Tumorigenesis and Genomic Stability
Caspases play complex roles in cancer biology, acting both to promote tumor proliferation in some contexts and suppress tumorigenesis in others. Our work focuses on caspase-2’s mechanistic roles and therapeutic potential across cancers where genomic stability is pivotal, including but not limited to AML and breast cancer.
Our Discoveries
Our findings are shaping new approaches to cancer treatment by elucidating caspase-2’s multifaceted functions and mechanisms across tumor contexts.
Caspase-2 is essential for AML cell self-renewal and mutant NPM1 relocalization
Caspase-2 regulates proliferation and self-renewal in NPM1-mutant AML through aberrant cytoplasmic relocalization and disruption of cell cycle and stress response pathways.
Preclinical caspase-2 inhibition suppresses AML progression
Pharmacologic inhibition of caspase-2 suppresses leukemia growth in patient-derived NPM1-mutant AML models, supporting its translational therapeutic potential.
Caspase-2 suppresses tumor growth by maintaining genomic stability
Caspase-2 functions as a tumor suppressor by preserving genomic stability through regulation of DNA damage responses and cell cycle progression.
Caspase-2 activation sites influence cancer outcomes
Spatially distinct activation of caspase-2 in the nucleolus versus cytoplasm drives divergent cellular outcomes that may underlie its context-dependent roles in cancer.
Caspase-targeted therapeutic strategy: sensitizing lung cancer cells to apoptosis
Proteasome inhibition enhances caspase-mediated cytotoxicity in lung cancer models, highlighting opportunities to therapeutically exploit caspase signaling pathways.
Join us in pioneering new therapies for cancer and inflammatory disease.
