Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on the incidence survey of leukemia and aplastic anemia (AA) from 1986 to 1988, Case control studies (1257 new leukemia cases and 339 new AA cases) were carried out according to the type of leukemia and AA in order to better understand the epidemiologic characteristics of the diseases. Controls were matched randomly (age, sex and ethnic group) from the same population. The data were analyzed with the conditional Logistic multi-regression model and calculated on an IBM-PC/XT. The risk factors of M2a were found to be X-rays, antipyretics, benzene, pesticides and bimolane; that of M3 was chloramphenicol; that of M5 was X-rays; and that of other ANLLs was phenylbutazone. The risk factors of ALL were chloramphenicol, phenylbutazone and family members with cancer; those of CML were X-rays and hepatitis; those of CLL were chloramphenicol and benzene; those of AAA were antipyretics and hepatitis; and that of CAA ws X-rays.
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PMID:[Risk factors analysis of leukemia and aplastic anemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 139 36

Growth and differentiation of hematopoietic progenitor cells is regulated by a complex network of stimulatory and inhibitory cytokines. Bone marrow failures can be due to a decrease of stimulators or an increase of inhibitors. T cells produce both, hematopoiesis stimulating and inhibiting cytokines. Therefore, a role of T cells in regulating hematopoiesis can only be assumed if the gene expression of these antagonistic acting cytokines can be differentially induced in T cells. To establish a model of selective cytokine induction, we investigated the induction of IFN gamma as inhibitor and GM-CSF as stimulator of hematopoiesis in T cells. Our results showed that IFN gamma mRNA accumulates in T cells which have been pre-activated via the signal transduction unit CD3, but not in unstimulated T cells. This accumulation depends on the expression of the high affinity IL2 receptor which is including the IL2 receptor alpha-chain (IL2R alpha, CD25). In a study on children with constitutional (CAA) versus acquired aplastic (EAA) anemia, we investigated the relevance of this model for the pathogenesis of aplastic anemia in childhood. We compared the following parameters: 1. Incidence of hematopoietic progenitor cells and cloning efficiency, 2. activation status and IL2R alpha expression of bone marrow T cells, 3. T cell cytokine expression profile. Our results show: 1. The relative incidence of bone marrow progenitor cells is decreased in children with CAA and normal in children with EAA. 2. Clonogenic growth of hematopoietic progenitor cells is suppressed in children with EAA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental principles of therapy-oriented pathogenetic classification of aplastic anemia in childhood]. 796 17

After studying of familial leukemias, Myelodysplastic Syndrome (MDS) and aplastic anemia (AA), we observed and analysed bone marrow (BM) cells hematologically and molecular-cytogenetically in 36 persons who are first degree relatives (FDRs) of patients with acute leukemias (AL), MDS and AA. The peripheral blood (PB) lymphocyte chromosome fragility sensitive to folic acid and unstability was also analysed in 18 FDRs. The abnormal BM megakaryocystic/erythroid cellularity and the rearrangement of c-erbB were found in 66%-86.1% of parents and siblings of patients. The associations of dysplastic megakaryopoiesis, including the presence of lymphoid small megakaryocytes, with the chromosomal monosomy or/and the rearrangement/amplification of C-erbB, were found in a few parents and siblings. These results were consistent with those of MDS, Fanconi Anemia (FA) and AL. The normal karyotype and SCD positive of BM cells and PB lymphocytes, and PB lymphocyte chromosomal fragility and unstability were found in most of patients' parents, while familial chromosomal monosomy of BM cells and PB lymphocyte chromosomal fragility were found in parents and siblings of familial leukemia patients. Based on the studies of a large family with 7 cases of acute erythroleukamia and relative myeloleukemias in three consecutive generations and a family with 3 CAA and 1 AML, the rearrangement of c-erbB might be inherited. The rearrangement/amplification of c-erbB and its PCR detected results could be the indicators of gene diagnosis of preleukemia and might be useful in genetic conselling of leukemias. The common origin of AL, MDS and AA was discussed.
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PMID:[Relationship between the occurrences of AL, MDS and AA and abnormal BM proliferation of patient's parents]. 975 8

The aim of this article was to explore the pathogenetic differences, as well as to provide a new way for the differential diagnosis of these two diseases by comparative analysis of CD(34)(+) cells numbers and their surface expression of granulocyte colony-stimulating factor receptor (G-CSFR) and granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) in patients with aplastic anemia (AA) and myelodysplastic syndrome (MDS). Twenty-seven patients with AA, 45 patients with MDS, and 20 normal controls were enrolled in this study. The ratio of CD(34)(+) cells and their surface expression of G-CSFR and GM-CSFR were detected by flow cytometry (FCM). The ratio of CD(34)(+) cells in BMMNC of AA, MDS patients and controls were 0.2438 +/- 0.1129%, 2.1677 +/- 1.1345% and 1.0792 +/- 0.3221%, respectively. Compared with normal controls as well as MDS patients, the ratio of CD(34)(+) cells in BMMNC of AA was significantly reduced (P < 0.05). The ratio of CD(34)(+) cells in MDS was significantly elevated than controls (P < 0.05). The ratio of CD(34)(+) cells in BMMNC of MDS-RA and MDS-RAEB patients were 1.2821 +/- 0.4658% and 3.7729 +/- 2.3360%, respectively. Compared with normal controls and MDS-RA patients, the ratio of CD(34)(+) cells in MDS-RAEB was significantly elevated (P < 0.05). The ratio of CD(34)(+) cells in MDS-RA was significantly elevated than AA patients (P < 0.05). The surface expression of G-CSFR on CD(34)(+) cells of AA, MDS patients and controls were 34.402 +/- 21.8357%, 26.376 +/- 15.2895% and 21.443 +/- 7.4465%, respectively. The surface expression of G-CSFR on CD(34)(+) cells of MDS-RA and MDS-RAEB patients were 22.788 +/- 14.7628% and 30.682 +/- 15.5346%. The surface expression of GM-CSFR on CD(34)(+) cells of AA, MDS patients and controls were 6.5961 +/- 4.4322%, 18.2737 +/- 10.9841% and 4.2753 +/- 2.6249%, respectively. Compared with AA and controls, the expression of GM-CSFR in MDS patients was significantly elevated (P < 0.05). The surface expression of GM-CSFR on CD(34)(+) cells of MDS-RA and MDS-RAEB patients were 16.1625 +/- 6.9487% and 22.1003 +/- 14.2983%. In AA patients, the ratio of CD(34)(+) cells in BMMNC less than 0.1% accounts for 75% (6/8) SAA patients, compared with 10.55% (2/19) in CAA (P < 0.05). The detection of CD(34)(+) cells and their surface expression of granulocyte (macrophage) colony-stimulating factor receptors G (M)-CSFR in AA and MDS are helpful in the differential diagnosis or prognosis of these two disorders.
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PMID:Comparative analysis of G-CSFR and GM-CSFR expressions on CD34+ cells in patients with aplastic anemia and myelodysplastic syndrome. 1863 7

This study was aimed to detect the ratio of CD34+ cells in bone marrow mononuclear cells (BMMNCs) and the expression rate of G(M)-CSFR on CD34+ cells in bone marrow of the patients with aplastic anemia (AA) and myelodysplastic syndrome (MDS). The ratio of CD34+ cells in BMMNCs and the expression rate of G(M)-CSFR on cells of 27 AA patients, 45 MDS patients and 20 controls were detected by flow cytometry (FCM). The results showed that the ratio of CD34+ cells in BMMNCs of AA patients reduced and was significantly different from controls (p<0.05), the ratio of CD34+ cells in MDS patients elevated and was significantly different from controls (p<0.05). Compared with controls and MDS-RA patients, the ratio of CD34+ cells in MDS-RAEB patients significantly elevated (p<0.05), but there was no significant difference between MDS-RA patients and controls (p>0.05). The ratio of CD34+ cells in MDS-RA patients was significantly higher than that in AA patients (p<0.05). There was no significant difference in expression rate of G-CSFR on CD34+ cells between AA patients and controls, MDS patients and controls, AA patients and MDS patients, MDS-RA patients and MDS-RAEB patients (p>0.05). The expression rate of GM-CSFR in MDS patients was significantly higher than that in AA patients and controls (p<0.05), but there was no significant difference between AA patients and controls, MDS-RA patients and MDS-RAEB patients (p>0.05). In AA patients, the ratio of CD34+ cells in BMMNCs was less than 0.1% accounts for 6/8 SAA patients, compared with 2/19 in CAA (p<0.05). There was no correlation between the expression rate of either G-CSFR or GM-CSFR and neutrophil count at diagnosis (r=0.058 and r=0.044). In MDS patients, there was no correlation between bone marrow CD34+ cells ratio and peripheral neutrophil count at diagnosis (r=-0.335). And there was no correlation between the expression of either G-CSFR or GM-CSFR and neutrophil count on diagnosis (r=0.064 and r=0.051). It is concluded the detection of CD34+ cells and their surface expression rate of G(M)-CSFR in AA and MDS is useful in diagnosis and differential diagnosis of these two diseases.
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PMID:[Expression of G-CSF and GM-CSF receptors on CD34 positive cells in aplastic anemia and myelodysplastic syndrome patients and its significance]. 1909 33