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T cells engineered to express chimeric-antigen receptors (CAR-T cells) can effectively control relapsed and refractory haematological malignancies in the clinic. However, the successes of CAR-T cell therapy have not been recapitulated in solid tumours due to a range of barriers such as immunosuppression, poor infiltration, and tumour heterogeneity.
Children with Down syndrome (DS, trisomy 21) are at a significantly higher risk of developing acute leukemia compared to the overall population. Many studies investigating the link between trisomy 21 and leukemia initiation and progression have been conducted over the last two decades.
Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes.
Transcription factors known to induce the epithelial-to-mesenchymal transition (EMT) (such as ZEB1/2 [zinc finger E-box binding homeobox 1/2], SNAI1/2/3, and TWIST1/2) have been undoubtedly implicated in tumorigenesis, cancer progression, metastasis, and chemoresistance in solid tumors; however, their role in normal and malignant hematopoiesis has been underappreciated for many years.
Here we report that CHAF1B is required for normal hematopoiesis while its overexpression promotes leukemia