BCR-ABL-negative chronic myeloid leukemia.
Constitutive activation of protein tyrosine kinases plays a central role in the pathogenesis of myeloproliferative disorders, including BCR-ABL-negative chronic myeloid leukemia. Current research is focused on elucidating the full spectrum of causative mutations in this rare, heterogeneous disease. Activated tyrosine kinases are excellent targets for signal transduction therapy, and an accurate diagnosis including morphology, karyotyping, and molecular genetics will become increasingly important to direct individualized treatment. In addition, new molecular findings need to be incorporated into disease classification systems.
Burgstaller
Sonja
S
Wessex Regional Genetics Laboratory, University of Southampton,Salisbury NHS Foundation Trust, Salisbury SP2 8BJ, UK.
Reiter
Andreas
A
Cross
Nicholas C P
NC
D000368:Aged; D000782:Aneuploidy; D004789:Enzyme Activation; D006801:Humans; D054438:Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / Q000145:classification / Q000175:diagnosis / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D008875:Middle Aged; D009154:Mutation; D015514:Oncogene Proteins, Fusion / Q000235:genetics / Q000502:physiology; D011494:Protein Kinases / Q000235:genetics / Q000502:physiology; D012307:Risk Factors; D015398:Signal Transduction / Q000235:genetics; D014178:Translocation, Genetic
D015514:Oncogene Proteins, Fusion; D011494:Protein Kinases