AACR Conference & Poster Presentation
I was very fortunate to attend the 101st Annual meeting of the American Association for Cancer Research in Washington, D.C. last week.
There were lots of promising compounds beginning pre-clinical testing by several companies that may someday have an application in treating bile duct cancers. Unfortunately, there were not many presentations on current clinical research with Cholangiocarcinoma. One poster presentation by a group of researchers in Japan showed evidence that a particular type of liver cell called a Hepatic Stellate cell, which has been known to cause fibrosis in chronic liver conditions, may play a key role in the formation of cholangiocarcinomas, and thus may direct future therapy development. I have summarized the study below.
In the meantime, I am looking forward to attending the CanLiv Hepatobiliary conference in May and ASCO in June, where there are numerous clinical trails that will be discussed. More on those later.
Poster title: Hepatic stellate cells promote progression of cholangiocarcinoma in vitro and in vivo
Authors: Hirohisa Okabe, Toru Beppu, Hiromitsu Hayashi, Takatoshi Ishiko, Toshiro Masuda, Ryu Otao, Masayuki Watanabe, Hiroshi Takamori, Hideo Baba. Kumamoto University, Kumamoto, Japan
Summary: The study was designed to identify if hepatic stellate (HS) cells, which have previously been shown to have as pivotal role in fibrogenesis (defn: Formation of fibrous scar tissue) in the liver, exist in the cancer stroma and architecture of intrahepatic cholangiocarcinoma (CCA) cells and what the interaction of these cells are in vitro (in the laboratory) and in vivo (in a living organism). HS cells are found in the sinuses between liver parenchymal spaces and exist in normal liver tissue in a quiescent state and only become activated when there is damage to the liver, as in cirrhosis or fibrosis. It is thought that HS cells play a pivotal role in storing vitamin A when quiescent, but then release collagen scar tissue when they are activated in periods of disease. The authors examined proteins secreted by the co-culture of HS cells and CCA cells in culture medium and in mice in multiple combinations.
This results of this study indicated that HS cells have an important role in accelerating cholangiocarcinoma growth progression. Several proteins including Interleukin1 (IL1β), which is a potent proinflammatory cytokine, induced by co-culture model may be therapeutic targets for chemotherapy which focus tumor-stromal interaction in cholangiocarcinoma.