An internationally recognized pancreatic cancer researcher, Dr. Eibl's laboratory was the first to demonstrate, in animal models, that a high-fat, high-calorie diet accelerates pancreatic cancer development — providing direct causative evidence for the link between obesity, inflammation, and one of the deadliest human malignancies.
Diet-induced obesity accelerates pancreatic cancer
Using the conditional KrasG12D (KC) mouse model, Dr. Eibl's team showed that a high-fat, high-calorie diet drives visceral obesity, hyperinsulinemia, and pancreatic inflammation — and dramatically increases the incidence and progression of pancreatic neoplasia. It was among the first work to establish a direct, causative link in a living system between diet-induced obesity and pancreatic cancer risk, reframing the disease as one that can be accelerated — and potentially intercepted — through metabolic and inflammatory pathways.
Background
Dr. Eibl is a Professor in Residence in the Department of Surgery at the David Geffen School of Medicine at UCLA and a member of the Jonsson Comprehensive Cancer Center. For two decades his research program has centered on the role of inflammation in the development and progression of pancreatic cancer, with a particular focus on how obesity and the metabolic state of the host shape tumor biology.
His work spans eicosanoid and cyclooxygenase signaling, the anti-inflammatory effects of omega-3 polyunsaturated fatty acids, and naturally derived compounds for cancer prevention. He has held a Program Project Grant investigating interventional strategies that address obesity-associated cancer risk — translating mechanistic insight into prevention and therapeutic opportunity.
Drug-development & targeted-therapy work
As a senior investigator, Dr. Eibl co-authored work defining how Src family kinase inhibition reshapes signaling in pancreatic cancer cells — showing that the Src inhibitor dasatinib combined with the MEK inhibitor trametinib synergistically suppresses colony formation and tumor growth in vivo, supporting combination targeted therapy for PDAC. His laboratory has likewise tested repurposed agents such as metformin and simvastatin, showing that low-dose combinations can blunt obesity-promoted pancreatic cancer development in genetically engineered mice.
Selected publications
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