2017 Grant Recipient Giulio Draetta, MD, PhD

Home Research Research Grants Program Grants Awarded Grants Awarded by Year 2017 Research Grant Recipients 2017 Grant Recipient Giulio Draetta, MD, PhD

2017 GRANTEE: Giulio Draetta, MD, PhD

MD Anderson Cancer Center
Research Project: Therapeutic Vulnerabilities of Mesenchymal Pancreatic Cancer Cells
2017 Pancreatic Cancer Action Network Translational Research Grant
Award Period: July 1, 2017 – June 30, 2019
Amount: $300,000

Biographical Highlights
Dr. Draetta earned his medical and graduate degrees from the University of Naples Medical School in Italy. Over the years, he held positions in both academic institutions (Cold Spring Harbor Laboratory, EMBL and the European Institute of Oncology), as well as industry. He co-founded several biotechnology companies and was a senior R&D executive with Pharmacia and Merck Research Laboratories. Before joining MD Anderson, Dr. Draetta served as chief research business development officer and deputy director of the Belfer Institute for Applied Cancer Science at the Dana-Farber Cancer Institute. Dr. Draetta currently serves as vice president, therapeutics discovery and is a professor of genomic medicine at the University of Texas MD Anderson Cancer Center.

Dr. Draetta was also the recipient of a $1 million Research Acceleration Network Grant from the Pancreatic Cancer Action Network in 2014, supported in honor of the legacy of Skip Viragh.

Project Overview
Cancer is a dynamic disease that evolves as it progresses, and in response to environmental pressures including drug treatment. Tumors, including pancreatic cancer, can regulate various processes to give them a survival advantage, and this contributes to disease aggressiveness and therapeutic resistance.

A mechanism that pancreatic cancer cells utilize to progress to more advanced stages is called epithelial-mesenchymal transition, or EMT. Higher levels of EMT that occur within a tumor correlate with poorer patient outcomes. Dr. Draetta and his colleagues identified a protein called SMARCB1 as a “gatekeeper” of EMT in pancreatic cancer cells, preventing the transition from epithelial to mesenchymal-like characteristics.

Based on these findings, the research team proposes to expand its studies to evaluate a large collection of patient-derived tissues to determine whether the absence of SMARCB1 could be considered a biomarker, or molecular clue. This biomarker could then be used to predict patients’ likelihood of responding to clinically available drugs.

For this Translational Research Grant project, Dr. Draetta and his team will evaluate several drugs and drug combinations for their effectiveness in the context of SMARCB1 deficiency. Further, they will determine whether other proteins involved in EMT may be therapeutically targetable. Based on the current evaluation of the biomarkers they will study, Dr. Draetta anticipates that this mechanism-based repositioning of clinically-available drugs may provide benefit to at least 10 percent of patients with pancreatic cancer.