Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

If bone marrow transplantation is to become widely applicable in the treatment of patients with leukemia and aplastic anemia, the necessity to have a perfectly histocompatible donor must be overcome. In an effort to define the roles of HL-A type and mixed lymphocyte culture (MLC) reactivity in the determination of successful engraftment and the occurrence of graftversus-host disease (GVHD), we have attempted transplantation of a child with acute myeloblastic leukemia (AML) using an HL-A identical, MLC-reactive sibling donor. Successful engraftment has been accomplished, as documented by the appearance of multiple donor genetic markers in the recipient. There is no evidence of severe GVHD. The recipient is alive, without evidence of leukemia, and has returned to full activities 9 mo after transplantation. The recipient now produces lymphocytes, which have the MLC reactivity that characterize the donor's lymphocytes, rather than that of her own pretransplant lymphocytes. This experience demonstrates that successful bone marrow transplantation in patients with leukemia can be accomplished in the face of MLC reactivity.
Blood 1976 Sep
PMID:Successful bone marrow transplantation against mixed lymphocyte culture barrier. 0 80

Fifty-seven patients with end-stage acute myeloblastic leukemia (AML) received a total of 65 bone marrow transplants between 1968 and 1976. Marrow from HLA genotypically identical allogeneic donors was administered to 32 patients, 13 received marrow from HLA-incompatible donors, donor-recipient HLA compatibility was undetermined for eight patients, and identical twins were marrow donors for four patients. None of the patients in the three latter groups survived beyond 9.4 months after transplantation. Two patients treated with marrow transplants from HLA-compatible donors currently are alive and free of leukemia with functioning grafts 13 and 38 months after transplantation. The 32 patients in the Registry series who received marrow from HLA-compatible donors were compared with a similar series of 46 patients in Seattle. Data for these 78 patients were pooled and analyzed for pretransplant factors that might have prognostic value. Patients with end-stage AML had approximately a 10% chance of surviving 20 months after high-dose chemoradiotherapy plus marrow transplantation. Patients younger than 21 years had a higher six-month survival rate than patients older than 30 years. Patients in the Registry series who received transplants with HLA-compatible marrow within eight months of diagnosis had a higher survival experience than patients who received transplants later.
JAMA 1978 Sep 15
PMID:Bone marrow transplantation for acute myeloblastic leukemia. 2 25

The pyrimidine analog, 5-azacytidine (NSC 102816), was administered by continuous intravenous infusion in Ringer's lactate in increasing doses to sets of patients with metastatic cancer to establish a dose sufficient to produce mild toxicity. Twenty-one patients (23 trials) were treated with doses of 50-200 mg/sq/m/day for 5 days every 2-4 wk. Nausea and vomiting were moderate and easily preventable. Doses of 100-200 mg/sq/m for 5 days every 14 days produced granulocytopenia, usually after two courses. Less toxicity was observed when courses were given every 21-28 days. Forty-five patients with previously treated and refractory acute myeloblastic leukemia were treated. The majority received doses of 150 mg/sq m for 5 days every 2 wk. Eleven (24%) complete remissions and four partial remissions were observed. The number of courses to achieve remission averaged three and required an average of 59 days. Nine patients with blastic crisis of chronic myeloblastic leukemia and four with refractory acute lymphoblastic leukemia failed to respond. 5-Azacytidine administered by continuous infusion is well tolerated and is an active compound in acute myeloblastic leukemia.
Blood 1976 Sep
PMID:5-Azacytidine (NSC 102816): a new drug for the treatment of myeloblastic leukemia. 6 Jan 56

Human B lymphocyte antigens analogous to the murine Ia determinants were found on myeloblasts and promyelocytes but not on more mature granulocytes. This was apparent by fluorescent staining with both human alloantisera and rabbit antisera to the isolated Ia-like proteins. The cells of patients with chronic myelocytic leukemia showed this difference especially clearly. Separation of the myeloblasts and promyelocytes by multistep density gradient fractionation produced a marked enrichment of the positive cells. The remaining cells from higher density fractions were more-mature neutrophils that were essentially negative. In acute myeloid leukemia, in which myeloid cells early in differentiation predominate, the vast majority of cells were strongly positive. Similar results were obtained with normal bone marrow cells. Here also, only the early forms of the myeloid series separated by gradient centrifugation had Ia antigens. Evidence was also obtained for the presence of Ia determinants on cells with the appearance of early erythroid precursors. Support for the presence of the Ia determinants on granulocyte-macrophage committed stem cells was provided by the inhibition of granulocyte colony formation in agar cultures following preincubation of normal bone marrow with antiserum and complement. Cross absorptions with purified preparations of immature cells provided evidence for the close similarity of the antigenic determinants on both myeloblasts and B cells. A 28,000-37,000-dalton bimolecular complex obtained from myeloblast membranes contained the Ia determinants and was similar to that obtained from peripheral blood B cell membranes.
Proc Natl Acad Sci U S A 1977 Sep
PMID:Expression of Ia-like antigen molecules on human granulocytes during early phases of differentiation. 7 38

We observed chromosome-banding abnormalities in leukemic cells of 46 of 90 (51 per cent) adults with acute nonlymphocytic leukemia at initial hospital admission. The difference in survival between 37 treated patients with an initially normal karyotype (10 months) and 43 with an initially abnormal karyotype (four months) was significant (P less than 0.01). When patients were classified as having acute myelogenous leukemia or acute myelomonocytic leukemia, this difference in survival was even more pronounced. Of 16 treated patients with acute myelogenous leukemia and a normal karyotype, 11 (69 per cent) had a complete remission and a median survival of 13 months. Of eight patients with acute myelogenous leukemia in whom only abnormal metaphases were observed, none had a complete remission, and the median survival was only two months (P approximately 0.50). Remission rate and median survival were not significantly different in patients with acute myelomonocytic leukemia grouped according to initial karyotypes.
N Engl J Med 1978 Sep 21
PMID:Correlation of clinical findings with quinacrine-banded chromosomes in 90 adults with acute nonlymphocytic leukemia: an eight-year study (1970-1977). 7 82

Identification of a "cluster" of cases of acute myeloid leukaemia and chronic myeloproliferative disorders in Lytham St. Annes, Lancashire, prompted an analysis of the incidence of myeloid leukaemias in Lancashire (excluding Ormskirk Health District), as recorded by the Manchester Cancer Registry. Although statistically there was no significant difference in the trend of incidence between the whole former borough of Lytham St. Annes and the other districts studied, the reported incidence of these diseases in the area as a whole had almost doubled, and in two districts nearly trebled, between two consecutive 6 year periods, beginning in 1965. This represents a substantially larger increase than mortality data suggests has occurred nationally in the same period, and is unlikely to be due solely to more accurate diagnosis or reporting.
Lancet 1979 Sep 15
PMID:Incidence of myeloid leukaemia in Lancashire. 8 57

Electrofocusing patterns of plasma fucosyltransferases provide information concerning marrow status of patients with myeloproliferative disorders. Three enzymes were detected in normal plasmas using an acceptor terminating in the sequence N-acetylglucosamine-galactose. The enzyme which focused at pH 4.7 was elevated during rapid proliferation of myeloid cells, e.g., acute myelogenous leukemias and certain infectious diseases. Activity at pI = 5.1 was decreased in acute myelogenous leukemia patients, and from other observations, appears related to the level of erythropoietic activity. Acceptor studies show this enzyme to be specified by the H gene. A third enzyme focused at pH 5.5 and appeared to be correlated with a later step in granulocytes maturation. Two other plasma fucosyltransferases (pl = 5.6 and 8.3) were detected with a high-molecular-weight acceptor terminating in N-acetylglucosamine. This activity was markedly elevated during regeneration of a normal marrow population during drug-induced remission of acute myelogenous leukemia. Additional isoenzymes were detected, using this acceptor, in plasma of patients with certain solid tumors and multiple myeloma. However, the new isoelectric points observed (pH 6.0, 6.9, and 7.8) suggest these enzymes are probably not derived from hematopoietic tissues.
Cancer Res 1979 Sep
PMID:Electrofocusing patterns of fucosyltransferases in plasma of patients with neoplastic disease. 8 96

Seventy-eight patients with Hodgkin's disease were treated with radiation therapy between July 1966 and July 1976 (30 Stage I, 28 Stage II, 20 Stage III). The mean follow-up period is greater than 5 years. 90% of Stage I, 86% of Stage II, 65% of Stage III, and 82% (64/78) of all patients are NED after radiotherapy alone. Since laparotomy option (1970) 89% (50/56) of patients are NED. Fourteen patients were failures. Chemotherapy "rescued" 6 of 14. Seven have died, 1 is alive with disease, and 1 died of leukemia. Absolute survival is 90% (70/78). Failures were more frequent in patients with unfavorable histological types (9/14), and Stage III disease, primarily IIIS+ or B category (7/14). Sites of failures were mainly extranodal, primarily lung (10/14) and bone (2/14), and are consistent with hematogenous dissemination. Laparotomy performed in 41 patients identified unsuspected splenic involvement in 9 cases (22%), but was a distinct failure in confirming most "small node" positive lymphangiograms. Two patients developed acute myelocytic leukemia, both while NED 5 years posttherapy. One patient had also received adjunctive MOPP. There has been no impairment in the quality of survival that could be directly attributed to radiotherapy.
Cancer 1978 Sep
PMID:Hodgkin's disease: radiotherapeutic management at a cancer oriented community hospital. 10 Jan 96

A 13-year-old boy with acute myelogenous leukemia resistant to conventional chemotherapy received a bone marrow transplant from his HL-A-identical, mixed lymphocyte culture-reactive sister. The recipient was prepared for transplantation with cyclophosphamide and total body irradiation. Despite cytogenetic evidence of engraftment, graft-versus-host disease was not observed. The patient died 38 days post-transplantation of Gram-negative bacteremia sepsis and recurrent leukemia of recipient origin.
Transplantation 1975 Sep
PMID:Bone marrow transplantation between mixed lymphocyte culture-reactive individuals. 12 39

Acquired enzymatic activity defects of erythrocyte pyruvate kinase, glucose phosphate isomerase and phosphofructokinase have been studied in patients with acute myeloid leukemias, sideroblastic refractory anemias and unclassified acquired dyserythropoiesis. 6 patients with acute myeloid leukemia had a lowered erythrocyte pyruvate kinase activity; in 5 of them the concentration of the "pyruvate kinase"-antigen was parallely decreased, in such a manner that the ratio enzyme activity/immunologic reactivity (i.e. the molecular specific activity) was normal. In 1 patient with acute leukemia, 4 with refractory anemia and 1 with acquired dyserythropoiesis the defect of the pyruvate kinase activity was associated with a normal antigen concentration (and, therefore, the molecular specific activity in whole hemolysate was lowered). The enzyme activity was restored by incubation with SH reagents in two cases and by partial purification as often as it was performed. The electrofocusing pattern of erythrocyte pyruvate kinase was normal in both these types of defects. In two patients with so-called "acquired dyserythropoiesis" an erythrocyte glucose phosphate isomerase deficiency has been detected; in both the cases it was associated with a parallel decrease of the antigen concentration. The residual enzyme had a normal electrofocusing and electrophoretic pattern and a normal heat stability; the enzyme activity could not be restored by any treatment. In 1 patient with erythroleukemia and in 1 other with acquired dyserythropoiesis the erythrocyte phosphofructokinase activity was lowered. The enzyme activity was not restored by cross incubation in isologous plasma or by the SH reagents. In one case immunologic study could be performed, indicating that the enzyme defect was mainly due to the decreased ratio of the muscle type subunit of the erythrocyte phosphofructokinase. The electrofocusing pattern of deficient phosphofructokinases was normal. Finally, we point out the probable existence of several direct mechanisms, genetic and post translational, accounting for the acquired enzyme defects of red blood cells in various blood disorders.
Clin Chim Acta 1976 Sep 20
PMID:Mechanisms of the acquired erythrocyte enzyme deficiencies in blood diseases. 13 55


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