Abnormalities in the tumor protein 53 (TP53) gene occur in approximately 5%-10% of patients with de novo acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Despite 4 decades of research, the prognosis of patients with TP53-mutated (TP53_mut) cancers remains poor as they often respond poorly to cytotoxic chemotherapy. These patients may have a median survival of 5 to 10 months, irrespective of therapies used. In a recent study, researchers from the University of Hong Kong’s Faculty of Medicine (HKUMed) identified the therapeutic potential of pololike kinase 4 (PLK4) inhibition in AML and the possible mechanisms behind its in vivo efficacy.

Abnormalities in the tumor protein 53 (TP53) gene occur in approximately 5%-10% of patients with de novo acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).1 Despite 4 decades of research, the prognosis of patients with TP53-mutated (TP53mut) cancers remains poor as they often respond po

A retrospective study on a pediatric population has shown that neurologic manifestations (NMs) in patients with acute leukemia (AL), relating to a greater mortality rate.1 AL is the most prevalent childhood cancer, which accounts for one-third of all cancers within the age range.1 Although the survi

One of the most common acute myeloid leukemia (AML) mutations is the FMS-like tyrosine kinase 3 (FLT3) mutation, which is made up of 2 major types. The more common FLT3-internal tandem duplication (ITD) mutation is associated with poor prognosis, high relapse rate, and poor overall survival (OS), while the prognosis of FLT3-tyrosine kinase domain (TKD) mutation remains unclear.¹

Children with Down syndrome are at an elevated risk of multiple malignancies and hematological disorders such as different types of leukemia.1,2 To better reflect the current risk association between Down syndrome and childhood leukemia, investigators from the United States had conducted a large, co