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1.
Science ; 162(3858): 1132-4, 1968 Dec 06.
Article in English | MEDLINE | ID: mdl-5698854

ABSTRACT

Direct in vivo estimates of DNA synthesis time in early and late erythroblasts were obtained by using the H(3)- and C(14)-thymidine double-la-beling technique. A double-emulsion autoradiographic procedure was used to resolve the two isotopes. Early erythroblasts were found to proliferate at a rate about five times that of late cells. This results primarily from a shorter mean DNA synthesis time in early cells (2.5 hours) than in late cells (6.5 hours).


Subject(s)
Bone Marrow Cells , Cell Division , DNA/biosynthesis , Erythrocytes , Erythropoiesis , Animals , Autoradiography , Carbon Isotopes , Male , Models, Biological , Rats , Thymidine/metabolism , Time Factors , Tritium
2.
J Natl Cancer Inst ; 55(5): 1123-7, 1975 Nov.
Article in English | MEDLINE | ID: mdl-1107569

ABSTRACT

To understand further the hematopoietic dyscrasias induced by a variant (a) of Rauscher leukemia virus (RLV), we used Escherichia coli endotoxin to stress the hematopoietic system of control and RLV/a-infected BALB/c mice. During the preleukemic stages of virus infection, there was slight splenomegaly without peripheral blood erythroblastosis. Granulocyte release and tissue mobilization mechanisms appeared unaffected by the RLV/a infection. Both RLV/a-infected and control mice reacted to endotoxin with peripheral granulocytosis and peritoneal granulocyte mobilization, though the circulating granulocyte levels in RLV/a-treated mice initially were lower than those in controls. Spleen of RLV/a-infected animals were larger than those of controls, but both responded to endotoxin with elevated numbers of granulocytes and erythroblasts. Since numbers of bone marrow erythroblasts in both groups of mice were decreased after endotoxin, stem cell competition and/or shunting of stem cells from marrow to spleen may have been involved. Endotoxin also induced rapid falls in hematocrit levels in both groups. These studies suggested that RLV/a-infected mice can be a model to study 1) erythropoietic dysfunction uncomplicated by defective granulopoietic release and tissue mobilization control mechanisms, and 2) progression of evolving granulocytic leukemia.


Subject(s)
Anemia/etiology , Granulocytes , Hematopoiesis , Leukocytes , Rauscher Virus , Anemia/blood , Animals , Bone Marrow Cells , Endotoxins/pharmacology , Erythropoiesis , Escherichia coli , Hematocrit , Mice , Mice, Inbred BALB C , Splenomegaly/etiology , Tumor Virus Infections/blood
3.
J Natl Cancer Inst ; 55(5): 1171-5, 1975 Nov.
Article in English | MEDLINE | ID: mdl-1206743

ABSTRACT

The function of phenylhydrazine (PHZ) hemolysis in ameliorating the anemia induced in mice by a slow-acting strain of Rauscher leukemia virus (RLV-A) was described. After cessation of treatment with PHZ, mid-stage RLV-A-infected, anemic mice responded with massive reticulocytoses and a rebound in hematocrit above control levels. RLV-infected mice, subjected to PHZ-induced hemolysis or phlebotomy, produced high levels of plasma erythropoietin (Ep); this suggested that Ep mediated the PHZ-induced differentiation. In addition, administration of exogenous Ep induced a wave of erythroid maturation in RLV-infected anemic mice, which indicated that virus-infected erythroid precursors could still respond to the hormone governing normal differentiation.


Subject(s)
Anemia/etiology , Cell Differentiation/drug effects , Erythropoiesis , Phenylhydrazines/pharmacology , Rauscher Virus , Anemia/blood , Anemia/physiopathology , Animals , Erythropoiesis/drug effects , Erythropoietin/blood , Erythropoietin/pharmacology , Female , Hematocrit , Hemorrhage/blood , Male , Mice , Mice, Inbred BALB C , Reticulocytes , Spleen/physiology , Splenectomy
4.
Biochim Biophys Acta ; 672(2): 176-90, 1981 Jan 21.
Article in English | MEDLINE | ID: mdl-6971652

ABSTRACT

Leukemia-associated inhibitory activity suppresses colony and cluster formation in vitro cells derived from granulocyte-macrophage progenitor cells of normal donors. It does not inhibit these same progenitor cells from patients with leukemia and it may contribute to the proliferative advantage leukemia cells appear to possess over normal hematopoietic cells during acute leukemia. The inhibitory activity was isolated by a combination of procedures including: ultracentrifugation, Sephadex G-200, carboxymethylcellulose, SDS-polyacrylamide gel electrophoresis, thin-layer and preparative isoelectric focusing and concanavalin A-Sepharose. Leukemia-associated inhibitory activity was characterized as a glycoprotein. it was inactivated by trypsin, chymotrypsin, pronase and periodate treatment. It bound to and was eluted by alpha-methylmannose from concanavalin A-Sepharose columns and had an apparent Mr range of 450-550 000 and an isoelectric focus value between pH 4.6 and 4.9. Crude leukemia associated inhibitory activity was temperature sensitive but the more purified preparations were heat stable.


Subject(s)
Colony-Stimulating Factors/antagonists & inhibitors , Ferritins , Granulocytes/analysis , Cell Aggregation/drug effects , Chromatography, Gel , Chromatography, Ion Exchange , Colony-Stimulating Factors/isolation & purification , Colony-Stimulating Factors/pharmacology , Humans , Isoelectric Point , Methylmannosides/metabolism , Molecular Weight
5.
Exp Hematol ; 13(8): 719-21, 1985 Sep.
Article in English | MEDLINE | ID: mdl-4043257

ABSTRACT

In vitro erythropoiesis by bone marrow and spleen cells was assessed in normal mice and during progression of Rauscher leukemia virus, variant-A (RLV-A) disease in mice. As RLV-A disease progressed from early through terminal stages, there was a marked increase in the numbers of in vitro splenic CFU-E and BFU-E. Conversely, bone marrow CFU-E and BFU-E demonstrated a concomitant decrease in numbers with disease progression. At no time were erythropoietin-independent (endogenous) erythroid colonies generated. The results suggest that compartmental alterations in erythroid precursors occur during progression of RLV-A.


Subject(s)
Erythrocytes/pathology , Erythropoiesis , Leukemia, Experimental/pathology , Stem Cells/pathology , Animals , Bone Marrow/pathology , Colony-Forming Units Assay , Leukemia, Experimental/blood , Leukemia, Experimental/physiopathology , Male , Mice , Mice, Inbred BALB C , Rauscher Virus , Spleen/pathology
6.
Exp Hematol ; 6(1): 91-5, 1978 Jan.
Article in English | MEDLINE | ID: mdl-272289

ABSTRACT

Erythropoietin (Ep) levels were measured in Shay chloroleukemic rats at various stages of anemia. Serum Ep was shown to increase logarithmically as the anemia became more severe. This increase in Ep levels was similar to that observed in normal rats subjected to acute blood loss. Significant levels of Ep were also demonstrated in ascitic fluid extracted from the peritoneal cavity of leukemic rats. These results indicate that the anemia of this disease is not due to a diminished production of Ep.


Subject(s)
Erythropoietin/blood , Leukemia, Myeloid/blood , Anemia/blood , Animals , Ascitic Fluid/analysis , Erythropoietin/analysis , Leukemia, Experimental/blood , Male , Rats
7.
Exp Hematol ; 8(3): 327-38, 1980 Mar.
Article in English | MEDLINE | ID: mdl-6936261

ABSTRACT

The pathogenesis of the anemia which occurs in rats bearing the Shay chloroleukemia (SCL) was investigated. Severe anemia, shown not to result from hemodilution, developed in the terminal stage of the disease. The rapid progression of the anemia suggested that reduced erythropoiesis was of no more than minor importance in the development of this anomaly. No evidence for a major hemolytic event was observed. Data are presented which suggest that hemostatic defects may be primarily responsible for the anemia of SCL. Because of many similarities with the pathogenesis of human myelogenous leukemia, SCL is proposed as a useful model for further studies on interreactions between the leukemic environment and the erythrocyte population.


Subject(s)
Anemia/complications , Leukemia, Myeloid/complications , Animals , Bilirubin/blood , Blood Volume , Erythrocytes , Hematocrit , Iron/blood , Leukemia, Myeloid/blood , Leukemia, Myeloid/etiology , Male , Rats , Reticulocytes , Spleen/pathology , Splenectomy
8.
Ann N Y Acad Sci ; 554: 88-115, 1989.
Article in English | MEDLINE | ID: mdl-2735654

ABSTRACT

Infection of BALB/c mice with the RLV-A virus typically results in an erythropoietic dysplasia characterized by hepatosplenomegaly, erythroblastosis, erythroblastemia and severe anemia without reticulocytosis. Mice hypertransfused weekly with 75%-packed red cells for 42 days prior to RLV-A infection and viral potency controls manifested this typical RLV-A response. Mice that were hypertransfused prior to and following RLV-A infection never developed the "typical" RLV-A pathogenesis. Instead, a transplantable myeloid leukemia was established. Although the reason for altered pathogenesis remains uncertain, it seems plausible that continued hypertransfusion, presumably after establishment of an altered granulopoietic microenvironment, resulted in a completely different viral expression and development of the transplantable myeloid leukemia.


Subject(s)
Hematopoiesis , Leukemia, Experimental/etiology , Leukemia, Myeloid/etiology , Animals , Blood Transfusion , Bone Marrow/pathology , Bone Marrow/ultrastructure , Female , Hematocrit , Leukemia, Experimental/pathology , Leukemia, Myeloid/pathology , Liver/pathology , Liver/ultrastructure , Male , Mice , Mice, Inbred BALB C , Microscopy, Electron , Neoplasm Transplantation , Rauscher Virus , Spleen/pathology , Spleen/ultrastructure
9.
Cancer Genet Cytogenet ; 35(1): 91-101, 1988 Oct 01.
Article in English | MEDLINE | ID: mdl-3180016

ABSTRACT

In vivo cytogenetic analyses have been performed using G-, C-, and nuclear organizing region (NOR)-banding techniques, and sister chromatid exchanges (SCE) on a transplantable monomyelocytic leukemia (MML) initially induced in female BALB/c mice by the Rauscher leukemia virus (RLV). Centromeric associations have been found to be greatly increased in MML transplanted mice. Transplantability of the disease has been demonstrated at the cytogenetic level by the presence of female cells in males transplanted with MML cells. G-banding analysis has shown the existence of a marker deleted chromosome 18 in all tissues examined (bone marrow, spleen, and peripheral blood) restricted to female transplanted cells. The NOR-banding analysis has shown a slight increase in the number of Ag-NOR sites per metaphase in MML transplanted mice compared with controls and the existence of an extra chromosome having NOR in MML transplanted mice. No differences were found in C banding between controls and MML transplanted mice. In MML transplanted males, female transformed cells showed a significant reduction in SCE frequency compared with host male cells or controls.


Subject(s)
Chromosome Aberrations , Leukemia, Myelomonocytic, Chronic/genetics , Animals , Bone Marrow/ultrastructure , Chromosome Banding , Female , Genetic Markers , Karyotyping , Male , Mice , Mice, Inbred BALB C , Neoplasm Transplantation , Nucleolus Organizer Region/ultrastructure , Sister Chromatid Exchange
10.
Cancer Genet Cytogenet ; 62(1): 9-14, 1992 Aug.
Article in English | MEDLINE | ID: mdl-1387833

ABSTRACT

Subsets of non-Hodgkin's lymphoma in humans have been shown to involve activation of protooncogenes such as MYC and BCL2 resulting from chromosome translocation involving the IGH and TCR genes. Malignant lymphomas in the canine present histologic and clinical subsets similar to those in humans. To study the genetic nature of these lymphomas, we undertook this study to determine, by Southern blotting analysis, the extent of homology between the human and canine genes MYC, BCL2, IGH, and TCRB using human gene probes. Our results, presented here, show that the organization of these genes in the two species is very similar.


Subject(s)
Genes, myc/genetics , Immunoglobulin Heavy Chains/genetics , Proto-Oncogene Proteins/genetics , Proto-Oncogenes , Receptors, Antigen, T-Cell, alpha-beta/genetics , Sequence Homology, Nucleic Acid , Animals , Blotting, Southern , Dogs , GTP-Binding Proteins/genetics , Humans , Protein-Tyrosine Kinases/genetics , Proto-Oncogene Proteins c-bcl-2 , Restriction Mapping
11.
Ann Clin Lab Sci ; 22(6): 385-97, 1992.
Article in English | MEDLINE | ID: mdl-1456728

ABSTRACT

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.


Subject(s)
Leukemia, Erythroblastic, Acute/microbiology , Rauscher Virus , Thrombocytopenia/microbiology , Animals , Blood Platelets/pathology , Cell Survival , Leukemia, Erythroblastic, Acute/blood , Leukemia, Erythroblastic, Acute/complications , Male , Mice , Mice, Inbred BALB C , Microscopy, Electron , Partial Thromboplastin Time , Prothrombin Time , Thrombocytopenia/blood , Thrombocytopenia/complications
12.
Adv Exp Med Biol ; 241: 191-8, 1988.
Article in English | MEDLINE | ID: mdl-3223406

ABSTRACT

Infection of BALB/c mice with the RLV-A virus normally induces an erythropoietic dysplasia characterized by hepatosplenomegaly, erythroblastosis, erythroblastemia and severe anemia without reticulocytosis. Time to death varies between 20-30 weeks. Mice were inoculated with RLV-A after being hypertransfused with 75% packed red cells for 42 days which has been shown to eliminate erythropoiesis and modify the microenvironment to favor granulopoiesis. Following RLV-A inoculation, one group did not receive further transfusion (short-term) and another group continued with hypertransfusion weekly (long-term). The pathogenesis of RLV-A in the short-term group paralleled the characteristic RLV-A response. In the long-term group however, the characteristic RLV-A response was never observed. Instead, a granulocytic leukemia was developed. Continued hypertransfusion presumably after establishment of an altered microenvironment resulted in a completely different viral pathogenesis and the development of a transplantable myeloid leukemia.


Subject(s)
Blood Transfusion , Erythropoiesis , Leukemia, Experimental/physiopathology , Rauscher Virus , Animals , Granulocytes , Hematopoiesis , Leukemia, Experimental/blood , Mice , Mice, Inbred BALB C , Time Factors
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