It has been established that genetic alterations cause initiation and malignant progression of cancer as generally accepted idea as “multistep tumorigenesis”. On the other hand, it has also been suggested that host responses play an essential role in cancer development. For example, infection-associated chronic inflammation promotes tumorigenesis through secretion of growth factors and inhibition of apoptosis.
In our laboratory, we have constructed gastrointestinal cancer mouse model that recapitulate human cancers from molecular mechanisms to gene expression profiles. Using these models, we are trying to elucidate the role of tumor microenvironment in cancer development. We believe that such maximizing cancer mouse models are important tools to uncover “cellular communications” between cancer cells and surrounding stromal cells.
Division of Genetics