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)

The effect of a leukemic environment on normal erythroid and granulocytic colony formation was examined in in vivo plasma clot diffusion chamber cultures implanted into Shay chloroleukemic rat hosts at varying stages of the disease. Normal bone marrow cells isolated in plasma clot diffusion chamber cultures in leukemic hosts displayed significant differences in the pattern of normal bone marrow colony growth. Granulocyte colony-forming units were significantly inhibited by leukemic hosts throughout the course of the disease. The size of developing colonies was reduced to under 100 cells; however, maturation within these clusters appeared unaffected. Erythroid colonies showed a slight inhibition during the early stages of the leukemia, a significant stimulation of 100 to 350% in the midleukemic period, and a significant inhibition of 50 to 65% during the terminal stages of the disease. Burst formation was also inhibited in the late leukemic stages. The transient increase in erythroid colony-forming units on Days 7 and 8 of the leukemia was concomitant with the onset of the anemia associated with the disease. Since the normal bone marrow cells were compartmentalized within the plasma clot diffusion chamber cultures, the suppression of erythroid and granulocytic colony development appears to be directly due to the release of diffusible inhibitory substances from the leukemic animal.
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PMID:Leukemic host influence on normal erythrocytic and granulocytic colony formation in in vivo plasma clot diffusion chamber cultures. 28 43

Male BALB/c mice that received prophylactic iv treatment with pyran had significantly enhanced splenomegaly, an increased number of splenic foci induced by the spleen focus forming virus (SFFV) in the Friend murine leukemia virus (F-MuLV) complex, and a slightly decreased mean survival time as compared with untreated controls infected with F-MuLV. A corresponding increase in the lymphatic leukemia virus component of the F-MuLV complex was not observed, which suggests that the enhancement of the disease was due primarily to a selective increase in the SFFV component of the F-MuLV complex. That the enhancement was related to an increased number of target cells for SFFV was substantiated by data concerning erythropoiesis in iv pyran-treated animals. Increases in splenic hematocrits and in uptake of 59Fe in the spleens of animals treated iv with pyran provided quantitative evidence for the histologic finding of increased erythroid precursors in the spleens.
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PMID:Enhancement of erythroid target cells for Friend murine leukemia virus by intravenous pyran treatment. 28 1

A 10-year-old boy, who had been in an uninterrupted remission of acute lymphocytic leukemia (ALL) for six years, developed polycythemia vera (PV). One and a half months after detection of PV, he was found to have active leukemia. Both the polycythemia and leukemia receded with anti-leukemia therapy. Three possible explanations for the development of PV in a child with ALL are discussed: 1) PV was a part of his original ALL and recurred whtn patient relapsed. The PV phase was detected only during relapse because the patient was under close observation. 2) PV was a second neoplasm independent of ALL. 3) PV was part of a second leukemia which was different from the original leukemia; this new ALL was derived from a pluripotential cell line involving both erythroid and lymphoid elements. A precedent for this explanation has been observed in chronic myelogenous leukemia.
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PMID:Polycythemia vera in a child with acute lymphocytic leukemia. 28 32

Bone marrow erythroid progenitor cells were examined from 50 cases of acute leukaemia and from 20 normal subjects using an in vitro semisolid culture method. Numbers of both primitive erythroid progenitor cells (BFU-e) and later-stage erythroid progenitor cells (CFU-e) were remarkably depressed in patient with acute leukaemia in active phase. However, both BFU-e and CFU-e recovered to within normal range when the patients achieved remission. Peripheral blood BFU-e of children with acute lymphocytic leukaemia in remission were also examined and found to have values not significantly different from those of control subjects. There was no distinct correlation between the numbers of erythroid bursts or colonies and the duration of remission in patients with acute leukaemia in remission. The reduction of BFU-e and CFU-e in active acute leukaemia suggests the involvement of erythropoietic progenitors in the pathophysiology of this type of leukaemia.
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PMID:Erythroid progenitors (BFU-e and CFU-e) in acute leukaemia. 29 1

One hundred consecutive newly diagnosed cases of leukemia and lymphoma in children from 0 to 16 years of age presenting at the University of Minnesota from 1973 to 1977 were studied. Clinical features were correlated with phenotypic features of blast cells, including surface markers and cytomorphology. Four groups with distinct clinical and pathologic features emerged from the study: a) The acute leukemias of the "null" or "undifferentiated" group were those in which the malignant cells carried distinctive null leukemia surface antigen and lacked features of either T cells (E-rosette positivity) or B cells (surface immunoglobulin positivity). These cases occurred most frequently in the series (56% of total cases), peaked in incidence at 6 years, were associated with extensive bone marrow involvement, lacked distinguishing cytomorphologic features, and had the best response to therapy of all groups. b) The acute myelogenous leukemias, including those with myeloid, monocytoid, or erythroid features or a combination of the above, had extensive bone marrow involvement and the characteristic morphology. This group was seen with intermediate frequency and showed an intermediate response to therapy. c) Leukemia-lymphomas of the T-cell group were frequently associated with mediastinal masses and other masses, a cytomorphology which was different from the B-cell group but similar to the null group, and high white cell counts. These cases occurred with intermediate frequency (14%) and had a worse prognosis than the null group. d) Leukemia-lymphomas of the B-cell group had monoclonal surface immunoglobulin with mu-heavy and either kappa or lambda light chain. These patients were least frequent in the series, frequently presented with abdominal masses, and had a characteristic Burkitt cell morphology. Prognosis was the worst of all patients in our series. These data suggest that the major phenotypic groups of childhood leukemia and lymphoma have differing prognoses and should receive differing forms of therapy. Clinical and pathologic features of each group are sufficiently distinctive to suggest that they may have different causes.
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PMID:The nature of childhood leukemia and lymphoma. 30 75

BALB/c mice depleted of T-cells by thymectomy at 3 to 5 days of age and by treatment with antithymocyte serum were inoculated with the lymphatic leukemia virus derived from Friend virus. After a long latent period, these animals developed erythroid leukemia. In contrast, intact control mice inoculated with Friend virus-associated lymphatic leukemia virus developed typical thymic (T-cell) lymphomas. Cell-free virus prepared from leukemic T-cell-depleted animals induced lymphoid, myeloid, and erythroid leukemias in intact mice. The erythroid leukemia-inducing virus differed from the spleen focus-forming component of Friend virus in its long latent period (88 to 225 days) and in its inability to induce spleen foci. End-point dilution experiments suggested that a hitherto undescribed component of the Friend virus complex might be responsible for these late-appearing erythroid leukemias.
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PMID:Erythroid leukemia induced by Friend lymphatic leukemia virus in T-cell-depleted mice. 31 86

Intraperitoneal (ip) inoculation of BALB/c mice with syngeneic hemopoietic cells results in the formation of 'Mesenteric Hemopoietic Colonies' (MHC). In lethally irradiated mice actively growing erythroid, myeloid and megakaryocytic, or mixed colonies form and soon become confluent. It is therefore concluded that in mice the mesentery is a suitable site for growth of hemopoietic cells. The mesentery might play an important role in the recovery of the hemopoietic system in lethally irradiated mice, being the primary site of proliferation of stem cells and/or CFU before their migration to bone marrow and spleen. Bone marrow and spleen cells from animals infected with Rauscher Leukemia Virus (R-MuLV) also produce MHC and spleen colonies after ip injection into lethally irradiated mice. In addition to the undifferentiated cells in the MHC, cells with limited differentiation and/or retarded maturation were identified. The cytologic pattern of the majority of cells in MHC was of mixed type.
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PMID:Mesenteric hemopoietic colonies: occurrence in BALB/c mice after transplantation of syngeneic normal or leukemic hemopoietic cells. 33 Jan 82

Bone marrow from inbred Wistar/Furth (W/Fu) rats, normal and 90% replaced by acute myelogenous leukemia (AML), was transplanted, respectively, to the left and right kidneys of adult W/Fu rats. After a transient period of hypocellularity, AML grafts repopulated to pre-transplant cellularity by day 9, whereas normal bone marrow (NBM) grafts required 25 days for repopulation to pre-transplant cellularity. Grafted leukemia cells remained localized to the kidney for 17 days. In NBM grafts phlebotomy accelerated erythroid proliferation, and intrathoracic inoculation of live Escherichia coli accelerated myeloid proliferation; in AML grafts only E. coli injection increased bone marrow proliferation. There was no morphologically detectable differentiation of W/Fu AML cells. These studies provide evidence of a myelopoietic response of AML blast cells in vivo and present a transplantation technique for comparison of localized grafts of leukemic and normal bone marrow in the same animal.
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PMID:Proliferative response of clonal acute myelogenous leukemia cells in localized grafts of normal bone marrow stroma to in vivo stimulation of myelopoiesis. 34 63

Studies are described employing two erythropoietic systems to elucidate regulatory mechanisms that control both normal erythropoiesis and erythroid differentiation of transformed hemopoietic precursors. Evidence is provided suggesting that normal erythroid cell precursors require erythropoietin as a growth factor that regulates the number of precursors capable of differentiating. Murine erythroleukemia cells proliferate without need of erythropoietin; they show a variable, generally low, rate of spontaneous differentiation and a brisk rate of erythropoiesis in response to a variety of chemical agents. Present studies suggest that these chemical inducers initiate a series of events including cell surface related changes, alterations in cell cycle kinetics, and modifications of chromatin and DNA structure which result in the irreversible commitment of these leukemia cells to erythroid differentiation and the synthesis of red-cell-specific products.
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PMID:Regulation of differentiation in normal and transformed erythroid cells. 34 91

Enzymatic studies were performed on erythroblasts obtained from marrows of 2 patients with untreated erythroleukemia. Cytochemically, erythroblasts showed abnormalities of several enzymes involved in carbohydrate metabolism, as well as abnormalities of specific and nonspecific esterases. Electrophoretic analysis of esterases extracted from predominatly erythroid marrows showed strong moderately fluoride-resistant nonspecific esterase activity with alpha-naphthyl acetate, and weak activity with alpha-naphthyl butyrate. Isoenzymatic patterns of specific esterase activity in erythroleukemia were indistinguishable from those found in myeloblastic leukemia. The results are consistent with the concept of the Di Guglielmo syndrome in which a preleukemic erythroid disorder may precede the emergence of acute myeloblastic or myelomonocytic leukemia.
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PMID:Enzymatic abnormalities in erythroleukemia. 41 53


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