Dr Laureano de la Vega

Stress Responses

Organisms need to be able to adapt to change in order to survive, and certain cellular programs (stress response pathways) have evolved to respond to a dynamic environment. Example of stress responses pathways include p53, NRF2, and HSF1 pathways. Stress responses are by definition acute, and their transient activation help normal cells to cope with cellular stresses. Interestingly, there is a large body of evidence showing that, in contrast to normal cells, cancer cells are constitutively under cellular stress (i.e. DNA damage/replication stress, proteotoxic stress, mitotic stress, metabolic stress, and oxidative stress) and they depend on the sustained activation of cytoprotective stress response pathways to survive.

The essential nature of the stress response pathways in cancer cells makes them attractive targets, and thus, a better understanding of how these pathways are regulated could help identify new ways to modulate stress responses to impair cancer cell survival. In that sense, our lab is focused in obtaining a detailed understanding of stress response pathways and their aberrations in cancer. For that, we are interested not only on key master regulators of stress responses (e.g. NRF2, HSF1 or P53) but as well in the upstream regulatory pathways that modulate their activity (i.e. upstream kinases).

Laureano is the Science and Health Communication MSc Programme Lead, where he is also module manager for three modules; he also leads the level 4 Cancer Pharmacology and Treatment module within the Biomedical and Biological sciences courses.