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)

Hybrid cell lines were derived from fusion of rodent cells with leukocytes from a t(9q+; 22q-)-positive chronic myeloid leukemia (CML) patient carrying a chromosome No. 9-linked adenylate kinase-1 (AK1) polymorphism (AK1 1-2). The AK1*2 allele was consistently expressed when 9q+ was present, whereas the AK1*1-coded isozyme was formed when the normal chromosome No. 9 was present. These results provide additional data confirming the clonal origin of the Ph1 translocation in CML.
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PMID:Clonal origin of the Philadelphia translocation in chronic myeloid leukemia demonstrated in somatic cell hybrids using an adenylate kinase-1 polymorphism. 628 97

Chinese hamster X human and mouse X human somatic cell hybrid lines were obtained using circulating leucocytes from six chronic myeloid leukemia patients. All six patients carried the Ph1 translocation, t(9q+;22q-), characteristic of chronic myeloid leukemia, in their dividing immature granulocytes. Analysis of independent hybrid clones yielded the following results: 1. The chromosome 9 markers, soluble aconitase and adenylate kinase-1, segregated with the 9q+ derivative. The latter marker has previously been localized to 9q34. 2. The chromosome 22 markers, mitochondrial aconitase, N-acetyl-alpha-D-galactosaminidase, and arylsulfatase-A, also segregated with the 9q+ derivative. Mitochondrial aconitase has recently been assigned to 22q11 leads to 22q13. No evidence was obtained either for reciprocity of the translocation or for variations in breakpoints in different patients. The results reported in this paper provisionally assign the gene for mitochondrial aconitase to a region distal to the breakpoint in 22q11.
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PMID:Characterization of the Philadelphia chromosome by gene mapping. 694 69