Despite being the most prevalent cancer among children, over 90% of pediatric acute lymphoblastic leukemia (ALL) cases are cured in most developed countries^.1 This has largely been attributed to the introduction of risk stratification protocols and risk-directed therapies.² However, there remains heterogeneity in treatment responses within risk groups which suggests the need for risk stratification to be further refined.² The predictive potential of CD9, a tetraspanin family protein that regulates cell motility, adhesion and signaling, in survival outcomes of patients with childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) was previously highlighted in a local single-center investigational study.³ Thereafter, researchers from The Chinese University of Hong Kong (CUHK) and clinicians in the Hong Kong Children’s Hospital conducted a nationwide, multicenter, retrospective study to validate clinical performance of CD9 as a prognostic biomarker in childhood ALL.²

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.

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