Recent advances in molecular biology of chronic myeloid leukaemia: is the pathogenetic puzzle approaching solution?
The great majority of patients with chronic myeloid leukaemia (CML) have a Philadelphia (Ph) chromosome which has proved at molecular level to be associated with the production of chimeric BCR-ABL gene which in turn is expressed as a fusion protein (P210) with tyrosine kinase activity. An equivalent but somewhat smaller chimeric gene and fusion protein (P190) is found in some cases of Ph-positive acute leukaemia. Though the consistency of these abnormal findings in patients with Ph-positive leukaemia is strong evidence for their pathogenetic role, there are still many unanswered questions.
Goldman
J M
JM
Royal Postgraduate Medical School, London.
D001752:Blast Crisis / Q000235:genetics / Q000473:pathology; D002891:Chromosomes, Human, Pair 21 / Q000648:ultrastructure; D016044:Fusion Proteins, bcr-abl; D006410:Hematopoiesis; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology; D014411:Neoplastic Stem Cells / Q000473:pathology; D010677:Philadelphia Chromosome; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000502:physiology
D009363:Neoplasm Proteins; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl