1. FLT3 inhibition upregulates HDAC8 via FOXO to inactivate p53 and promote maintenance of FLT3-ITD+ acute myeloid leukemia.
2. The study found that FLT3 inhibition could reduce the expression of p53, which is a tumor suppressor gene, and increase the expression of HDAC8, which is an epigenetic regulator.
3. This suggests that FLT3 inhibition may be a potential therapeutic strategy for treating FLT3-ITD+ acute leukemia.
The article is generally reliable and trustworthy as it provides evidence from a scientific study conducted by Long et al., published in Blood journal. The authors have provided detailed information about their research methods and results, as well as discussed the implications of their findings. However, there are some potential biases that should be noted. Firstly, the study was conducted using cell lines derived from patients with FLT3-ITD+ acute leukemia, so the results may not be applicable to all patients with this type of cancer. Secondly, the authors did not explore any possible risks associated with FLT3 inhibition or discuss any potential side effects that could arise from this treatment approach. Additionally, there is no mention of any alternative treatments or therapies that could be used to treat this type of cancer. Finally, while the authors provide evidence for their claims, they do not present any counterarguments or explore any other possible explanations for their findings.