IMPROVING SURVIVAL RATES IN PATIENTS WITH RELAPSED AND REFRACTORY ACUTE MYELOID LEUKEMIA
Foreword
L
eukemia is a relatively rare form of cancer,
high risk and poor outcome.3 The array of leukemic
accounting for roughly 1% of new cancer
subtypes and prevalence of FLT3 mutations in AML
diagnoses each year. Acute myeloid leukemia
highlight the importance of genetic profiling at the
(AML) is the deadliest and most common type of
time of diagnosis for comprehensive prognostics
leukemia, making up approximately one-third of all
and for identifying targetable oncogenic pathways.
leukemia diagnoses. At just over 11,000 deaths a
As FLT3 inhibitors entered the treatment landscape,
year, AML accounts for nearly half the number of
FLT3 profiling at diagnosis shifted from being purely
annual leukemia deaths (23,100).1 In broad terms,
prognostic to being predictive of patient response
AML can be further categorized based on genetic
and overall survival.4
aberrations, clinical manifestations, and patient
With their distinct immunophenotypic profiles,
prior treatment. The World Health Organization
AML and acute lymphoblastic leukemia (ALL) are
(WHO) divides AML into no fewer than two dozen
distinguished through flow cytometry, which is
subtypes with differing prognostic factors.2 Distinct
performed for 99.1% of all AML patients. Karyotyping,
leukemia molecular subtypes are identifiable by
which 98% of AML patients receive, further
immunophenotype, chromosomal mutation, and
distinguishes clonal cytogenetic abnormalities as
gene mutation.
subtypes of AML.5,6 A 2016 survey found that only
The most common AML mutation is the FMS-like
51% of AML patients were tested for FLT3 genetic
tyrosine kinase 3 (FLT3) gene, which is detected in
mutations, ostensibly leaving a significant portion
approximately 30% of AML cases. Of FLT3 mutation
of AML patients with a gap in treatment options.5
subtypes, internal tandem duplication (ITD) is the
However, that gap is quickly closing.
most common, with FLT3-ITDs found in 25% of all AML cases.3 According to the National Comprehensive Cancer Network (NCCN) and European LeukemiaNet (ELN), the FLT3-ITD mutation is associated with
Anna Love Editor
Dr. Anna Love earned her bachelor’s degree in English in 2009, before returning to school in 2011 for post-baccalaureate studies in science. In 2014, Dr. Love completed her master’s degree in biomedical sciences at William Carey College of Medicine. After which, Dr. Love pursued a Ph.D. in molecular biosciences at Middle Tennessee State University with a focus on developmental and cell biology. Dr. Love currently works as a research fellow at Vanderbilt University Medical Center in the Department of Medicine.
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