The onset of CML in blastic crisis: molecular features.
The lack of distinguishing characteristics between lymphoid blastic crisis (BC) of Philadelphia (Ph)+ chronic myeloid leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL) remains an exciting dilemma. Indeed, the genetic defect of approximately half of Ph+ ALL patients is identical to that identified in CML. Here we report the case of one patient admitted with immunological and molecular patterns indicative of Ph+ ALL. The patient was brought into complete remission by chemotherapy and was transplanted with an HLA identical sibling donor, but relapsed a few months later with immunological and molecular evidence of BC of CML, displaying myeloid markers and lacking lymphoid antigens and immunoglobulin heavy chain (IgH) rearrangement. This suggest a CML case with an initial BC without a previous chronic phase or supervening on a subclinical CML.
Gregorini
A
A
Istituto di Biologia e Genetica, Università degli Studi, Ancona, Italy.
Filippetti
A
A
Luchetti
F
F
Walker
A
A
Lillington
D M
DM
Papa
S
S
Valentini
M
M
D000328:Adult; D001752:Blast Crisis / Q000235:genetics / Q000276:immunology; D016026:Bone Marrow Transplantation; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D006801:Humans; D016130:Immunophenotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000628:therapy; D012008:Recurrence
D016044:Fusion Proteins, bcr-abl