Background: Chronic myeloid leukemia is caused by a chromosomal translocation that
results in an oncogenic fusion protein, Bcr-Abl. Bcr-Abl is a tyrosine kinase whose activity is …

The tyrosine kinase activity of the Bcr/Abl oncogene is required for transformation of
hematopoietic cells. The tyrosine kinase inhibitor STI571 (formerly called CGP57148B …

The 2-phenylaminopyrimidine derivative STI571 has been shown to selectively inhibit the
tyrosine kinase domain of the oncogenic bcr/abl fusion protein. The activity of this inhibitor …

Targeting the tyrosine kinase activity of Bcr-Abl with STI571 is an attractive therapeutic
strategy in chronic myelogenous leukemia (CML). A few CML cell lines and primary …

The major mechanism of action of STI571 is a competitive interference with the ATP-binding
site of the Bcr/Abl tyrosine kinase. In the BCR/ABL-positive cell line KBM5, we studied …

STI571, an Abl‐specific tyrosine kinase inhibitor, selectively kills Bcr‐Abl‐containing cells in
vitro and in vivo. However, some chronic myelogenous leukemia (CML) cell lines are …

Despite the efficacy of STI571 (Glivec, Novartis, Basle, Switzerland) in treating chronic
myeloid leukemia (CML), drug resistance has already been noted both in vitro and in vivo …

Clinical studies with the Abl tyrosine kinase inhibitor STI-571 in chronic myeloid leukemia
demonstrate that many patients with advanced stage disease respond initially but then …

A characteristic feature of chronic myeloid leukaemia (CML) is the inevitable advancement
from a treatable chronic phase to a fatal, drug-resistant stage referred to as blast crisis. The …

Philadelphia chromosome-associated leukemias are among the most well-understood
human malignancies. The importance of BCR-ABL enzymatic activity in the proliferation of …