Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 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

Twenty-nine patients with acute myelocytic leukemia (AML) and 14 patients with Philadelphia chromosome-positive chronic myelocytic leukemia (CML) were analyzed to detect the presence of mutations in their ras genes by the polymerase chain reaction and oligonucleotide hybridization methods. Deoxyribonucleic acid (DNA) isolated from blood or bone marrow samples was screened for mutations in codons 12, 13 and 61 of N-ras and in codons 12 and 61 of K-ras and H-ras. We detected mutations of the ras gene in 7 patients with AML (7/29), all in N-ras. The mutations were 3 GGT- greater than GAT transitions in codon 12, 1 GGT- greater than TGT transition in codon 13, and 3 CAA- greater than AAA transitions in codon 61. No correlation has been observed between French-American-British subtypes and the incidence of N-ras mutation, nor between cytogenetic changes and the incidence of N-ras mutation. All ras gene mutations detected by the oligonucleotide hybridization method were further confirmed by direct sequencing. No mutations were detected in ras genes in samples from the 14 Philadelphia chromosome-positive CML patients (12 in chronic phase, 2 in blastic phase). These findings are in line with previous results indicating that ras gene mutations in the codons tested play only a small role in the tumorigenesis of CML.
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PMID:Mutation analysis of the ras gene in myelocytic leukemia by polymerase chain reaction and oligonucleotide probes. 168 80