Abstract
A plethora of new molecular abnormalities has been identified to be associated with acute myelogenous leukemia (AML). These markers have contributed to a more accurate prognostic stratification of these patients, and have nurtured hopes for effective targeted therapies. One such abnormality is the FMS-like tyrosine kinase 3, or FLT3 gene mutation, present in approximately 30 % of AML patients. The presence of the FLT3 internal tandem duplication (FLT3-ITD) confers a poorer prognosis with higher risk of relapse for this subset of AML patients. Rapid development of a large number of FLT3 tyrosine kinase inhibitors (TKIs) has enabled an exciting era of research and treatment for patients with these abnormalities. The expectation is that FLT3 inhibition may offer improvements in outcomes in this poor prognosis group of patients. Early data suggest that this promise may be materializing for patients. This chapter will focus on two of these FLT3 inhibitors, sorafenib (Nexavar®) and AC220 (quizartinib).
| Original language | English (US) |
|---|---|
| Title of host publication | Targeted Therapy of Acute Myeloid Leukemi |
| Publisher | Springer New York |
| Pages | 233-249 |
| Number of pages | 17 |
| ISBN (Electronic) | 9781493913930 |
| ISBN (Print) | 9781493913923 |
| DOIs | |
| State | Published - Jan 1 2015 |
| Externally published | Yes |
Keywords
- AML
- FLT3
- Quizartinib
- Sorafenib
- Tyrosine kinase inhibitor
ASJC Scopus subject areas
- General Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)
- General Biochemistry, Genetics and Molecular Biology
- General Immunology and Microbiology