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 5q- syndrome is a recently described entity characterized by partial deletion of the long arm of chromosome No. 5 and by hematologic findings of chronic anemia with reticulocytopenia, nonlobulated megakaryocytes, and megathrombocytes. We report on a patient with the hematologic features of the 5q- syndrome who progressed to acute leukemia and whose uniqueness consisted of 1) lack of additional cytogenetic abnormalities, 2) presence of blasts with Auer rods, and 3) bone marrow cells positive for terminal deoxynucleotidyl transferase. His leukemia was refractory to conventional chemotherapy.
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PMID:Chronic anemia progressing to Auer rod-positive and TdT-positive acute leukemia with 5q- chromosomal anomaly. 609 6

Jaundice and hepatomegaly developed in a boy with Fanconi anemia after he had undergone treatment with oxymetholone for nine years. A liver scan showed patchy uptake consistent with the presence of space-occupying lesions. After oxymetholone treatment was stopped, the jaundice resolved, the liver size decreased, and the filling defects were no longer detectable on the liver scan. A year later, 5% of his white blood cells showed a consistent chromosomal abnormality. His leukocyte count increased and 85% of these cells showed the same chromosomal abnormality. The rapid replication of this abnormal clone suggests that it was leukemic. The significance of oxymetholone therapy and the occurrence of hepatic tumors and leukemia is discussed.
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PMID:Fanconi anemia. Oxymetholone hepatic tumors, and chromosome aberrations associated with leukemic transition. 625 60

Murine leukemia viruses contain a low molecular weight basic protein, designated p10, which binds to single-stranded nucleic acids. The complete amino acid sequence of p10 from the Rauscher strain of virus has been determined. The partial amino acid sequences of p10s from Moloney, Friend, AKR, Gross, radiation leukemia, and BALB/2 viral strains have also been determined using microsequencing techniques. Rauscher p10 is composed of 56 amino acid residues; the other p10s are similar in size but differ from Rauscher by a few conservative amino acid substitutions. The structure of Rauscher p10 was compared to the structure of a functionally homologous protein from Rous avian sarcoma virus. The comparison revealed regions of amino acid sequence homologies which indicate a phylogenetic relationship between the murine and avian viral strains. The analyses revealed a periodic placement of three Cys residues and a Gly-His sequence. A structure involving these residues is found once in the murine protein and twice in the avian protein. A similar structure is seen in the single stranded nucleic acid binding protein of bacteriophage T4. However, in the latter case, the order of amino acid residues is inverted.
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PMID:Primary structure of the low molecular weight nucleic acid-binding proteins of murine leukemia viruses. 626 42

A 56-year-old black man with nonendemic adult T-cell leukemia is reported, who presented with severe hypercalcemia and leukemic leptomeningeal infiltration but had no evidence of bone marrow involvement. His malignant cells were characterized by light and transmission electron microscopy, cytogenetics, and flow cytometry. The cells demonstrated the deeply indented or convoluted nuclei characteristic of endemic human T-cell lymphoma virus-associated cases. Surface phenotyping indicated the cells' origin to be from the mature, helper/inducer subset of T-lymphocytes. However, there was no clinical or laboratory evidence that the malignant cells retained immunoregulatory function. The clinical and immunologic features of this and other nonendemic cases are compared with those of patients from the endemic regions of Japan, the Caribbean islands, and the southeastern United States.
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PMID:Adult T-cell leukemia: clinical and immunologic characterization of a nonendemic case. 638 15

Until the late 1940s, no therapy was available for leukemia other than blood transfusion and a few antimicrobial agents. The disease ran its course uninfluenced by this treatment; most children died in a matter of a few months. The success of nitrogen mustard in the treatment of lymphomas and chronic leukemias encouraged efforts to try various drugs in the treatment of acute leukemia. In 1948, Farber and colleagues at the Boston Children's Hospital reported that aminopterin produced complete remissions in about one-third of children with acute leukemia. The dramatic success of this trial proved to be a monumental step forward for the field of cancer chemotherapy. Dr. Wolff was a pediatric resident and hematology fellow at the Boston Children's Hospital during the time that this important study was done. His first-hand experience gives valuable historical insight into how this giant step in cancer therapy research was accomplished.
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PMID:Dr. James A. Wolff. II. First successful chemotherapy of acute leukemia. 639 32

Since there was no position for a full-time pediatric hematologist, Dr. Wolff practiced general pediatrics for 10 years while he volunteered as director of the hematology clinic at the Babies Hospital. He was appointed full-time Director of Pediatric Hematology in 1959. His early clinical studies were concerned with treatment of erythroblastosis fetalis and use of frequent transfusions and desferroxamine in children with thalassemia. The combined tumor clinic at the Babies Hospital, established in 1952, was one of the first to use the multidisciplinary approach to treatment of the child with cancer. In 1957, the Children's Leukemia Group A, later called the Children's Cancer Study Group, was established by Dr. Joseph Burchenal. Dr. Wolff was one of the first members. This group led to the establishment of various national intergroup committees for clinical study of cancers in children. In 1954, Farber began to use dactinomycin for treatment of Wilms' tumor. At first this drug was used only for treatment of metastatic tumors, but later it was also used to prevent metastases. Subsequently, other childhood tumors were found to be amenable to chemotherapy.
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PMID:Dr. James A. Wolff. III. First pediatric hematologist at Babies Hospital. 639 33

Nineteen patients with adult T-cell leukemia (ATL) have been found in the last seven years along the east coast of Kii Peninsula in Japan. The leukemic cells were of the immunologically inducer/helper T-cell phenotype. The prognosis was very poor (median survival time, 85 days), and most of the patients had fatal complications of pulmonary infections. Antibody against ATL-associated antigen (anti-ATLA) was detected in sera from 9 of 10 patients who were born along the coast. However, it was not detected in one patient who was born in a district surrounded by mountains. Although he had neither superficial lymphadenopathy nor skin lesions, he showed rapid clinical deterioration. His leukemic cells appeared to be extremely bizarre with marked nuclear deformation compared with those of the other patients. In surface marker studies the leukemic cells reacted positively with OKT3, OKT4 and OKIa-1 monoclonal antibodies. The characteristics of the anti-ATLA-negative case are discussed in comparison with the other ATL cases.
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PMID:Adult T-cell leukemia on the east coast of Kii Peninsula--presentation of an anti-ATLA-negative case. 660 35

A 19-year-old man with severe pure red-cell aplasia is described. An unusually high proportion of this patient's lymphocytes were large granular lymphocytes (LGL), both in the blood (40%) and in the bone marrow (50%). His blood leukocytes displayed a strongly elevated natural killer (NK) cell activity in vitro against the erythroblastic leukemia line K562. The patient's non-T blood lymphocytes inhibited in vitro erythroid colony formation (BFU-E and CFU-E) but not the granulocyte-monocyte colony growth (CFU-GM) from autologous and allogeneic bone marrow. Neither T-cell-mediated cytotoxicity nor circulating antibodies against erythroid precursors could be demonstrated. The patient's haemoglobin values returned to normal levels after three weeks of glucocorticoid treatment and have since then remained stable with continued prednisone administration. Attempts to reduce the prednisone dose to less than 10 mg/day have led to relapses. It is tempting to suggest that the patient's disease might be caused by hyperactivity of cytotoxic non-T (NK) cells specific for K562 cells and early erythroid precursors.
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PMID:Acquired pure red-cell aplasia: a consequence of increased natural killer cell activity? 670 Feb 59

We have demonstrated previously that L-histidinol, a structural analogue of the essential amino acid L-histidine, protects a variety of phenotypically normal cell lines from certain proliferation-dependent anticancer drugs without decreasing the toxicity of these agents for corresponding tumorigenic derivatives of the normal cells. Histidinol modulates the toxicity of selected anticancer drugs in tissue culture systems by its ability to arrest, specifically and reversibly, cells of normal phenotype in a G0-like, noncycling state while allowing continued cell cycle transit in most of their tumorigenic counterparts. Thus, in the presence of comparable levels of histidinol, the toxicities of the proliferation-dependent anticancer drugs 1-beta-D-arabinofuranosylcytosine and 5-fluorouracil are eliminated for a variety of normal cell lines but significantly increased for a number of tumorigenic lines. We report here that histidinol confers substantial protection upon the bone marrow cells of DBA/2J mice from the drugs 1-beta-D-arabinofuranosylcytosine and 5-fluorouracil. The protective responses were evaluated by quantitative cell survival assays and by animal survival studies. We report also that the histidinol-mediated protection to bone marrow cells persists in L1210 leukemia-bearing DBA/2J mice treated with combinations of histidinol and 1-beta-D-arabinofuranosylcytosine or 5-fluorouracil without diminishing the toxicities of these agents for in situ leukemia cells.
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PMID:Histidinol-mediated improvement in the specificity of 1-beta-D-arabinofuranosylcytosine and 5-fluorouracil in L 1210 leukemia-bearing mice. 672 19

The histidine ammonia-lyase from bacterial strain CAMR 5315 was partially purified to assess its effect on the growth of murine tumours. This strain was selected as the source after an extensive screening programme for histidine ammonia-lyases. The enzyme was partially purified by ammonium sulphate fractionation, chromatography on DEAE-cellulose and Sephadex G-150. The enzyme reduced circulating L-histidine levels in Wistar rats and in mice persisted with a half-life of 6-7 h. Neither LDH virus nor chemical modification with ethylacetimidate increased the half-life as observed with L-asparaginase and L-glutaminase. The enzyme was tested in mice against Ehrlich carcinoma, L5178Y lymphoblastic leukaemia, Mc/S sarcoma, B16 melanoma, P8157 mastocytoma, P1798 lymphosarcoma and the Gardner 6C3HED lymphosarcoma. The only tumours to show sensitivity to the enzyme were the Mc/S sarcoma against which a 65% increase in life span was observed at the highest enzyme dose, 1000 U/kg on alternate days over 14 days and the Ehrlich ascites carcinoma where cures were obtained at 250 U/kg on alternate days over 14 days, but only at inocula levels of 10(5) and 10(3) cells/animal respectively.
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PMID:The effect of histidine ammonia-lyase on some murine tumours. 688 63


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