title: Detection of trisomy 8 in donor-derived Ph- cells in a patient with Ph+ chronic myeloid leukemia successfully treated with Imatinib (STI571) in relapse after allogeneic transplantation.
abstract: Recent data suggest that STI571 (Imatinib) induces complete cytogenetic responses in patients with chronic myeloid leukemia (CML) who relapse after allogeneic stem cell transplantation (SCT). However, little is known about molecular responses to STI571 and the duration of leukemia-free survival in these patients. We report on a 43 year old female patient who presented with a relapse from Ph+ CML in December 2000. Five years earlier she had received an SCT from an unrelated male donor in accelerated phase. At the time of relapse, she presented with marked leukocytosis (89,000 microl) and 10% blasts. In December 2000, therapy with Imatinib was started. After 3 months, the karyotype showed an XY, with trisomy 8 in about 50% of all metaphases, but without evidence of residual Ph+ cells. Moreover, in response to Imatinib, BCR/ABL transcripts decreased and were no longer detectable after 6 months. After a total observation period of 36 months, the patient is still in complete cytogenetic and molecular remission without signs of occurrence of a donor-type hematopoietic neoplasm or CML relapse. These data suggest that Imatinib is a useful agent for long term treatment of relapsed CML after allogeneic SCT.
authors.affiliation: Department of Internal Medicine I, Medical University of Vienna, Austria.
authors.forename: Hermine
authors.initials: H
authors.lastname: Agis
authors.forename: Christine
authors.initials: C
authors.lastname: Mannhalter
authors.forename: Wolfgang R
authors.initials: WR
authors.lastname: Sperr
authors.forename: Felix
authors.initials: F
authors.lastname: Keil
authors.forename: Peter
authors.initials: P
authors.lastname: Kalhs
authors.forename: Hendrati
authors.initials: H
authors.lastname: Pirc-Danoewinata
authors.forename: Maria-Theresa
authors.initials: MT
authors.lastname: Krauth
authors.forename: Oskar A
authors.initials: OA
authors.lastname: Haas
authors.forename: Klaus
authors.initials: K
authors.lastname: Geissler
authors.forename: Klaus
authors.initials: K
authors.lastname: Lechner
authors.forename: Peter
authors.initials: P
authors.lastname: Valent
mesh_terms: D000328:Adult; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000032:analysis; D006801:Humans; D000068877:Imatinib Mesylate; D007621:Karyotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000473:pathology; D008297:Male; D014411:Neoplastic Stem Cells / Q000187:drug effects* / Q000648:ultrastructure; D036102:Peripheral Blood Stem Cell Transplantation; D010677:Philadelphia Chromosome; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D012008:Recurrence; D012074:Remission Induction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016879:Salvage Therapy; D018183:Transplantation Chimera; D014184:Transplantation, Homologous; D014314:Trisomy
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D004791:Enzyme Inhibitors; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl