Cellular and Molecular Life Sciences CMLS

, Volume 61, Issue 23, pp 2897–2911

Oncogenic protein tyrosine kinases

Abl: the prototype of oncogenic fusion proteins
Multi-author Review

DOI: 10.1007/s00018-004-4271-0

Cite this article as:
Saglio, G. & Cilloni, D. CMLS, Cell. Mol. Life Sci. (2004) 61: 2897. doi:10.1007/s00018-004-4271-0


Since it was first recognized, chronic myeloid leukemia (CML) has always represented a unique model to understand the molecular mechanisms underlying the onset and progression of a leukemic process. CML was the first recognized form of cancer to have a strong association with a recurrent chromosomal abnormality, the t(9;22) translocation, which generates the so-called Philadelphia (Ph)-chromosome. Twenty years later, this abnormality was shown to cover a specific molecular defect, a hybrid BCR-ABL gene, strongly implicated in the pathogenesis of the disease through the production of a protein with a constitutive tyrosine-kinase activity. Although we still lack a complete definition of all the transformation pathways activated by Bcr-Abl, the recent introduction into clinical practice of tyrosine kinase inhibitor represents a major breakthrough to the management of CML and, furthermore, promises to usher in molecularly targeted therapy for other types of leukemia, lymphoma and cancer.

Key words.

c-Abl BCR-ABL Ph-chromosome CML tyrosine-kinase 

Copyright information

© Birkhäuser Verlag, Basel 2004

Authors and Affiliations

  1. 1.Dept. of Clinical and Biological SciencesUniversity of Turin, San Luigi HospitalOrbassano-TorinoItaly

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