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)

Osteogenic sarcoma developed in a 14-year-old boy 13 years after he had partially recovered from chloramphenicol-induced aplastic anemia. A possible relationship is considered between aplastic anemia, chloramphenicol, testosterone, prednisone, and osteogenic sarcoma. Leukemia has been reported following chloramphenicol-induced aplastic anemia and liver tumors have been associated with testosterone therapy. Certain chemicals have caused osteogenic sarcoma in animals. Thus, we believe there are sufficient a priori reasons to question an etiologic relationship between the cause or treatment of aplastic anemia and osteogenic sarcoma.
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PMID:Osteogenic sarcoma in a patient with aplastic anemia. 26 29

The authors report a case of subacute myelocytic leukemia presenting some severe aspects. The cytogenetic findings show the Philadelphia chromosome ; t (9-22) and a second translocation between the chromosome 12, and the other chromosome 9 : t (9-12). They think that this second translocation represents a supplementary cytogenetic argument for the isolation of "Subacute myeloid Leukemia with Philadelphia chromosome" within chronic myeloid Leukemia.
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PMID:Subacute myelocytic leukemia associated with the philadelphia chromosome and supplementary translocation : 9-12. 26 21

The sera of 21 adult patients with acute leukemia were studied for the presence of antibody reacting with surface antigens of autologous leukemia cells. Sequential serum samples were obtained from patients and were tested on cryopreserved leukemia cells in immune adherence assays. Three patients showed autologous serum reactivity and the serum of one of them was analyzed in detail. This antibody reacted with autologous acute lymphocytic leukemia cells but not with autologous cells obtained from peripheral blood, bone marrow, or spleen during clinical remission. In absorption tests, the antigen could not be detected on normal autologous or allogeneic blood lymphocytes, lymphoblastoid lines of T- or B-cell origin, or cells infected with simian sarcoma virus, baboon C-type virus, or Mason-Pfizer virus. Leukemia cells from two other patients with acute lymphocytic leukemia and one patient with acute nonlymphocytic leukemia absorbed specific reactivity. These studies indicate that certain acute leukemia cells express a common antigen that elicits a humoral immune response in the autologous host.
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PMID:Detection of antibody to autologous human leukemia cells by immune adherence assays. 27 Jul 2

Since the initial development of the "passage A" mouse leukemia virus in 1957, this virus has been propagated in our laboratory by serial passage in newborn C3H(f) mice. At the present time, 10(-2)-10(-3) dilutions in physiological saline solution of this mouse-passaged virus induce lymphatic leukemia in practically all inoculated mice after a latency of 3-5 months. On the other hand, when the same virus was propagated on NIH 3T3 mouse embryo cells in tissue culture for more than 10 years, its leukemogenic potency became considerably reduced. Recent bioassay experiments carried out in our laboratory demonstrated that after such prolonged propagation in tissue culture this virus now induced leukemia in less than 15% of the inoculated suckling C3H(f) mice; only undiluted or 10% dilutions of the tissue culture fluid (very occasionally 10(-2) or 10(-3) dilutions) induced leukemia after a prolonged latency varying from 5.5 to 18 months. The passaged and the tissue-culture-grown virus strains are identical immunologically and indistinguishable in their morphology when examined by electron microscopy. The tissue-culture-grown virus, attenuated in its leukemogenic potency, does not, however, confer immunity against a challenge with the mouse-passaged virus.
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PMID:Relative loss of oncogenic potency of mouse leukemia virus (Gross) after prolonged propagation in tissue culture. 27 14

A case of a child with acute lymphocytic Leukemia is reported. The roentgenograms of the skull show intracerebral "railroad-track-like" calcifications mimicking those seen in Sturge-Weber syndrome. These calcifications are described and their etiology is discussed. The frequency of such observations in cases of acute lymphocytic leukemia with CNS-treatment is increasing.
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PMID:[Intracerebral calcifications associated with intrathecal methotrexate therapy in acute lymphocytic leukemia (author's transl)]. 28 72

In previous studies, intradermal inoculation of small doses of L2C leukemic cell suspensions into strain 2 guinea pigs induced immunity against challenging reinoculation with leukemic cells; however, 50% of the guinea pigs developed leukemia in the course of immunization. We have now attempted to induce immunity by inoculation of L2C leukemic cells inactivated by in vitro gamma irradiation ranging from 750 to 8000 rads (1 rad = 0.01 gray). In preliminary experiments, irradiation with 750 to 2750 rads had no significant effect on leukemogenic potency of leukemic cells; however, doses exceeding 3000 rads inactivated the leukemogenic potency of L2C cells. Eighty-nine guinea pigs that survived intradermal, subcutaneous, or intraperitoneal inoculations with irradiated (1000-8000 rads) L2C cells were subsequently challenged by reinoculation with nonirradiated leukemic cells, and 83 of them (93%) developed leukemia. L2C leukemic cells contain spherical particles, about 103 nm in diameter; it is reasonable to assume that these particles represent the causative virus responsible for the development of L2C leukemia. Inactivation of leukemogenic potency of L2C leukemic cells by gamma irradiation in vitro does not necessarily imply that the virus particles consistently present in these cells were also inactivated. In previous experiments carried out on mouse leukemia, doses exceeding 1,000,000 rads were needed in order to inactivate the mouse leukemia virus in vitro.
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PMID:Attempt to immunize guinea pigs against L2C leukemia with leukemia cells inactivated by gamma irradiation. 29 Oct 16

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

Antisera have been raised in rabbits to the lymphoblastoid cell line NALM 1 precoated with anti-lymphocyte serum (ALS). Following absorption with chronic lymphocytic leukemia cells (CLL) the antisera reacted mainly with acute lymphocytic leukemia (ALL) cells, and were very similar in specificity to antisera raised to ALL cells precoated with ALS. Leukemia cells from the following numbers of patients were positive for the anti-NALM 1 sera in a complement-dependent cytotoxicity test; 11/14 ALL, 3/15 acute myelocytic leukemia (AML), 1/5 chronic myelocytic leukemia (CML) and 0/8 CLL. Normal B and T peripheral blood lymphocytes were negative. The titer of the anti-NALM 1 sera against positive cells was 1:64 to 1:256 whereas the undiluted sera did not react with negative cells. Ten out of 11 of the positive ALL cells were of the non-B non-T type. However, cells from 1/4 T ALL patients and a cultured T ALL line 8402 were also positive. Six of 12 cultured lymphoblastoid cell lines were positive, all of which were of malignant origin. The molecular weight of the ALL antigen detected by anti-NALM-1 serum was determined by immunoprecipitation and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) to be approximately 98,000 daltons.
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PMID:Heteroantiserum against acute lymphocytic leukemia raised to the lymphoblastoid cell line NALM-1. 30 68

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

In May 1972, the Cancer and Leukemia Group B initiated a randomized study comparing the effectiveness of CCNU and methyl-CCNU in patients with advanced malignant lymphomas, including Hodgkin's disease (HD), lymphosarcoma (LYS) and reticulum cell sarcoma (RCS). A single dose of 100 mg/m2 of CCNU or 150 mg/m2 of methyl-CCNU was given orally every 6 weeks. In patients with leukopenia or thrombocytopenia, due to prior treatment, this dose was reduced to 70 mg/m2 of CCNU and 100 gm/m2 of methyl-CCNU. Of 109 evaluable patients, 60 received CCNU and 49 received methyl-CCNU. Response rates (complete and partial) to CCNU and methyl-CCNU were respectively 42% (14/33) and 15% (3/20) in HD, 21% (3/14) and 21% (3/14) in LYS, 15% (2/13) and 27% (4/15) in RCS. Responses to methyl-CCNU, but not to CCNU, were seen only in patients who developed significant hematologic toxicity. Responses to both drugs were generally of short duration due to the advanced stage of the disease. Renal, hepatic or neurological toxicity was not observed. In conclusion, CCNU proved to be superior to methyl-CCNU for the treatment of advanced HD. CCNU was also observed to be of higher activity in Hodgkin's than in non-Hodgkin's lymphomas.
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PMID:Comparison of methyl-CCNU and CCNU in patients with advanced forms of Hodgkin's disease, lymphosarcoma nad reticulum cell sarcoma. 34 94


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