title: P185BCR-ABL in two patients with late appearing Philadelphia chromosome-positive acute nonlymphocytic leukemia.
abstract: Two patients with acute nonlymphocytic leukemia (ANLL) who had normal karyotypes at diagnosis and developed the Philadelphia (Ph) translocation during leukemia relapse are described in this report. Patient 1 relapsed with Ph-positive acute leukemia, FAB classification M1. The Ig heavy chain locus and T cell receptor gamma and beta genes of relapse cells from this patient were all found to be germline configuration confirming the diagnosis of M1 acute leukemia. Patient 2 displayed a complex karyotypic evolution leading to Ph-positive M4 relapse. Ph-positive relapse specimens from both patients expressed P185BCR-ABL protein and RNA gene products that were identified serologically and by polymerase chain amplification of the BCR-ABL RNA junction. In vitro derived myeloid cell lines from relapse M1 leukemia cells of patient 1 also expressed the P185BCR-ABL protein. In two described patients, late appearance of the Ph translocation that encodes P185BCR-ABL coincided with relapse of acute leukemia. We conclude that P185BCR-ABL may be a strong indicator of Ph-positive acute leukemias.
authors.affiliation: Tumor Cytogenetics, Polly Annenberg Levee Hematology Center, Mount Sinai Medical Center, New York, New York 10029.
authors.forename: V
authors.initials: V
authors.lastname: Najfeld
authors.forename: J
authors.initials: J
authors.lastname: Cuttner
authors.forename: A
authors.initials: A
authors.lastname: Figur
authors.forename: E S
authors.initials: ES
authors.lastname: Kawasaki
authors.forename: O N
authors.initials: ON
authors.lastname: Witte
authors.forename: S S
authors.initials: SS
authors.lastname: Clark
mesh_terms: D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000032:analysis*; D015870:Gene Expression; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010677:Philadelphia Chromosome
chemical_list: D016044:Fusion Proteins, bcr-abl