David Cheresh,
Distinguished Professor of Pathology ,
University of California-San Diego
David Cheresh, PhD, studies the molecular basis of angiogenesis and tumor progression. He spent to early part of his career at The Scripps Research Institute and moved to the UC San Diego Moores Cancer Center in 2005 where he has led efforts to develop new collaborations and programs in clinical and basic science with an emphasis on translational medicine. He is Associate Director for Innovation and Industry Alliances at the Cancer Center, and Vice Chair and Distinguished Professor of Pathology. Dr. Cheresh studies the signaling networks that regulate angiogenesis, tumor stemness, drug resistance and metastasis. He identified that integrin a?ß3 – a receptor on the surface of tumor-associated blood vessels – as a critical biomarker of angiogenesis. More recently his team discovered that this molecule drives tumor stemness, drug resistance and progression. He successfully translated laboratory discoveries into biologically-based drugs that are now in various stages of clinical development.
Targeting Cancer Stem Cells Using avß3 Integrin as Oncology Biomarker
Thursday, 15 January 2015 at 14:30
Add to Calendar ▼2015-01-15 14:30:002015-01-15 15:30:00Europe/LondonTargeting Cancer Stem Cells Using avß3 Integrin as Oncology BiomarkerPrognostic, Predictive, and POC: Biomarkers from Research to Clinic in San Diego, California, USASan Diego, California, USASELECTBIOenquiries@selectbiosciences.com
Tumor cells, with stem-like properties, are highly aggressive and often display drug resistance. Here, we reveal that integrin avß3 serves as a marker of breast, lung and pancreatic carcinomas with stem-like properties that are highly resistant to receptor tyrosine kinase inhibitors such as erlotinib. This was observed in vitro and in mice bearing patient-derived tumor xenografts or in clinical specimens from lung cancer patients that had progressed on erlotinib. Mechanistically, avß3, in the unligated state, recruits KRAS and RalB to the tumor cell plasma membrane, leading to the activation of TBK-1/NFkB. In fact, avß3 expression and the resulting KRAS/RalB/NFkB pathway were both necessary and sufficient to promote tumor initiation, anchorage-independence, self-renewal, and erlotinib resistance. Pharmacological targeting this pathway with Bortezomib reversed both tumor stemness and erlotinib resistance. These findings not only identify a?ß3 as a marker/driver of carcinoma stemness but they reveal a therapeutic strategy to sensitize such tumors to RTK inhibition.
Add to Calendar ▼2015-01-15 00:00:002015-01-16 00:00:00Europe/LondonPrognostic, Predictive, and POC: Biomarkers from Research to ClinicPrognostic, Predictive, and POC: Biomarkers from Research to Clinic in San Diego, California, USASan Diego, California, USASELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2015-01-15 14:30:002015-01-15 15:30:00Europe/LondonTargeting Cancer Stem Cells Using avß3 Integrin as Oncology BiomarkerPrognostic, Predictive, and POC: Biomarkers from Research to Clinic in San Diego, California, USASan Diego, California, USASELECTBIOenquiries@selectbiosciences.com
