I came to The Cancer Institute of New Jersey in 2008 after completing a fellowship in surgical oncology at the Memorial Sloan-Kettering Cancer Center. There, I received specialized training in the surgical management of hepatobiliary and pancreatic cancers. I completed my internship and residency in general surgery at the UCLA Medical Center. During my surgical residency I completed a PhD in Molecular, Cell and Developmental Biology through UCLA’s STAR program (Specialized Training in Advanced Research) which is a program designed to provide formalized training in research to post-graduate medical trainees.
As a member of the Liver Cancer and Bile Duct Cancer Program at CINJ, I oversee the management of patients with liver and biliary cancers of all stages. I am trained in radiofrequency ablation techniques and intrahepatic arterial chemotherapy as well as in minimally invasive surgical approaches to gastrointestinal cancers. At CINJ we are a high volume pancreatic surgery center, and I am currently leading a clinical protocol designed to improve quality and efficiency with our patients undergoing pancreaticoduodenectomy (Whipple Procedure) at our Flagship hospital Robert Wood Johnson University Hospital.
Recurrence of patients’ cancers following surgery for gastrointestinal cancers is one of the most significant clinical problems facing surgical oncologists today. Unfortunately recurrence is a problem that can only be remedied by more effective chemotherapy. Therefore, the focus of my laboratory research is in Developmental Therapeutics (novel anti-cancer drugs). Pancreas cancer is a disease that is not only very aggressive, but also the chemotherapy is only marginally effective. I am leading a translational clinical trial to study a novel class of drugs called Hedgehog inhibitors in patients with surgically resectable pancreas cancer so that we may understand more completely how these exciting drugs work in humans.
The next generation of anticancer drugs is defined by compounds that selectively kill cancer cells while leaving normal cells undisturbed. My colleagues at CINJ and I have identified a compound targeting one of the most commonly mutated genes in human cancer, TP53. TP53 is second only to K-Ras as the most commonly mutated gene in pancreatic cancer with point mutations occurring in 75 percent of patients. Considered a tumor suppressor, the protein p53’s normal function is to tightly regulate cellular growth and division, making sure that cells only divide in the appropriate time and place. However, upon mutation, p53 loses its function and allows uncontrolled proliferation of cells, a hallmark of tumor formation. This compound selectively kills cancer cells with one of the most commonly found p53 mis-sense mutants, p53-R175H, by restoring the normal structure and function to this mutant p53 protein. This work was recently published in the journal Cancer Cell (2012) and I have received a grant from the Pancreatic Cancer Action Network to further examine the functions of p53.
Liver, bile duct, pancreatic, gastric and colorectal cancers; metastatic colon cancer to the liver
- Career Development Award, Pancreatic Cancer Action Network-American Association for Cancer Research, 2012
- IMPACT award, The Cancer Institute of New Jersey Foundation, 2011
- UCLA Longmire Scientific Day Research Award, University of California at Los Angeles, 2006
- UCLA Longmire Scientific Day Research Award, University of California at Los Angeles, 2005
- American Association for Cancer Research-Scholar in Training Award, American Association for Cancer Research, 2003
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