New insights into the complex regulation and function of ASPP2 tumor suppressor: the discovery of the ΔN-ASPP2 isoform

Cancer remains the second leading cause of death in the United States, despite recent declines in mortality. Tumor progression involves evading cellular checkpoints, including apoptosis, a key defense against malignancy. Resistance to apoptosis often occurs through disruption of tumor suppressor pathways, notably p53. As a critical transcription factor, p53 mediates responses to genetic damage and oncogenic stress by inducing cell cycle arrest, DNA repair, and apoptosis. Understanding how p53-driven apoptotic signaling is regulated—and how it becomes impaired during tumor evolution—is essential for developing therapies aimed at restoring apoptotic sensitivity, a major goal in cancer treatment.