Our results indicate that the NF1 tumor suppressor gene is a direct transcriptional target of RUNX1 and the t(8;21) fusion protein, suggesting that suppression of NF1 expression contributes to the molecular pathogenesis of AML.
Since neurofibromatosis-type 1 (NF1) patients are at an increased risk to develop malignancies, we used the fluorescence in situ hybridization (FISH) replication assay and evaluated the level of replication synchrony of three cancer-implicated genes (RB1, AML1, and CMYC) in lymphocytes derived from patients with NF1 without malignancy.