Rate My Professor Hiroko Oshima

Associate Professor Hiroko Oshima is a faculty member of the Cancer Research Institute at Kanazawa University, affiliated with the Division of Pharmacy in the Graduate School of Medical Science and the Division of Genetics laboratory. She earned her bachelor's degree from Kumamoto University in March 1992 and holds a Doctor of Pharmacy degree from the same institution. Her prior career includes positions at Banyu Tsukuba Research Institute from 1992 to 1997, Merck Research Laboratory from 1997 to 2000, and Kyoto University from 2001 to 2005.

Professor Oshima specializes in experimental pathology with a research focus on inflammatory responses in gastrointestinal tumorigenesis. Her work examines the roles of prostaglandin E2, Wnt signaling, and BMP pathways in gastric tumor development using mouse models, including those involving COX-2 and mPGES-1 transgenic expression or Helicobacter infection leading to SPEM and adenocarcinoma. Key publications include Activation of epidermal growth factor receptor signaling by the prostaglandin E2 receptor EP4 pathway during gastric tumorigenesis (Cancer Science, 2011), Induction of prostaglandin E2 pathway promotes gastric hamartoma development with suppression of bone morphogenetic protein signaling (Cancer Research, 2009), and Prostaglandin E2 signaling and bacterial infection recruit tumor-promoting macrophages to mouse gastric tumors (Gastroenterology, 2011). Additional papers address topics such as Sox17 expression changes during gastrointestinal tumorigenesis (Gastroenterology, 2009) and intestinal cancer progression by mutant p53 (Oncogene, 2017). She has contributed to numerous studies on tumor-promoting macrophages, stromal fibroblasts, and genetic mechanisms in colorectal and gastric cancers, often collaborating on organoid and mouse model experiments. Her research themes also encompass the generation of inflammation-associated gastric cancer models demonstrating the necessity of inflammatory responses alongside Wnt activation or BMP suppression for tumorigenesis.