作者: Gayle E. Woloschak , Gordon W. Dewald , Rebecca S. Bahn , Robert A. Kyle , Philip R. Greipp
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摘要: Previous work has established the presence of an unbalanced chromosome abnormality [+der(1),t(1;7)(p11;p11)] in some therapy-associated myelodysplastic disorders. Recently EGF receptor been found to reside at 7p11. Using a probe specific for erb B oncogene, which encodes truncated form receptor, we examined RNA and DNA derived from bone marrow peripheral blood mononuclear cells three patients with syndromes (MDS) one acute lymphocytic leukemia (ALL), all bearing abnormal clone their similar 1;7 translocation. DNA-excess slot blot hybridization 5′-32p-labeled cellular revealed ten- thirtyfold enhancement accumulation mRNA both MDS when compared normal controls. In addition, H-ras was detected some, though expression other genes such as actin, N-ras, myc, src, B-lym, 20 not be enhanced. Increased apparent hematologic disorders chronic leukemia, Hodgkin's disease, or lymphoma. Southern analysis restriction-enzyme-cleaved translocation that gene amplified least twentyfold white cells, while levels actin were comparable those No amplification evident ALL patient. Our data suggest +der(1),t(1;7)(p11;p11) chromosomal anomalies can specifically associated sequences.