Chad Pecot, MD
Professor
About
- Department Affiliations:
- Medicine
I am a professor at the UNC School of Medicine and am a Lineberger Comprehensive Cancer Center member, and I specialize in solid tumor malignancies. As a prior cancer patient, my passion is to uncover important findings in cancer biology and translate these to the clinic as rapidly as possible. Since August 2013 I have been an independent investigator at UNC-Chapel Hill. My research career thus far has quickly led to several high-impact discoveries as a result of innovative ideas and establishment of synergistic collaborative teams. I also have a passion for training the next generation of scientists at the doctoral and postdoctoral level. My research is characterized by a harmonization of therapeutic RNA interference, sophisticated modeling of cancer metastasis and the tumor microenvironment, and the integrative use of complex bioinformatic and systems biology approaches to uncover key nodes in cancer networks. Because metastatic spread accounts for the greatest proportion of cancer-related deaths in the U.S. and worldwide, most of my current work uses lung and triple-negative breast cancers as disease models with the hopes that our discoveries will also fundamentally impact treatment paradigms in other aggressive malignancies.
My Research
I am a lung cancer specialist with a particular interest in how RNA interference (RNAi) can regulate cancer metastases. Because metastases are responsible for the death of nearly all cancer patients, the ability to control this process is vital. In collaboration with our Carolina Center of Cancer Nanotechnology Excellence, I am studying how nanoparticle-based platforms can be exploited to target the metastatic process. Currently I have three areas of focus centered on this problem:
First, our group helped discover and characterize how the miR-200 family regulates tumor angiogenesis. We found that miR-200 directly targets IL-8 and CXCL1 cytokines secreted from cancer cells, which are important mediators of angiogenesis and metastasis. We demonstrated that miR-200 regulation of angiogenesis is a novel regulatory network across several cancer types; namely lung, ovarian, renal and triple-negative breast adenocarcinomas. Several metastatic models demonstrated that nanoparticle-mediated delivery of miR-200 members could potently silence IL-8 and CXCL1, leading to therapeutic inhibition of angiogenesis and metastases. Current efforts are on further characterizing how this miRNA family regulates cancer progression.
Second, I am studying novel miRNA mediators of lung cancer metastasis. Our group is utilizing the Cancer Genome Atlas dataset to investigate key regulatory networks within lung adeno- and squamous carcinomas. We are establishing new metastases models to study candidate miRNAs of interest. The ultimate goal will be to explore and develop systemically delivered miR-based therapeutics to inhibit metastases in these models.
Finally, since the classic KRAS oncogene is largely considered “non-druggable”, I am investigating how nanoparticle delivery of KRAS siRNAs can be used to therapeutically inhibit KRAS-driven cancers. Using metastatic models of lung and colorectal cancers, we have found that systemically delivered KRAS siRNAs can potently inhibit metastases formation. We are interested in further developing this approach as a novel therapeutic to enter early-phase clinical trials.