Abstract
Chronic myeloid leukemia (CML) is characterized at the molecular level by the presence of the Philadelphia chromosome (Ph) and the resultant oncogenic signaling by the BCR-ABL fusion protein. The treatment and outlook for CML were revolutionized by the introduction of imatinib, but resistance is a substantial barrier to successful treatment in many patients. Introduction of the second-generation tyrosine kinase inhibitors (TKI) dasatinib and nilotinib has provided effective therapeutic options for many patients with resistance to front-line imatinib. However, the T315I mutation remains a significant clinical issue because it is insensitive to all currently available agents. A number of new agents are in development and many hold the promise of activity in T315I-mutated disease. Successful treatment of patients with disease harboring T315I might lie in the effective combination or sequencing of these new agents with existing TKI therapies.
Original language | English (US) |
---|---|
Pages (from-to) | S272-279 |
Journal | Clinical lymphoma & myeloma |
Volume | 9 Suppl 3 |
DOIs | |
State | Published - 2009 |
Externally published | Yes |
ASJC Scopus subject areas
- Hematology
- Oncology
- Cancer Research