Previous Rocco Lab Members

I worked on deciphering how expression of the p16 tumor suppressor product of the CDKN2A gene is regulated. My primary focus was how loss of the C-terminal binding protein (CtBP) could release the Polycomb–based repression of CDKN2A so that p16 protein is expressed constitutively, thus inhibiting cell proliferation. Targeting CtBP to activate p16-based tumor suppression could then lead to a novel therapeutic strategy to prevent head and neck squamous carcinogenesis.

I brought a background in the study of genetics, replication stress and disease to the Rocco Lab. I expanded the use of adenoviral delivery of CRISPR technology for genetic editing in cells, in particular to elucidate the cellular pathways associated with the p16 and p14 products of the cyclin-dependent kinase inhibitor 2A (CDKN2A) gene and the tumor suppressor p53. I was also responsible for day-to-day lab functions, ordering supplies and organizing the lab.

I played a fundamental role in establishing the Rocco Lab at Ohio State after its move from Boston in 2015. I was responsible for day-to-day lab functions, overseeing staff training and safety, ordering supplies and performing equipment maintenance and upkeep. I found, expanded, organized and documented the many cancer cell lines and other reagents that came from Boston, allowing the laboratory’s work to proceed efficiently. After two years in the Rocco Lab as the self-described “lab mom,” I took a position in the Clinical Trials Office at the OSUCCC – James.

I investigated the properties of cancer stem cells (CSC) in cell lines derived from head and neck squamous cell carcinoma (HNSCC). I used the ability of single cells to form tumorspheres, floating sphere-shaped structures, as a model to understand how CSC differ from other cancer cells and to find ways to target the CSC population.

I worked to determine the ways that carcinogenic stimuli normally lead to expression of the p16 tumor suppressor from the CDKN2A gene. This tumor suppression is almost always lost before HNSCC develops. I investigated a protein complex including the C-terminal binding protein (CtBP), which helps determine whether p16 expression is kept off or turned on. Understanding the ways that p16 normally is engaged to prevent tumor development may provide ways to detect and treat disease at an early stage before dangerous heterogeneity can develop.

I provided scientific and technical support in histopathology and immunohistochemistry for the laboratory. I developed patient-derived tumor xenografts (PDX) in mice from human head and neck tumors or cells grown in culture to evaluate intra-tumor heterogeneity and devise preclinical screens for the development of novel cancer therapeutics. I also helped other lab members establish and monitor animal experimental models.