title: Is cure for chronic myeloid leukemia possible in the tyrosine kinase inhibitors era?
abstract: OBJECTIVE
  The advent of tyrosine kinase inhibitors (TKI) has remarkably changed the treatment of chronic myeloid leukemia (CML). Patients treated in chronic phase can enjoy an expected survival similar to the general population. In the last few years we have found that some patients with an excellent therapeutic response can have their TKI discontinued and still remain in molecular remission.
  
  
  RESULTS
  The fact that some patients can apparently have their therapy discontinued, and stay in remission for more than 2 years, is surprising, as in-vitro work suggests the CML cell is dependent on BCR-ABL signaling and mathematical models predict that extinction of the CML stem cell reservoir will take decades of therapy. However, given that unopposed BCR-ABL causes progression and CML cells can have a rather long latency (e.g., Hiroshima survivors), it may be some time until we can be completely assured that discontinuation is without risk.
  
  
  CONCLUSIONS
  If we can safely discontinue TKI in some patients, it will have a profound effect on both the strategy and medical economics of CML therapy. A key future finding will be factor(s) that predict which patients can be discontinued without relapse, thus targeting only the patients where discontinuation will be successful.
authors.affiliation: aPharmaceutical Outcomes Research and Policy Program, University of Washington bPublic Health Sciences Division, Fred Hutchinson Cancer Research Center cClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
authors.forename: Aasthaa
authors.initials: A
authors.lastname: Bansal
authors.forename: Jerald
authors.initials: J
authors.lastname: Radich
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000235:genetics; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D008962:Models, Theoretical; D058990:Molecular Targeted Therapy; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D016044:Fusion Proteins, bcr-abl