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

Patients with multiple myeloma (MM) are highly susceptible to developing relapsed and refractory (RR) disease towards lenalidomide and proteasome inhibitors (PIs) and require new active treatments at relapse. As such, novel treatment options like isatuximab, a monoclonal antibody (mAb) that targets