Two cell lines of t(8;21) acute myeloid leukemia with activating KIT exon 17 mutation: models for the ‘second hit’ hypothesis
Copyright policy )Two cell lines of t(8;21) acute myeloid leukemia with activating KIT exon 17 mutation: models for the ‘second hit’ hypothesis
In up to 30% of acute myeloid leukemia (AML), chromosomal translocations disrupt one of the core binding factor (CBF) genes most frequently by the t(8;21)(q22;q22). Although patients with CBF leukemia generally have a higher complete remission rate and disease-free survival as compared to those with a normal karyotype or other chromosomal aberrations, additional distinct mutations in genes involved in signal-transduction pathways, particularly in receptor tyrosine kinases (RTKs), herald a higher relapse rate (see below).
- University Medical Center Freiburg Germany
- Memorial Sloan Kettering Cancer Center United States
- University of Freiburg Germany
Leukemia, Myeloid, Acute, Proto-Oncogene Proteins c-kit, Chromosomes, Human, Pair 21, Cell Line, Tumor, Mutation, Humans, Exons, Models, Biological, Translocation, Genetic, Chromosomes, Human, Pair 8
Leukemia, Myeloid, Acute, Proto-Oncogene Proteins c-kit, Chromosomes, Human, Pair 21, Cell Line, Tumor, Mutation, Humans, Exons, Models, Biological, Translocation, Genetic, Chromosomes, Human, Pair 8
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