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Advanced Genome Medicine Lab
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The lab uses mice to investigate how inflammation and cancer arise in the digestive tract.

AboutAbout the lab
Exploring how digestive diseases develop
The Advanced Genome Medicine Lab studies diseases of the digestive organs, including the esophagus, stomach, intestines, liver, bile ducts, and pancreas.
Its main targets are inflammatory diseases such as gastritis and colitis, and cancers such as gastric cancer and liver cancer.
Focusing on the functions of genes and molecules, the lab clarifies how diseases arise and carries out translational research aimed at new therapies, using mouse models and other approaches.
It investigates from many angles, including stem cell differentiation, the proliferation and death of epithelial cells, and interactions with immune cells and pathogens.
Key terms
- Translational research
- Research that bridges the results of basic research to the diagnosis and treatment of patients
- Genetically modified mice
- Mice in which a specific gene has been disrupted or activated. They are used to study the roles of genes and the mechanisms of disease
- Lineage tracing
- An experimental method that follows what types of cells a labeled cell develops into
ResearchResearch themes
The lab aims to clarify the mechanisms underlying cancers and inflammatory diseases of the digestive tract and to establish new treatments. Using genetically modified mice, it studies how gastritis, cholangitis, and inflammatory bowel disease develop, and, in cancer, stem cell differentiation and interactions with immune cells and microorganisms.
*Illustrative imageGastric Inflammation and IL-33
In collaboration with the Department of Gastroenterology at the University of Tokyo, the lab used mice that produce large amounts of IL-33 in the stomach and found that IL-33 is involved in gastritis, particularly in recruiting specific immune cells to the stomach. Mice lacking the acetylcholine receptor in the epithelium develop IL-33-induced gastritis more easily, so acetylcholine signaling may offer a clue for treatment.
*Illustrative imageA Model of Primary Biliary Cholangitis
Primary biliary cholangitis is an autoimmune liver disease whose cause is not well understood. In collaboration with Chiba University, the lab found that mice lacking dendritic cells show the same features as the human disease. Immune responses driven by autoantibodies and immune suppression by dendritic cells are thought to be important.
*Illustrative imageGastric Cancer and Sox9
Sox9 is a transcription factor involved in development, stemness, and carcinogenesis. In collaboration with the Department of Gastroenterology at the University of Tokyo, the lab found that mice in which Sox9 is deleted only in the stomach develop gastritis and gastric tumors, and that malignant lesions form when CDH1 is also deleted. The lab is now investigating the underlying mechanism.
*Illustrative imageCancer at the Squamocolumnar Junction of the Stomach
It is not well understood where tumors arising at the squamocolumnar junction of the stomach, where two different types of epithelium meet, originate or how they form. Using mouse models and lineage tracing, the lab searches for the cells of origin of these cancers and for stem cells specific to this site.
MembersFaculty
- Associate ProfessorYoshihiro HirataPublications ↗
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Report an errorAbout the images
The top and research theme images are illustrative and were not taken at the lab. They are cropped from Wikimedia Commons images. Cropped CC BY-SA images are provided under the same CC BY-SA license as the original (version shown on each line).
- Top image: “Knockout Mice5006-300” Maggie Bartlett, NHGRI. / Public domain (cropped)
- Gastric Inflammation and IL-33: “Normal gastric mucosa intermed mag” Nephron / CC BY-SA 3.0 (cropped)
- A Model of Primary Biliary Cholangitis: “Primary biliary cirrhosis intermed mag” Nephron / CC BY-SA 3.0 (cropped)
- Gastric Cancer and Sox9: “Gastric adenocarcinoma” Nephron / CC BY-SA 3.0 (cropped)
- Cancer at the Squamocolumnar Junction of the Stomach: “Histopathology of autolytically denuded gastric mucosa at the gastroesophageal junction” Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: None Mikael Häggström, M.D.Consent note: Consent from the patient or patient's relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance). / CC0 (cropped)
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