FLT3-ITD

[Leukemia] Utilizing a Flt3-ITD knock-in, Dnmt3a haploinsufficient mouse model, researchers demonstrated that Gab2 was essential for the development of Flt3-ITD driven acute myeloid leukemia in vivo, asGab2 deficient mice displayed prolonged survival, presented with attenuated liver and spleen pathology and reduced blast counts.

[Leukemia] Researchers discovered that FMS-like Tyrosine Kinase 3 (FLT3)-internal tandem duplication (ITD) directly binded to CSF2RB in acute myeloid leukemia (AML) cell lines and blasts isolated from AML patients.

[Nature Genetics] Researchers applied an integrated genomic approach to a murine allelic series that modeled the two most common mutations in acute myeloid leukemia (AML): Flt3-ITD and Npm1c, then deconvoluted the contribution of each mutation to alterations of the epigenetic landscape and genome organization.

[British Journal of Cancer] The ability of CCT245718 to overcome TKD-mediated resistance was evaluated in a cell line-based model of drug resistance to Fms-like tyrosine kinase 3 (FLT3) inhibitors.

[Communications Biology] Midostaurin resistance was overcome by a combination of midostaruin, the BCL-2 inhibitor venetoclax and the RAC1 inhibitor Eht1864 in midostaurin-resistant acute myeloid leukemia (AML) cell lines and primary samples, providing the first evidence of a potential new treatment approach to eradicate FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication + AML.

[Cancer Gene Therapy] The authors reported that cabozantinib could promote differentiation in erythroid leukemia cells and found that K562 erythroid leukemia cells treated with 1 μM cabozantinib for 72 hours underwent erythroid lineage differentiation.