Clinical algorithms for the treatment of patients with chronic myeloid leukemia: the 2010 perspective.

Elias Jabbour, Amber Fullmer, Jorge E. Cortés, Hagop Kantarjian

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Chronic myeloid leukemia (CML) is a progressive and often fatal myeloproliferative disorder. The hallmark of CML is an acquired chromosomal translocation known as the Philadelphia chromosome (Ph) that results in the synthesis of the BCR-ABL fusion protein, a constitutively active tyrosine kinase (TK). The introduction of imatinib, a TK inhibitor (TKI) specific for BCR-ABL, was a major breakthrough in CML therapy. Although most patients respond to first-line imatinib therapy, some experience a loss of response (resistance) or require treatment discontinuation because of toxicity (intolerance). In patients for whom standard-dose imatinib therapy (400 mg/day) fails, imatinib dose escalation (600-800 mg/day) is a second-line option. However, high-dose imatinib is not an appropriate approach for patients experiencing drug toxicity, and there remain questions over the durability of responses achieved with this strategy. Alternative second-line options include the newer TKIs dasatinib and nilotinib. A substantial amount of long-term data for these agents is available. Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status. To optimize therapeutic benefit, clinicians should select treatment based on each patient's historical response, adverse event tolerance level, and risk factors.

Original languageEnglish (US)
Pages (from-to)S6-13
JournalClinical lymphoma, myeloma & leukemia
Volume10 Suppl 1
StatePublished - Jun 2010
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Cite this