We study signaling networks that are often deregulated in cancer, in an effort to understand why they are deregulated, and how it may be possible to correct this.
Most of our projects concern cellular stress signaling pathways, from ER stress, hypoxia, and cellular response to external (radiation and chemotherapy) and internal (reactive oxygen radicals) stress.
Among key pathways we focus on are ubiquitin ligases and stress activated kinases and respective transcription factors. These players affect ER stress, hypoxia and mitochondrial biogenesis and dynamics.
We use melanoma, prostate and breast cancer related models and patient samples to validate our findings and develop potential new therapeutic modalities.