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Sunrise CE Course: A Great Start to the Annual Meeting

By Betina Lew posted 03-23-2015 10:22 AM

  

On Sunday morning I attended the Sunrise Continuing Education Course "New Horizons in Chemical Carcinogens: Advances in Mode of Action (MoA) and Mechanisms of Cancer Pathogenesis." The course featured two speakers, who were also the Co-Chairs for the session: Dr. James Klaunig from Indiana University, and Dr. Udayan Apte from the University of Kansas Medical Center.  The course started at 7:00 AM and despite the early Sunday morning schedule, the session was extremely well attended by the many Toxicologists who, like me, are directly or indirectly involved in chemical carcinogenicity.

Dr. Klaunig opened the course with a very nice overview of carcinogenicity.  He reminded us of basic concepts in cancer: terminology, stage of the disease development and possible mechanisms of actions of chemical carcinogens (with emphasis on hepatic carcinogens).   He then focused his presentation on the “traditional” MoA of chemical carcinogens,” and talked about the mechanisms of action through activation of PPARα, CAR, PXR, ER and AhR.

Dr. Apte, focused on the “new” receptors involved in Chemical Carcinogenesis. As a “Hepatomaniac” [sic], his research is also conducted with the liver.  Dr. Apte started his presentation adding the HNF4α to the table of the “traditional” Nuclear Receptors involved in chemical carcinogenesis.  He explained that HNF4α is considered “the new tumor suppressor” that can inhibit cell proliferation and cancer in multiple organs, such as colon and liver. He presented some results of research conducted with the help of combinatorial genomics that shows that HNF4α inhibits pro-mitogenic and EMT (Epithelial-Mesenchymal Transition) genes through several different mechanisms such as inhibition of Cyclin D1 and cMyc functions, and Snail mediated EMT.  Dr. Apte explained that HNF4α deletion promotes Hepatocellular Carcinoma (HCC) pathogenesis in mice. He finally applied the findings to create hypothesis on the roles of HNF4α on Human HCC Pathogenesis. He ended his talk presenting data on HNF4α gene expression profile compared to several stages of HCC. 

Both talks were very informative and a wonderful way to kick off the 54th Annual Meeting of the SOT.

 

This blog discusses highlights from the SOT Annual Meeting Sunrise CE Course "New Horizons in Chemical Carcinogens: Advances in Mode of Action (MoA) and Mechanisms of Cancer Pathogenesis."  

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