Our laboratory is interested in understanding the mechanisms by which myeloid cells fuel and facilitate tumor initiation, progression and metastasis.

Myeloid cells, which constitute the first barrier of the innate immune system upon an insult, are equipped to provide sensing, recognition, pro-inflammatory and homeostatic functions. Thus, their unique presence in tissues places them at the forefront of tumor cell recognition and inception.

Innate immune cells possess a circadian molecular clock that time the functional properties of these cells, driving temporal windows of action for cell-type-specific processes. In a similar manner, circadian oscillations have also been described in cells of the adaptive immune system, such as T cells. We aim to decipher clock-controlled tissue immune surveillance in order to promote cancer cell clearance thus, preventing tumor growth and invasion.

Epigenetic reprogramming of myeloid cells upon exogenous or endogenous insults leads to an altered response to subsequent triggers, which can favor disease progression. Our lab aims to understand the mechanisms by which myeloid cells in metastatic sites are co-opted by signals raised in primary tumor.

With the help of integrated single cell transcriptomics, proteomics and multiplex imaging, we seek to understand myeloid functional programs at the very early stages of tumorigenesis, and how these cells may be harnessed to better enable an anti-tumor response.

Our ultimate goal is to identify myeloid determinants of tumor progression in pre-malignant lesions.