Raquel Buj-Gomez, PhD

Dr. Buj's research is focused on understanding the fundamental metabolic and epigenetic mechanisms that drive malignant transformation and tumorigenesis downstream p16 loss. p16 is an important tumor suppressor protein suppressed in ~50% of human cancers and is highly upregulated in many types of senescence. Senescence is a stable cell cycle arrest also characterized by high metabolic activity and epigenomic reorganization. Senescence acts as a double-edge sword in human cancer. On one hand, senescence is a tumor suppressor mechanism that maintains the cell cycle arrest in part by overexpressing p16. On the other hand, senescent cells acquire a senescence-associated secretory phenotype (SASP) that promotes chronic inflammation and tumorigenesis. Dr. Buj's research program aim to understand the metabolic and epigenetic mechanisms that promote senescence-bypass and malignant transformation downstream of p16 loss with the ultimate goal of developing new targeted therapies for patients with null or very low p16 expression.
 
Currently, Dr. Buj is involved in two major lines of research:
 
1) To investigate whether altered metabolism and epigenome downstream of p16 loss leads to reprogrammed SASP and tumor microenvironment, impairing tumor immunosurveillance.

2) To investigate the coordinated mechanism between mTORC1 and the Hippo pathway to alleviate oxidative stress and promote malignant transformation downstream of loss of p16.