Christine Chio, PhD

Lab Members

Christine ChioChristine Chio, Ph.D.

Assistant Professor of Genetics & Development

Location: Room 505
Phone: 212-851-4967

Post Doctoral training
11/2012 - Present: Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. Postdoctoral fellow

09/2006 - 10/2012: University of Toronto, Dept of Medical Biophysics, Toronto, Canada.  PhD, June 2012
09/2002 - 06/2006: University of Toronto, Department of Genetics, Toronto, Canada. HBSc, June 2006

2003, 2004, 2005: University of Toronto Scholar award
2003, 2004, 2005: University of Toronto, St. Michael’s College in course scholarship
2004: Charles Lester Mills Scholarship in Science
2004, 2005: Pang Shou Yun scholarship
2005: Life science Fellowship (U of T, Dept of Medical Genetics)
2005: Starbucks Clinical Genetics Studentship (Hospital of Sick children)
2006: University of Toronto, St Michael’s College Silver Medal (Graduation award for student with high cGPA)
2006, 2007, 2008: University of Toronto Fellowship
2006-2011: University of Toronto Connaught Scholarship
2009: 12th International TNF conference award
2009, 2010: Ontario Graduate Scholarship (OGS 2009-2010)
2011, 2012: Medical Biophysics Excellence Award
2012-2013: Human Frontiers post doctoral fellowship
2013-2017: Damon Runyon post doctoral fellowhip
2003-Present: Member of Golden Key International Honour Society
10/2013- Present: Damon Runyon Research Fellow
7/2016: Aspen Cancer Fellowship
4/2015-Present: Member of American Association for Cancer Research
2/2017-Present: Editorial board member of “Gastroenterology and Liver Clinical and Medical Issues”


Pancreatic ductal adenocarcinoma (PDA) is the third leading cause of cancer death in the United States. Lethality of PDA owes largely to the advanced disease stage at the time of diagnosis and to its profound resistance to existing therapies. Targeted therapy is a cornerstone of precision medicine, and is currently the focus of much anticancer drug development. However, in the context of pancreatic cancer, no chemical inhibitors exist for the most common KRAS mutations (G12D, G12V) even though it is well established that the oncogenic KRAS promotes drug resistance. Thus, a detailed understanding of the role of specific genetic lesions and their signaling surrogates in the initiation and progression of PDA is critical to improving treatment efficacy and patient outcome for this disease.

A key histopathological feature of PDA that is also associated with its innate clinical and biological aggressiveness is its pronounced desmoplastic (stromal) reaction. Desmoplasia generates a nutrient and oxygen-deprived environment in PDA that is unique to the disease. The resultant redox and metabolic adaptations thus create cancer-specific vulnerabilities that could potentially be exploited. My central hypothesis is that PDA cells harness reactive oxygen species (ROS) as selective secondary messengers to support cancer cell viability and tumor-stroma co-evolution. The goal of my research to leverage the ability of PDA cells to regulate levels of reactive oxygen species towards the development of more effective therapies for this highly lethal malignancy. The cytoprotective transcription factor NRF2 is a central regulator of redox homeostasis and is up-regulated in PDA. As transcription factors are difficult to target therapeutically, the Chio laboratory seeks to comprehensively characterize the mechanisms used by NRF2 to promote PDA such that more feasible approaches to counter its effects in PDA may be developed. In pursuit of this goal, genetically engineered mouse models (GEMM), ex-vivo organoid co-culture systems, and patient-derived organoid transplantation models will be used to establish a discovery pipeline and in vivo validation platforms that will facilitate the design of integrated intervention strategies for a disease involving complex interactions between the tumor and the stroma.

You can find out more about her work and the field of redox here: