The University of Tokyo · Medicine
Professor T. Nakatsuka's research lab focuses on the molecular mechanisms underlying hepatocellular carcinoma (HCC) development, particularly the interplay between metabolic liver diseases such as non-alcoholic fatty liver disease (NAFLD) and diabetes mellitus. The lab investigates epigenetic regulators—especially histone methyltransferase G9a—in DNA damage response and early hepatocarcinogenesis, using genetic and pharmacological models. Additionally, the lab explores hemodynamic and imaging biomarkers, such as hepatic vein waveforms and deep learning-based pathological analysis, to detect early liver fibrosis and carcinogenesis in high-risk populations.
Figures are computed from collected data and may differ slightly.
The incidence of diabetes mellitus and hepatocellular carcinoma (HCC) has been increasing worldwide during the last few decades, in the context of an increasing prevalence of obesity and non-alcoholic fatty liver disease (NAFLD). Epidemiologic studies have revealed that patients with diabetes have a 2- to 3-fold increased risk of developing HCC, independent of the severity and cause of the underlying liver disease. A bidirectional relationship exists between diabetes and liver disease: advanced
Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease, affecting approximately 25% of the world's population. Recently, because of the sedentary lifestyle and overnutrition resulting from urbanisation, the burden of NAFLD has rapidly increased in many Asian countries. Currently, the prevalence of NAFLD in Asia is approximately 30%, as is the case in many Western countries. In Asia, the prevalence and presentation of NAFLD vary widely across regions becau
The ability of the DL model to capture subtle pathological features beyond fibrosis suggests its potential for identifying early signs of hepatocarcinogenesis in patients with steatotic liver disease.
While the significance of acquired genetic abnormalities in the initiation of hepatocellular carcinoma (HCC) has been established, the role of epigenetic modification remains unknown. Here we identified the pivotal role of histone methyltransferase G9a in the DNA damage-triggered initiation of HCC. Using liver-specific G9a-deficient (G9a<sup>ΔHep</sup>) mice, we revealed that loss of G9a significantly attenuated liver tumor initiation caused by diethylnitrosamine (DEN). In addition, pharmacologi
Hepatic vein waveforms change in accordance with liver fibrosis progression in Fontan patients, and can be a useful indicator of liver fibrosis after the Fontan procedure.
Free transverse colon transfers based on the middle colic vessels were used to reconstruct a pharyngoesophageal defect in 9 patients. In all patients, cancer invaded up to the oropharynx. Resection resulted in a larger pharyngostoma than normally seen following standard total pharyngolaryngoesophagectomy. In such cases, it can be difficult to achieve good swallowing function after reconstruction using the free jejunal transfer. This mainly results from a significant discrepancy between the diame
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