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)

Folic acid binding protein (FABP) has been measured in the supernatant of leukocytes of 12 patients affected with chronic granulocytic leukaemia (CGL). The folate binding capacity ranged from 1.37 to 697.52 pg/mg protein, showing a considerable heterogeneity. When the supernatant was preincubated with methotrexate (MTX), the inhibition of folic acid binding was complete in some cases whereas in others it was negligible: these findings have been confirmed by studying the 3H-MTX binding capacity by the same supernatants. In this case the range of bound 3H-HTX varied from 0.00 to 927 pg/mg protein. The presence of a binder in the cytoplasm of leukocytes might represent a new step in the regulation of endogenous folate metabolism. The MTX, widely used as an antifolate drug, may also be bound by FABP of CGL leukocytes, although in different amounts from case to case: this finding suggests a new point of interference of MTX in the folate metabolism. It has also been demonstrated that FABP, which is present in serum, may reduce the uptake of folate by leukocytes opening a new field of investigation on the megaloblastic transformation.
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PMID:Folic acid binding protein in chronic granulocytic leukaemia: the effect of methotrexate. 10 54

Using a method involving elution of hemoglobin bands from cellulose acetate strips following electrophoresis of hemolysates, hemoglobin A2 (Ab A2) was quantitated in bloods from 300 healthy individuals and 904 patients. The percentage of Hb A2 was elevated in beta-thalassemia heterozygotes and some patients who had megaloblastic anemia. In the latter, the highest Hb A2 levels were observed in patients with the most severe anemia. Low Hb A2 percentages were found in iron-deficiency anemia, hereditary persistance of fetal hemoglobin, and Hb H disease. In iron-deficiency anemia, the lowest levels of Hb A2 were observed in association with the most severe anemia. Iron and folate deficiency each suppressed Hb A2 levels in beta-thalassemia heterozygotes; however, vitamin B12 deficiency did not alter the percentage of Hb A2 in thalassemia. Malignant tumors, renal and hepatic insufficiency, chronic infections and inflammation, hemolytic disease, lead poisoning, aplastic anemia, leukemia, myelofibrosis, and hypothyroidism did not change Hb A2 levels. The pathogenesis of altered Hb A2 levels and their clinical significance in various diseases are discussed.
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PMID:Hemoglobin A2 levels in health and various hematologic disorders. 26 35

The six cases of Preleukemia (or Preleukemic States) are described. The peripheral blood was characterised with Pancythopoenia in 5 and bicytopoenia in 1 patient. Morphological alterations of Erythrocytes were present in all cases. The Bone Marrow was hypercellular in 3 and hypocellular in 3 patients. Erythropoiesis was megaloblastic or partly megaloblastic in 5 cases, with "ring" sideroblasts present in all cases. The percentage of Leukemic blast cells was as follow: 0, 5, 6, 10, 30 and 33. The duration of the preleukemic phase varied from 3-53 months. With the manifestations of overt Acute Nonlymphatic Leukemia the agressive therapy was applied. The results were poor in 5 patients (the survival 1, 5-4 m.). Only one survived more than 60 months and is still in full remission.
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PMID:[Preleukemia]. 60 31

Several forms of drug-induced anemia are discussed. Anemia resulting from toxic effects on the marrow may occur after large doses or long treatment courses of alkylating agents, the plant alkaloids vinblastine and vincristine, and antibiotics used in cancer chemotherapy. A lesion of the stem cells in bone marrow is thought to be caused. Aplastic anemia has been produced by chloramphenicol in a small percentage of cases. This has led to its disuse except when no suitable alternative is available or where the mortality of the disease being treated is high. Some nonnarcotic analgesics, e.g., amidopyrine, have caused agranulocytosis. Gold injections have also been implicated. Insecticides or an inhaled agent such as benzine or a glue solvent may cause hypoplastic anemia. A list is given of drugs that have been reported as having caused aplastic anemia. Chromosomal changes have rarely been reported. An alleric mechanism is sometimes responsible for drug-induced aplastic anemia. There may be individual variations in ability to metabolize a drug. Treatment of drug-induced aplastic anemia requires transfusions. Bone marrow transplants have also been used. Antibiotic therapy is needed. Oral contraceptives may be of value if there is menorrhagia. Megaoloblastic anemia may be due to defective metabolism of folate. Anticonvulsant drugs may also cause megaloblastic anemia, especially primidone. Giving folic acid with these drugs may prevent this development. Oral contraceptives have been reported to cause folate depletion but megaloblastic anemia has not been shown to follow. Alimentary bleeding with peptic ulcer or following drug use may cause anemia. Sideroblastic anemia may be a congenital abnormality of iron metabolism or an acquired form induced by drugs or lead poisoning. Pyridoxine therapy is used. Drug-induced leukemia may follow use of radioactive compounds or may develop in patients with a drug-induced aplastic anemia.
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PMID:Drug-induced anaemias. 78 36

Peripheral blood lymphocytes from 24 patients were cultured in vitro in the presence of autologous peripheral serum and bone marrow blood serum, with and without PHA stimulation. Bone marrow serum showed a well defined effect, in the absence of PHA stimulation, on lymphocytes from 4 patients (2 affected by acute leukaemia, 1 by megaloblastic anemia and 1 by benign idiopathic paraproteinaemia), and a less defined effect on lymphocytes from 2 donors (1 affected by iron deficiency anemia and 1 by thalassemia minor). No difference attributable to the source of blood serum was observed in PHA stimulated cultures. These results do not allow defined statements. Peripheral blood lymphocytes cultured in vitro were affected by bone marrow blood serum only in some subjects. A clear cut correlation between this effect and the clinical features of our patients was not evident.
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PMID:[Blastogenetic activity of medullary blood serum of patients with various blood diseases]. 90 42

Cerebral cortical calcification identical to that of the Sturge-Weber syndrome was observed in two children. In one child the calcification appeared after intrathecal administration of methotrexate and skull irradiation because of leukemia involving the central nervous system. In the other child, who had coeliac disease and epilepsy, the calcification appeared after treatment with anticonvulsants. This treatment was also contributing to the development of profound megaloblastic anemia. The unspecificity of the Sturge-Weber calcification is stressed and the hypothesis is put forward that the calcification may be secondary to folic acid deficiency interfering with the matabolism in the central nervous system.
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PMID:Intracranial calcification mimicking the Sturge-Weber syndrome: a consequence of cerebral folic acid deficiency? 101 95

An analysis of the underlying pathology and different clinico-haematological features of 202 adult pancytopenic patients is presented. Aplastic anaemia (40.6%), megaloblastic anaemia (23.26%) and acute myeloblastic leukaemia (12.8%) together accounted for most of the cases. Our aplastic anaemia cases showed several different features compared to the cases reported in western literature. Aplastic anaemia and megaloblastic anaemia patients revealed significant differences in the incidence of hepatosplenomegaly, anisocytosis, circulating erythroblasts, relative lymphocytosis (P < 0.001 for all) and reticulocytosis (P < 0.01). The present study stresses the importance of physical and peripheral blood findings in the management of pancytopenic patients.
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PMID:A reappraisal of underlying pathology in adult patients presenting with pancytopenia. 129 41

We have investigated proliferation in bone marrow trephine biopsies from 32 patients with normal or abnormal haemopoiesis, using the monoclonal antibody PC10, which detects proliferating cell nuclear antigen (PCNA), together with immunohistochemical markers of haemopoietic cell lineage. PCNA immunostaining revealed the pattern of proliferation within individual haemopoietic lineages in normal marrow. Two unexpected observations were made: of erythroid cells, only pro-erythroblasts and occasional early normoblasts reacted, and positivity of megakaryocytes was unrelated to nuclear lobulation or CD61 expression. The pathological cases represented conditions in which haemopoiesis is increased (reactive hyperplasia, chronic granulocytic leukaemia, myeloproliferative and myelodysplastic syndromes, megaloblastic anaemia). Increases in the number, and disturbances of the spatial organization, of PCNA-expressing cells were present to a variable extent in all cases. Sheets of PCNA-positive megaloblastoid erythrocytes were frequently found in myelodysplastic and myeloproliferative tissue, associated with marked disturbances in the spatial organization of all haemopoietic lineages. Cases of megaloblastic anaemia due to vitamin B12/folate deficiency also demonstrated greatly increased erythroid PCNA expression, with positivity in some giant metamyelocytes. In addition to reflecting increased proliferation, elevated PCNA expression in some bone marrow pathologies may be due to altered kinetics of the protein induced by disturbances in growth factor production.
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PMID:A study of cell proliferation in formalin-fixed, wax-embedded bone marrow trephine biopsies using the monoclonal antibody PC10, reactive with proliferating cell nuclear antigen (PCNA). 134 81

The human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origin and spread of human leukemia. 143 86

Some patients with hypoplastic marrow disorders, including aplastic anemia (AA), are at risk for clonal evolution to myelodysplastic syndromes (MDS) and leukemia. Magnetic resonance imaging (MRI) of marrow of the spine, pelvis, and femurs was performed in 24 patients with hypoplastic marrow disorders. In 12 patients (three AA, nine MDS) MRI was compatible with the clinical and biopsy diagnoses and served to define the spectrum of marrow patterns in these disorders. In eight patients with hypocellular marrow biopsies and a clinical diagnosis of AA, MRI showed an unexpected inhomogeneous or diffuse cellular pattern. Concurrent or subsequent marrow or cytogenetic studies have led to diagnoses of hypoplastic MDS in seven of these patients. In four patients with prolonged hypoplasia after bone marrow transplantation for lymphoma, a speckled pattern superimposed on a fatty background appeared in serial MRI studies. One case evolved to AML, two developed megaloblastic foci, and one remains hypoplastic at 19 months. This study suggests that MRI is able to detect early clonal disease in patients with AA, and can distinguish AA from hypoplastic MDS.
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PMID:Evidence for clonal disease by magnetic resonance imaging in patients with hypoplastic marrow disorders. 195 75


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