Enrique Torchia

We study how the fidelity of cell division (e.i., the formation of two genetically identical daughter cells) is regulated during increased proliferation in normal tissues or can be compromised in cancer to contribute to tumor progression. We are focusing on three questions: 1. How is mitosis regulated in highly proliferative conditions? 2. How is mitotic fidelity maintained during highly proliferative conditions? 3. How does mitotic infidelity contribute to cancer progression and metastasis? We use physiological models coupled to basic biochemical and cell biology techniques as well as new emerging single cell and bioinformatic approaches. We have defined the role of the mitotic kinase AURORA A in skin cancers and shown how enhanced genomic instability can accelerate metastasis prone skin cancers. We have also described mechanisms that regulate mitosis in rapidly diving tissues under normal (e.g., development) and precancer conditions using genetically engineered animal models.