed BMMC released higher amounts of PGD2 upon immunologic stimulation. After an additional 14-day period of DM exposure, an intense peroxidase activity was detected in the perinuclear envelope and the endoplasmic reticulum of BMMC, which, under immunologic stimulation, released as much as 42.4 +/- 14.7 ng of PGD2/1 x 10(6) cells. Aminotriazole (20 and 50 mM) extinguished both peroxidase activity and PGD2 release from BMMC whereas indomethacin (1 microM) suppressed PGD2 production, but did not alter endogenous peroxidase activity. Previous cell fixation with glutaraldehyde totally inhibited endogenous peroxidase reaction in DM-exposed BMMC. Moreover, 14-day DM-exposed BMMC exhibited morphologic characteristics of mature mast cells and possessed alcian blue+/safranin+ granules. Therefore, the present data suggest that appearance of peroxidase activity in the nuclear envelope and the endoplasmic reticulum of DM-exposed BMMC is associated with the ability of the cells to synthetize PGD2 and appears as a cytochemical marker of the in vitro maturation of mouse bone marrow-derived mast cells.

Aldehydes↗
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↗
PubMed1988

In vitro inhibition of normal human hematopoiesis by marrow CD3+, CD8+, HLA-DR+, HNK1+ lymphocytes.

We previously demonstrated that after allogeneic bone marrow transplantation (BMT) a subset of CD8, HNK1, and DR-positive T lymphocytes are able to inhibit CFU-GM and BFU-E growth with an HLA-DR restriction. In this study we investigated whether these cells, present in normal marrow in low concentration (less than 1%), play the same role. HNK1-positive sorted marrow cells forming rosettes (E+C) were able to inhibit BFU-E and CFU-GM growth when added back to the marrow E-C at a ratio of 1:10 (HNK1+ E+C/E-C) in a range from 40% to 60%. This inhibitory effect was also detected for a cellular ratio of 1:100, which is the normal marrow value for this subset of T cell. HNK1+ DR+-sorted E+C after double-immunofluorescent labeling also showed the same inhibitory activity as the HNK1+ E+C, whereas the negative fraction including all the other E+C had no detectable inhibitory activity. CD3 and CD8 antigens were also present on the membrane of these cells, as demonstrated in two cases by double-immunofluorescent labeling performed with anti-CD3 or anti-CD8 monoclonal antibodies (MoAbs) and HNK1 MoAb, respectively, and subsequent cell sorting. Blocking experiments, performed by adding in culture anti-CD4 and anti-CD8 MoAbs to HNK1+ T cells showed that only the last MoAb was able to prevent inhibition of hematopoietic colony growth. These results confirmed that one subset of CD3+, CD8+, HNK1+, and DR+ T cells was responsible for in vitro inhibition of normal hematopoiesis. In addition, this inhibition was genetically restricted to HLA-class II antigens, since in three co-culture experiments with unrelated bone marrow cells inhibition occurred only when cells with one haplo-identical HLA-DR antigen was added back to the culture. Indeed, this effect was really HLA-DR restricted, since in blocking experiments with different anti-HLA class II MoAbs (anti-DR, anti-DP, and anti-DQ MoAbs) only an anti-HLA-DR MoAb was able to prevent the colony growth inhibition by CD3+ HNK1+, or CD8+ HNK1+ E+C. In conclusion, the CD3+, HNK1+, CD8+, DR+ cells may be the T-cell subset able to inhibit normal hematopoiesis with an HLA-DR restriction.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

Ultrastructural demonstration of tubular inclusions coinciding with von Willebrand factor in pig megakaryocytes.

The appearance of von Willebrand factor (vWF) in bone marrow megakaryocytes was studied by standard electron microscopy (EM) and immuno-EM using an original purification technique. Eighty percent pure megakaryocytes were isolated from porcine rib bone marrow using Percoll gradients followed by counterflow centrifugation. Activation was prevented by prostacyclin and prefixation with low concentrations of glutaraldehyde. In early megakaryoblasts, standard EM revealed the presence of tubular structures in the small vesicles located in the Golgi area, in the small immature alpha-granules and in the rare mature alpha-granules. Immunolabeling for vWF was simultaneously observed in small vesicles and small alpha-granules, mainly in the Golgi zone. In mature megakaryocytes, standard EM showed that tubular structures were numerous, regularly spaced, and aligned in parallel. Immunolabeling for vWF was intense, restricted to the alpha-granules, and distributed in a similar manner to porcine platelets. Gold particles were located eccentrically at one pole of the alpha-granule, labeling only its periphery or outlining one side of an elongated granule. Tubule profiles could be seen underlying the immunolabeling and were usually located at one side of the granule. In conclusion, this study demonstrates the presence of tubular structures in megakaryocyte alpha-granules, their association with vWF, and the appearance of both in the Golgi-associated vesicles.

Animals↗
PubMed1987

Biosynthesis of major platelet proteins in human blood platelets.

We studied de novo protein biosynthesis in platelets of normal adult donors and in newly formed platelets isolated from splenectomized patients with idiopathic thrombocytopenic purpura (ITP). After metabolic labelling of platelet proteins, performed with different radiolabelled amino acids or carbohydrates, a tenfold increase in incorporation of radioactivity into trichloroacetic-acid-precipitable material was obtained with ITP platelets compared to control platelets. Electron microscopic studies of ITP platelets revealed the presence of rough endoplasmic reticulum and polyribosomes, providing morphological evidence for protein synthesis. SDS-PAGE of radiolabelled ITP platelet proteins followed by autoradiography showed that [35S]methionine and [3H]leucine were incorporated into almost all Coomassie-blue-stained proteins whereas [3H]carbohydrates only labelled a few bands. Using crossed-immunoelectrophoresis we identified some of the labelled platelet compounds and demonstrated that major membrane glycoproteins (GPIb, IIb, IIIa) and alpha-granule proteins, such as fibrinogen, thrombospondin, albumin and von Willebrand factor, were synthesized in newly formed circulating platelets.

Adult↗
PubMed1987

Ultrastructural localization of lysozyme in human neutrophils by immunogold.

The subcellular localization of lysozyme (LZ) has been investigated by immunogold electron microscopic cytochemistry in human neutrophils from bone marrow and blood. Intact cells or subcellular granule fractions were fixed in glutaraldehyde and embedded in glycol methacrylate. Thin sections were incubated with monospecific antibodies followed by antiglobulins coupled to colloidal gold. LZ was detected within both elliptical and spherical primary granules in bone marrow neutrophil promyelocytes. In myelocytes and more mature neutrophils immunolabeling for LZ was observed within the primary granules, although fainter than in promyelocytes. However secondary granules from bone marrow and blood neutrophils were not consistently labeled by gold particles. Immunogold staining was then performed on sections of subcellular fractions of secondary granules: immunogold staining of lactoferrin demonstrated 95% of secondary granules in this fraction. Labeling for LZ of this granule fraction was intense, and except that the few primary granules were also labeled, looked similar to that of lactoferrin. In conclusion, this study is the first to utilize electron microscopic cytochemistry to show that LZ is present in both the primary and secondary granules of blood and bone marrow neutrophils. This technique has the advantage of allowing LZ distribution to be studied within a single organelle and/or in relation to the rest of the cell structure.

Bone Marrow↗
PubMed1987

Detection of cells of megakaryocyte lineage in haematological malignancies by immuno-alkaline phosphatase labelling cell smears with a panel of monoclonal antibodies.

Immuno-alkaline phosphatase staining (by the APAAP technique) has been used to identify promegakaryoblasts in cell smears from 10 cases of leukaemia (three acute leukaemia, seven blast transformations). In all cases promegakaryoblasts were labelled by at least two anti-platelet glycoprotein (gp) antibodies, the highest percentages being obtained with anti-gp IIIa (antibody C17). HLA-DR was expressed by a variable percentage of neoplastic cells in all cases, the T11 (CD2) antigen (sheep red cell receptor) in four of seven cases tested and the p150,95 antigen in three of the six cases tested. In some cases of acute myeloid leukaemia APAAP staining of blood smears revealed circulating promegakaryoblasts and micromegakaryocytes (which superficially resemble small lymphoid cells). It is concluded that immuno-alkaline phosphatase staining of cell smears offers a convenient means of diagnosing acute megakaryoblastic leukaemia in the routine laboratory.

Acute Disease↗
PubMed1987

Characterization of the blast cell population in two neonates with Down's syndrome and transient myeloproliferative disorder.

The phenotype and in vitro growth properties of blood and marrow blast cells detected in two neonates with Down's syndrome and a transient leukaemic picture are presented. In both patients, blast cells at diagnosis were heterogeneous and expressed predominantly megakaryocyte and erythroid markers identified by membrane fluorescence using monoclonal antibodies or ultrastructural detection of platelet peroxidase and ferritin. An additional trisomy involving chromosome 22 was detected in blast cells from one patient. Blood and marrow cells colony-assays performed at diagnosis revealed precursors with an abnormal differentiation capacity similar to those found in acute myelogenous leukaemia colony assays. However, an unusual feature was the persistence of high numbers of precursor cells (namely erythroid) following a normal differentiation pathway. Phenotypically and cytogenetically abnormal cells spontaneously disappeared by week 4-6, but overt relapse occurred in one patient 20 months later. These results bring strong arguments in favour of the neoplastic nature of the transient leukaemic picture observed in some neonates with Down's syndrome. Furthermore, we suggest that this disorder can be individualized as a separate entity with specific phenotypic and biological properties.

Bone Marrow↗
PubMed1987

In vitro inhibition of hematopoiesis by HNK1, DR-positive T cells and monocytes after allogeneic bone marrow transplantation.

Blood CFU-GM and BFU-E, grown from 17 patients who had undergone allogeneic bone marrow transplantation (BMT), were studied by the plasma-clot technique before day 45, and at a time when their blood count was approximately normal. The number of colonies varied from one patient to another, but was always lower than in normal subjects. Removal of cells forming rosettes with sheep erythrocytes (E+C) increased colony growth in four out of eight cases, whereas removal of adherent cells (AC) had the same effect in five out of six cases. Addition of E+C or AC after their initial removal restored the inhibition of colony growth. This suppression was noted at a 1:1 to 8:1 cellular ratio and ranged from 25% to 75%. The phenotype of the suppressive cells was further characterized by complement-mediated lysis with monoclonal antibodies (MoAbs) and fluorescent labeling. Two types of cells associated with inhibition of colony growth were identified: the first were E+C positive, characterized by the T3, HNK1, DR, and T8 determinants; the second were identified by the MO2 MoAb, indicating their monocytic origin, together with their properties of adherence. Similar suppressor cells of CFU-GM were found in the marrow of two other allogeneic BMT patients. A direct suppressive effect of the two types of cells was demonstrated in one experiment when MO2+ and/or HNK1+ cells collected by cell sorting were added back to cultures depleted in MO2+ and HNK1+ cells by complement-mediated lysis and were both found to decrease colony growth. Purified HNK1+ cells led to moderate inhibition of colony growth, which was not enhanced by increasing their concentration. This suppressive effect of hematopoiesis could be the consequence of an allogeneic reaction, since no inhibition was affected by T cells or monocytes in seven autologous BMTs and one syngeneic BMT.

Adolescent↗
PubMed1987

Ultrastructural and cytochemical characterization of blasts from early erythroblastic leukemias.

Among nine cases of early erythroblastic leukemia previously diagnosed using a panel of antibodies, two patients have erythroid blasts expressing glycophorin A, seven patients have blasts with a more immature phenotype. These immature blasts were labeled by the FA6-152 monoclonal antibody when studied with the immunogold technique. The blasts exhibited large nucleoli, and their cytoplasm contained numerous ribosomes and large mitochondria. In the Golgi apparatus several granules resembled the theta granules as previously described and contained ferritin molecules in the absence of rhopheocytosis. A large proportion of these blasts exhibited a platelet peroxidase (PPO)-like activity. As the blasts from the two other patients with a more mature phenotype and glycophorin A reactivity lacked this PPO, this enzyme seems to be restricted to the more immature cells. Since in these leukemic samples immature erythroid blasts were admixed to promegakaryoblasts, immunogold labeling was also performed with antiplatelet antibodies. This latter population which was labeled with C17, a monoclonal antibody to platelet glycoprotein IIIa, showed strong PPO activity but lacked theta granules and ferritin. In the normal bone marrow enriched by panning for CFU-E (8%) and depleted in progenitors of other lineages, blast cells showing characteristics similar to leukemic erythroid blasts were seen. They exhibited theta granules and ferritin and a proportion of them also had a PPO-like activity. Thus, a PPO reaction is not restricted to the platelet-megakaryocyte line. In conclusion, a PPO-like activity and ferritin molecules were present in immature leukemic erythroid blasts. Similar cells could be identified from normal bone marrow.

Antibodies, Monoclonal↗
PubMed1987

Effects of granulocyte-macrophage colony-stimulating factor and erythropoietin on leukemic erythroid colony formation in human early erythroblastic leukemias.

Erythroid colonies from five patients with an early erythroblastic leukemia were obtained in "serum-free" cultures in the presence or absence of recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) and homogeneous native erythropoietin (Epo). Erythroid colonies with abnormal morphology and karyotype could be grown in different culture conditions. Their erythroid nature was ascertained by the presence of carbonic anhydrase I and glycophorin A. Leukemic erythroid progenitors strongly differed from normal progenitors in that spontaneous colonies were always obtained, sometimes with an extremely high plating efficiency (up to 5.7%). Colonies were found to be autonomous from exogenous hematopoietic growth factors because they were still obtained with a high plating efficiency at an average of one cell per culture in the absence of any added growth factor. No evidence for an autocrine secretion of Epo or GM-CSF emerged because Epo or GM-CSF could not be detected by biologic or radioimmunologic assays from the culture supernatant or cellular extracts of the leukemic cells and that Epo or GM-CSF antibodies did not block autonomous growth. In all cases, however, hematopoietic growth factors increased the plating efficiency of the abnormal erythroid progenitors. In the two "de novo" leukemias, leukemic erythroid progenitors responded primarily to Epo, whereas in the three other patients' (chronic myeloid leukemia) blast crisis they responded maximally to GM-CSF plus Epo. Recombinant erythroid-potentiating activity had no effect in any of these cases. These results suggest that the leukemic erythroid clonogenic cells arise from expansion of erythroid progenitors at different levels of differentiation (ie, CFU-E or BFU-E, depending upon the disease) and that autonomous growth is not related to a secretion of Epo or GM-CSF.

Cell Cycle↗
PubMed1987

Expression of blood group A antigen during erythroid differentiation in A1 and A2 subjects.

The expression of blood group A antigen on marrow and blood cells from A1 and A2 subjects was investigated by the binding of Helix pomatia and Dolichos biflorus lectins using immunofluorescence. These two lectins stained BFU-E-derived colonies from A subjects in the early days of culture before the expression of glycophorin. The erythroid origin of these cells was ascertained by the coexpression of two other very early erythroid markers. In bone marrow, the ultrastructural immunogold method revealed that the entire erythroid lineage including proerythroblasts was labeled by HPA, whereas no staining was observed on granulomonocytic cells including myeloblasts. Platelets from A subjects were HPA-labeled and so were platelets from an O subject preincubated in A plasma. Megakaryocytes obtained in CFU-MK-derived colonies were weakly and heterogeneously labeled by the HPA lectin. Cultures from A1 and A2 subjects were the reflection of the genetic differences only when investigations were performed on mature erythroblasts. In contrast, the great majority of immature erythroblasts both from A2 and A1 subjects were equally labeled by both lectins; during further erythroid maturation, binding of both lectins markedly diminished only on A2 erythroblasts. When marrow erythroblasts were investigated at electron microscopic level, heterogeneity of labeling among all stages of maturation was clearly observed in A2 subjects, with staining stronger on immature than on mature erythroblasts. Therefore, the genetic differences between A1 and A2 subjects are revealed during terminal erythroid differentiation.

ABO Blood-Group System↗
PubMed1987

Monoclonal antibodies specific for human platelet membrane glycoproteins bind to monocytes by focal absorption of platelet membrane fragments: an ultrastructural immunogold study.

The membrane labeling of monocytes by monoclonal antibodies directed against platelet glycoproteins Ib (AN51), IIb (Tab), IIIa (C17), IIb-IIIa complex (J15) and to antigens common to platelets and monocytes (anti-monocyte platelet antigen and FA6 152) has been investigated by an ultrastructural immunogold method. Only with FA6 152, which identifies a structure shared by erythroblasts, platelets, and monocytes, was labeling obtained on membranes of both platelets and monocytes from normal blood. With all the other monoclonal antibodies, platelets were highly labeled but monocytes lacked quantitatively significant label; however, focal microparticles which exhibited gold particles were adherent to the membrane of monocytes. This localized labeling, interpreted as resulting from the fragmentation of platelet membranes during monocyte isolation with adhesion of the fragments to monocyte surfaces, was verified by two approaches. First, double staining with C17 visualized by an anti-IgG coupled to 40 nm gold particles and MO2 recognizing exclusively a surface monocyte antigen, as visualized by an anti-IgG coupled to 15 nm gold particles, was performed. The absence of colocalization of large and small gold particles either on monocytes or on microparticles confirmed the exclusive cell origin. Second, when analyzed by quantitative x-ray analysis, monocyte associated gold following C17 treatment was restricted to platelet pseudopods and fragments on whole mount spread cells. Finally, when monocytes were spread immediately after blood collection in the absence of sedimentation and centrifugation to prevent platelet activation, platelet rosetting was avoided and the number of microparticles markedly decreased. Thus, the attachment to monocyte membranes of microparticles originating from platelets may be confused with true labeling of monocytes by antibodies to platelet glycoproteins if analysis is limited to immunofluorescence.

Adsorption↗
PubMed1986

Expression of platelet glycoprotein Ib alpha in HEL cells.

We have previously shown that platelet glycoprotein Ib is expressed in a minority of cells of the human leukemic cell line HEL (Tabilio, A., Rosa, J. P., Testa, U., Kieffer, N., Nurden, A. T., Del Canizo, M. C., Breton-Gorius, J., and Vainchenker, W. (1984) EMBO J. 3, 453-459). In this report, we have selected a stable HEL subclone with increased expression of glycoprotein (GP) Ib as assessed by 6 different monoclonal antibodies in order to investigate the biochemical characteristics of this glycoprotein. A single polypeptide chain of apparent Mr = 60,000 was precipitated under reducing and nonreducing conditions by a specific polyclonal anti-platelet glycocalicin antibody and two anti-GPIb alpha monoclonal antibodies (AN51 and AP1), both from surface-labeled and metabolically labeled HEL cells. We were unable to demonstrate the presence of a polypeptide corresponding to the beta subunit of GPIb or GPIX which is closely associated with GPIb. Competitive immunoprecipitation performed in the presence of an excess amount of cold platelet glycocalicin completely displaced the Mr = 60,000 polypeptide. Synthesis of N-linked oligosaccharide chains on this Mr = 60,000 polypeptide was inhibited by the antibiotic tunicamycin, and a shift of the apparent Mr from 60,000 to 48,000 was observed. O-Linked oligosaccharide chains identical to platelet GPIb hexasaccharides were deficient or incomplete since no peanut agglutinin binding to the Mr = 60,000 polypeptide was observed after neuraminidase treatment of HEL cells. Thus, our results provide evidence that the Mr = 60,000 polypeptide expressed on the surface membrane of HEL cells is closely related to platelet GPIb and corresponds to an incompletely or abnormally O-glycosylated GPIb alpha subunit.

Asialoglycoproteins↗
PubMed1986

HLA-DR restriction in suppression of hematopoiesis by T cells from allogeneic bone marrow transplants.

Three allogeneic bone marrow transplantation patients who exhibited a suppressive subset of T cells for in vitro hematopoiesis have been investigated to determine whether this T cell suppressive effect was genetically restricted. In the three cases, T cells separated by sheep red cell rosetting inhibited blood colony-forming units granulocyte-monocyte (CFU-GM) and burst-forming unit erythroid (BFU-E) growth from the patients and from the bone marrow donors who were HLA identical, but not from randomly chosen unrelated subjects. In one case, cocultures were performed between the patient T cells and the T-depleted cells from eight siblings and from the mother. A marked inhibition (30 to 60%) of CFU-GM and BFU-E growth was found in the relatives who shared a haplo-identical HLA-DR 5. The same degree of suppression was found with respect to whether the siblings were homozygous or heterozygous for the HLA-DR 5 antigen, and whether or not they shared common class I antigens. This inhibition was totally abolished when a monoclonal antibody against HLA-DR was added, whereas a monoclonal antibody against class I histocompatibility antigen had no effect. To additionally demonstrate that this inhibition was mediated by a single HLA-DR haplotype, T cells from the patient were co-cultured with cells from three normal unrelated individuals, one with a phenotypically identical DR and two with only one haploidentical DR. Inhibition was similarly found in the subject exhibiting complete DR identity, and the subject with only the DR 5 haploidentical phenotype. These results demonstrate that a unique subset of T cells present in allogeneic bone marrow transplants specifically suppress differentiation of hemopoietic progenitors that bear one phenotypically haplo-identical HLA-DR antigen.

Adult↗
PubMed1986

Phenotype of early erythroblastic leukemias.

Nine cases of early erythroblastic leukemia, unidentified by usual criteria, have been diagnosed using a panel of antibodies. Three cases arose in patients with Down's syndrome, one in a patient with therapy-related leukemia, and four patients were in blast crisis of chronic myeloid leukemia; only one case arose de novo. Blast cells could be assigned to two main stages of erythroid differentiation: presence of all erythroid-specific proteins in two patients, a phenotype corresponding to an immature erythroblast; absence of the erythroid markers such as glycophorin A and spectrin in the presence of carbonic anhydrase isoenzyme I, ABH group antigens, and the antigen defined by FA6 152 monoclonal antibody in six patients, a phenotype related to a late erythroid progenitor (CFU-E). One patient had an intermediate phenotype. All patients except one demonstrated a megakaryocytic component. In three patients, chromosomal abnormalities were present, detected both in blasts and in erythroid colonies. In conclusion, these findings indicate that most "cryptic erythroleukemias" are blocked at a "CFU-E-like" stage of differentiation, it may be a frequent event in Down's syndrome and chronic myeloid leukemia, and these erythroleukemias are phenotypically heterogeneous.

Acetylcholinesterase↗