title: Chronic myeloid leukemia.
abstract: The molecular origin of the BCR-ABL chimeric gene is now reasonably well defined; a new breakpoint cluster region in the BCR gene, designated mu-bcr, has recently been identified. p210BCR-ABL binds with or phosphorylates a wide variety of intracellular proteins but the mechanism by which it exerts its oncogenic potential is not yet known. Treatment decisions for younger patients are often complex. Interferon alfa prolongs life in comparison with conventional cytotoxic drugs but the optimal starting dosage, the definition of response, and the management of interferon alfa responders remain controversial. Allografting is the treatment of choice for younger patients with HLA-identical siblings but its precise role for patients lacking such donors is still unclear. The transfusion of donor lymphoid cells is very effective in reinducing molecular remission in patients who relapse after allografting; the mechanism for this graft-versus-leukemia effect remains speculative. Autografting with Philadelphia-negative progenitor cells appears promising. A working algorithm for the management of patients not entered into prospective clinical studies is proposed; such an algorithm will need to be updated at frequent intervals.
authors.affiliation: Department of Haematology, Royal Postgraduate Medical School, London, UK.
authors.forename: J M
authors.initials: JM
authors.lastname: Goldman
mesh_terms: D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000276:immunology / Q000628:therapy