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7 results on '"MESH: Leukemia, Experimental"'

1. Murine APOBEC1 Is a Powerful Mutator of Retroviral and Cellular RNA In Vitro and In Vivo

Author

Denise Guetard, Marc Sitbon, Jean-Pierre Vartanian, Anne Keriel, Myrtille Renard, Simon Wain-Hobson, Vincent Petit, Rétrovirologie Moléculaire, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Institut de Génétique Moléculaire de Montpellier ( IGMM ), and Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS )

Subjects
Hypoxanthine Phosphoribosyltransferase, MESH : Molecular Sequence Data, MESH : RNA, Messenger, MESH : DNA, Complementary, MESH : NIH 3T3 Cells, viruses, Muscle Proteins, MESH: Base Sequence, Nucleic Acid Denaturation, MESH : Retroviridae Infections, MESH: Animals, Newborn, Mice, chemistry.chemical_compound, MESH : Hypoxanthine Phosphoribosyltransferase, Structural Biology, Murine leukemia virus, MESH : RNA, MESH: Animals, APOBEC Deaminases, MESH : Cytidine Deaminase, Gammaretrovirus, MESH : Muscle Proteins, 0303 health sciences, biology, Nucleotides, MESH : Animals, Newborn, 030302 biochemistry & molecular biology, MESH: Leukemia Virus, Murine, Cytidine, Cytidine deaminase, MESH: Apolipoproteins B, 3. Good health, Leukemia Virus, Murine, MESH: Retroviridae Infections, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, MESH : Mutation, MESH: Genome, Viral, MESH : Genome, Viral, MESH : Leukemia Virus, Murine, MESH : Nucleic Acid Denaturation, APOBEC, DNA, Complementary, MESH: Mutation, APOBEC-1 Deaminase, Molecular Sequence Data, MESH: Leukemia, Experimental, Genome, Viral, MESH: Nucleic Acid Denaturation, [ SDV.MP.VIR ] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, MESH: Muscle Proteins, 03 medical and health sciences, MESH: RNA, Cytidine Deaminase, MESH : Mice, MESH : RNA Editing, Animals, Humans, MESH: RNA Editing, RNA, Messenger, MESH: Mice, Molecular Biology, Apolipoproteins B, MESH: RNA, Messenger, MESH: Cytidine Deaminase, 030304 developmental biology, Messenger RNA, Leukemia, Experimental, MESH: Molecular Sequence Data, MESH: Humans, Base Sequence, APOBEC1, MESH : Humans, MESH: Tumor Virus Infections, RNA, MESH : Apolipoproteins B, MESH: DNA, Complementary, biology.organism_classification, MESH: Hypoxanthine Phosphoribosyltransferase, Molecular biology, MESH: Nucleotides, Tumor Virus Infections, Animals, Newborn, chemistry, Mutation, NIH 3T3 Cells, MESH : Nucleotides, MESH : Leukemia, Experimental, MESH : Base Sequence, MESH : Animals, RNA Editing, MESH : Tumor Virus Infections, Retroviridae Infections, MESH: NIH 3T3 Cells
Abstract

International audience; Mammalian APOBEC molecules comprise a large family of cytidine deaminases with specificity for RNA and single-stranded DNA (ssDNA). APOBEC1s are invariably highly specific and edit a single residue in a cellular mRNA, while the cellular targets for APOBEC3s are not clearly established, although they may curtail the transposition of some retrotransposons. Two of the seven member human APOBEC3 enzymes strongly restrict human immunodeficiency virus type 1 in vitro and in vivo. We show here that ssDNA hyperediting of an infectious exogenous gammaretrovirus, the Friend-murine leukemia virus, by murine APOBEC1 and APOBEC3 deaminases occurs in vitro. Murine APOBEC1 was able to hyperdeaminate cytidine residues in murine leukemia virus genomic RNA as well. Analysis of the edited sites shows that the deamination in vivo was due to mouse APOBEC1 rather than APOBEC3. Furthermore, murine APOBEC1 is able to hyperedit its primary substrate in vivo, the apolipoprotein B mRNA, and a variety of heterologous RNAs. In short, murine APOBEC1 is a hypermutator of both RNA and ssDNA in vivo, which could exert occasional side effects upon overexpression.

Published
2009

2. Effects of benzyl alcohol on transferrin and low density lipoprotein receptor mediated endocytosis in leukemic guinea pig B lymphocytes

Author

Jean Philippot, M. Vignes, Jacques Sainte-Marie, Michel Vidal, Alain Bienvenüe, Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM), Plasticité cérébrale (PC), Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Neurobiologie de l'audition-plasticité synaptique, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Lipoproteins, LDL, L2C cell, Biochemistry, chemistry.chemical_compound, 0302 clinical medicine, Structural Biology, Membrane fluidity, MESH: Animals, Inhibition, chemistry.chemical_classification, B-Lymphocytes, MESH: Iron, 0303 health sciences, Transferrin, Endocytosis, Lipoproteins, LDL, MESH: Benzyl Alcohols, Benzyl alcohol, 030220 oncology & carcinogenesis, MESH: Endocytosis, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH: Transferrin, MESH: Benzyl Compounds, Iron, Guinea Pigs, MESH: Leukemia, Experimental, Biophysics, Transferrin receptor, Biology, Receptor endocytosis, MESH: Guinea Pigs, Guinea pig, 03 medical and health sciences, MESH: B-Lymphocytes, Benzyl Compounds, Receptors, Transferrin, Genetics, Animals, Humans, MESH: Receptors, Transferrin, Molecular Biology, Benzyl Alcohols, 030304 developmental biology, Leukemia, Experimental, MESH: Humans, Cell Biology, Molecular biology, Receptors, LDL, chemistry, MESH: Receptors, LDL, LDL receptor, MESH: Benzyl Alcohol, Lipoprotein
Abstract

International audience; We demonstrated that benzyl alcohol, a neutral local anesthetic drug, inhibits the uptake and degradation of lowdensity lipoprotein and endocytosis of transferrin receptors of guinea pig leukemic B lymphocytes (L2C). This inhibition is very rapid, concentration dependant and reversible by simple washing. Membrane fluidity of the living cells is also modified.

Published
1990

3. A new model of pre-B acute lymphoblastic leukemia chemically induced in rats

Author

Michel Arock, Lionel Devevey, Philippe Helissey, Jean-Jacques Guillosson, Joëlle Nafziger, Pascale Chrétien, Natacha Bernard, Céline Jacquemont, Université Pierre et Marie Curie - Paris 6 (UPMC), Littoral, Environnement, Télédétection, Géomatique (LETG - Nantes), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-École pratique des hautes études (EPHE)-Université de Brest (UBO)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS)-Institut de Géographie et d'Aménagement (IGARUN), Université de Nantes (UN)-Université de Nantes (UN), Institut de Recherche en Electrotechnique et Electronique de Nantes Atlantique EA4642 (IREENA), Ecole Polytechnique de l'Université de Nantes (Polytech Nantes), Littoral, Environnement, Télédétection, Géomatique (LETG - Brest), Littoral, Environnement, Télédétection, Géomatique UMR 6554 (LETG), Normandie Université (NU)-Normandie Université (NU)-Université d'Angers (UA)-Université de Nantes (UN)-École pratique des hautes études (EPHE)-Université de Brest (UBO)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS)-Université de Caen Normandie (UNICAEN), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS), Unité sous contrat biologie environnementale, Institut National de la Recherche Agronomique (INRA)-Université de Franche-Comté (UFC), Epidémiologie, santé publique et développement, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de médecine interne, CHU Bordeaux [Bordeaux]-Hôpital Saint-André, Laboratoire de génie électrique de Paris (LGEP), Université Paris-Sud - Paris 11 (UP11)-Université Pierre et Marie Curie - Paris 6 (UPMC)-SUPELEC-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Biologie et de Pharmacologie Appliquée (LBPA), École normale supérieure - Cachan (ENS Cachan)-Centre National de la Recherche Scientifique (CNRS), Normandie Université (NU)-Normandie Université (NU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Brest (UBO)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS)-Institut de Géographie et d'Aménagement Régional de l'Université de Nantes (IGARUN), Institut Universitaire de Technologie Saint-Nazaire (IUT Saint-Nazaire), Université de Nantes (UN)-Université de Nantes (UN)-Ecole Polytechnique de l'Université de Nantes (EPUN), Université de Nantes (UN)-Institut Universitaire de Technologie - La Roche-sur-Yon (IUT La Roche-sur-Yon), Normandie Université (NU)-Normandie Université (NU)-Université d'Angers (UA)-École pratique des hautes études (EPHE), Université de Nantes (UN)-Université de Nantes (UN)-Université de Caen Normandie (UNICAEN), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Université Paris-Sud - Paris 11 (UP11)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Ecole Supérieure d'Electricité - SUPELEC (FRANCE)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université de Brest (UBO)-École pratique des hautes études (EPHE)-Université de Nantes (UN)-Université d'Angers (UA)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Université de Rennes 2 (UR2), and Normandie Université (NU)-Normandie Université (NU)

Subjects
Male, Cancer Research, Pathology, MESH: Carcinogens, Nitrosourea Compounds, 0302 clinical medicine, Immunophenotyping, hemic and lymphatic diseases, MESH: Animals, Gene Rearrangement, B-Lymphocyte, Gene Rearrangement, 0303 health sciences, Acute leukemia, Leukemia, MESH: Gene Rearrangement, B-Lymphocyte, B-Lymphocyte, Hematology, 3. Good health, medicine.anatomical_structure, 030220 oncology & carcinogenesis, MESH: Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.medical_specialty, MESH: Rats, MESH: Leukemia, Experimental, Pre-B Acute Lymphoblastic Leukemia, Biology, 03 medical and health sciences, Experimental, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, MESH: Nitrosourea Compounds, Genetics, medicine, Animals, B Acute Lymphoblastic Leukemia, Molecular Biology, 030304 developmental biology, Leukemia, Experimental, Cell Biology, Gene rearrangement, medicine.disease, MESH: Male, Rats, Transplantation, MESH: Karyotyping, Karyotyping, Carcinogens, Bone marrow, MESH: Neoplasm Transplantation, Neoplasm Transplantation
Abstract

OBJECTIVE: Although B acute lymphoblastic leukemia (B-ALL) is the most common leukemia among children, no chemically inducible model of this leukemia has yet been described in vivo. METHODS: Leukemia was chemically induced in male WKAH/Hkm rats by a nitrosourea derivative, N-butylnitrosourea (BNU), an alkylating agent, administered orally 5 days a week for 24 weeks. Development of leukemia was monitored by clinical observation, follow-up of blood parameters, and appearance of blast cells in peripheral blood samples. The phenotype of the leukemia was determined by cytological examination, cytochemical reactions, and by immunophenotyping of bone marrow cells using various markers. The feasibility of leukemia transplantation was investigated. Clonality and karyotype analyses were also performed. RESULTS: We observed the appearance of acute leukemia in 60% of the rats treated with BNU. Of these, 65% developed pre-B-ALL, which was serially transplantable to healthy WKAH/Hkm male rats. Karyotype analysis did not reveal clonal abnormalities. Clonality determined by immunoglobulin gene rearrangement sequencing disclosed that the pre-B-ALL were mostly oligoclonal. CONCLUSION: This new in vivo model of inducible pre-B-ALL might be useful for investigating the effects of co-initiating or promoting agents suspected to be involved in leukemia development, and for disclosing new molecular events leading to leukemogenic processes.

Published
2005

4. A retrovirus carrying the promyelocyte-retinoic acid receptor PML-RARalpha fusion gene transforms haematopoietic progenitors in vitro and induces acute leukaemias

Author

Catherine Lavau, Suk-Chul Bae, Anne Dejean, Madeleine Garcia, Jacques Samarut, Muriel Altabef, Centre National de la Recherche Scientifique (CNRS), École normale supérieure - Lyon (ENS Lyon), Recombinaison et Expression Génétique, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by grants from the Association pour la Recherche contre le Cancer (ARC), Region Rhone-Alpes and Ligue Departementale de l'Yonne contre le Cancer to J.S., and from ARC and EEC Biotech and Biomed programs to A.D. M.A. is the recipient of fellowships from the Ministere de la Recherche et de l'Enseignement Superieur and ARC., École normale supérieure de Lyon (ENS de Lyon), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Cheriet Rauline, Samia

Subjects
MESH: Neoplasm Proteins, MESH: Oncogenes, Receptors, Retinoic Acid, viruses, [SDV]Life Sciences [q-bio], MESH: Amino Acid Sequence, Promyelocytic Leukemia Protein, Translocation, Genetic, MESH: Hematopoietic Stem Cells, Fusion gene, 0302 clinical medicine, Retrovirus, MESH: Promyelocytic Leukemia Protein, MESH: Animals, 0303 health sciences, MESH: Retinoic Acid Receptor alpha, biology, leukaemic transformation, General Neuroscience, Retinoic Acid Receptor alpha, MESH: Bone Marrow Cells, MESH: Chickens, Nuclear Proteins, virus diseases, MESH: Transcription Factors, MESH: Translocation, Genetic, Cell biology, Neoplasm Proteins, [SDV] Life Sciences [q-bio], Haematopoiesis, Cell Transformation, Neoplastic, haematopoietic differentiation, 030220 oncology & carcinogenesis, Acute Disease, MESH: Acute Disease, Research Article, Recombinant Fusion Proteins, Molecular Sequence Data, MESH: Leukemia, Experimental, Bone Marrow Cells, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Promyelocytic leukemia protein, MESH: Recombinant Fusion Proteins, Animals, Humans, Point Mutation, MESH: Tumor Suppressor Proteins, Amino Acid Sequence, Molecular Biology, 030304 developmental biology, MESH: Point Mutation, MESH: Receptors, Retinoic Acid, Leukemia, Experimental, MESH: Humans, MESH: Molecular Sequence Data, General Immunology and Microbiology, Tumor Suppressor Proteins, Oncogenes, biology.organism_classification, Hematopoietic Stem Cells, Fusion protein, Molecular biology, Retinoic acid receptor, nuclear hormone receptor, Retinoic acid receptor alpha, MESH: Cell Transformation, Neoplastic, biology.protein, PML-RARa, Chickens, MESH: Nuclear Proteins, Promyelocyte, Transcription Factors
Abstract

International audience; The promyelocyte (PML)-retinoic acid receptor alpha (RARalpha) fusion gene results from a t(15;17) chromosome translocation in acute promyelocytic leukaemia. We have analysed the oncogenic potential of the human fusion PML-RARalpha product in chicken using retrovirus vectors. We show that PML-RARalpha transforms very early haematopoietic progenitor cells in vitro and induces acute leukaemias. Neither PML nor RARalpha domains alone achieve such a transformation. The PML-RARalpha viruses recovered from the transformed cells carry two point mutations in the PML domain, one of which alters both the pattern of intracellular localization of the fusion protein and its functional interference with AP-1, thus defining an essential domain in PML for oncogenic transformation.

Published
1996

5. Effect of pyridoxine on the inhibition by dexamethasone of murine erythroleukemia cell differentiation

Author

Howard Beverley Osborne, Laboratoire de Biologie Moléculaire et Cellulaire (ER199), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), and Osborne, Howard Beverley

Subjects
MESH: Cell Differentiation, Receptors, Steroid, medicine.medical_specialty, MESH: Receptors, Glucocorticoid, MESH: Pyridoxine, medicine.medical_treatment, Cellular differentiation, MESH: Leukemia, Experimental, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Dexamethasone, Cell Line, Hemoglobins, Mice, Receptors, Glucocorticoid, Glucocorticoid receptor, Internal medicine, medicine, Extracellular, Animals, MESH: Animals, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH: Mice, Molecular Biology, Leukemia, Experimental, MESH: Kinetics, Pyridoxine, Cell Differentiation, Cell Biology, MESH: Cell Line, Cell biology, Kinetics, Steroid hormone, MESH: Hemoglobins, Endocrinology, Cell culture, MESH: Dexamethasone, hormones, hormone substitutes, and hormone antagonists, Glucocorticoid, MESH: Receptors, Steroid, medicine.drug
Abstract

International audience; Glucocorticoids are known to inhibit the induced differentiation of murine erythroleukemia cells. I show here that the binding of glucocorticoid receptors to the intact nuclei of these cells is reduced by exogenous extracellular pyridoxine (1-4 mM). This reduction of glucocorticoid-receptor binding did not abrogate the inhibition by dexamethasone of the induced differentiation.

Published
1983

6. Comparison of dexamethasone binding and resistance to inhibition of induced differentiation in subclones of murine erythroleukemia cells

Author

H. Beverley Osborne, Osborne, Howard Beverley, Laboratoire de Biologie Moléculaire et Cellulaire (ER199), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Cell Differentiation, endocrine system, medicine.medical_specialty, MESH: Receptors, Glucocorticoid, MESH: Leukemia, Experimental, Drug Resistance, Biophysics, Chromosomal translocation, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Diamines, Biology, Biochemistry, Dexamethasone, Hexamethylene bisacetamide, Mice, Receptors, Glucocorticoid, Internal medicine, Acetamides, polycyclic compounds, medicine, Animals, MESH: Animals, Erythroleukemia cell, MESH: Mice, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Molecular Biology, ComputingMilieux_MISCELLANEOUS, Leukemia, Experimental, MESH: Clone Cells, Cell Differentiation, MESH: Diamines, Cell Biology, MESH: Acetamides, Molecular biology, Clone Cells, Chromatin, Endocrinology, Hormone receptor, MESH: Dexamethasone, Time course, MESH: Drug Resistance, Leukemia, Erythroblastic, Acute, MESH: Leukemia, Erythroblastic, Acute, hormones, hormone substitutes, and hormone antagonists, medicine.drug, Hormone
Abstract

Subclones of the murine erythroleukemia cell line DS 19 with different sensitivities towards inhibition by dexamethasone (DEX) of the hexamethylene bisacetamide induced differentiation have been obtained. Scatchard analysis of DEX binding to whole cells and the time course of DEX binding to nuclei show that resistance to inhibition of erythrodifferentiation by DEX is neither associated with a reduction in specific binding of the hormone nor in a lack of activation or translocation to the nuclei of hormone receptor complexes. Hence resistance in these subclones must result from a defect at an event after binding of hormone-receptor complexes to chromatin if inhibition of differentiation is mediated by these complexes.

Published
1981

7. Reactivation and dedifferentiation of differentiated murine erythroleukemic cell nuclei

Author

A.C. Bakke, John Yu, H. B. Osborne, Laboratoire de Biologie Moléculaire et Cellulaire (ER199), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Scripps Clinic and Research Foundation, Scripps Research Foundation, and Osborne, Howard Beverley

Subjects
MESH: Cell Differentiation, MESH: Cell Nucleus, Cancer Research, Thymidine kinase activity, Cellular differentiation, Cell, MESH: Leukemia, Experimental, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Hybrid Cells, Hexamethylene bisacetamide, Cell Line, Cell Fusion, chemistry.chemical_compound, Mice, medicine, Animals, MESH: Animals, Molecular Biology, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH: Mice, ComputingMilieux_MISCELLANEOUS, MESH: Bromodeoxyuridine, Cell Nucleus, Leukemia, Experimental, Cell growth, Cell Differentiation, Cell Biology, Cell biology, MESH: Cell Line, medicine.anatomical_structure, Biochemistry, chemistry, Bromodeoxyuridine, Cell culture, Thymidine kinase, MESH: Cell Fusion, MESH: Cell Division, MESH: Hybrid Cells, Cell Division, Developmental Biology
Abstract

A murine erythroleukemic cell line, 745 A4-TG, deficient in hypoxanthine-guanine-phosphoribosyl transferase, can be induced with 3 mM hexamethylene bisacetamide to yield at least 50% of cells undergoing irreversible erythroid differentiation and finally losing capacity for cell divisions. The effects of such induced differentiation of 745 A4-TG on its ability to form viable and proliferating hybrids when fused with 3T3 1T22 fibroblasts were investigated. We found that when the induced 745 A4-TG cells were used, more continuously proliferating hybrids were obtained than could be accounted for by the residual uninduced cells which remained in these induced preparations. This suggests that some of the induced 745 A4-TG cells, when fused with 3T3 1T22 reverted from the induced phenotype of a limited capacity for cell proliferation to an uninduced state of continuous proliferation. This observation was further confirmed with the use of fully differentiated 745 A4-TG cells, which were obtained after selection with a bromodeoxyuridine suicide treatment to eliminate the uninduced and the partially differentiated cells in the preparations. When these selected, fully differentiated cells, as characterized by their lack of proliferation capacity and thymidine kinase activity, were fused with 3T3 1T22 (also deficient in thymidine kinase), it was found that not only were viable hybrid colonies obtained in a selection medium, which precluded the proliferation of either parental cells, but these hybrids continued to proliferate for more than two months in selection medium. These data thus confirmed that some fully differentiated erythroleukemic nucleus components in the hybrids were reactivated to regain capacity for cell proliferation and to dedifferentiate to synthesize thymidine kinase for survival in the selection medium. The lack of hemoglobin synthesis by these hybrids also indicates dedifferention of these murine erythroleukemic components in the hybrids.

Published
1982

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