Kyoto University · Medicine
Professor Akihisa Fukuda's research lab focuses on the molecular and epigenetic mechanisms underlying pancreatic development and tumorigenesis, with a particular emphasis on transcriptional regulators such as Ptf1a, chromatin remodeling complexes (e.g., SWI/SNF and BRG1), and tumor suppressor genes like RECK. The lab investigates how dysregulation of these factors contributes to pancreatic cancer initiation, progression, and metastasis, especially in the context of pancreatic ductal adenocarcinoma (PDAC) and precursor lesions such as PanIN and IPMN. Using genetically engineered mouse models and clinical correlation studies, the lab explores the roles of epigenetic regulators, EMT, and tumor microenvironment remodeling in cancer pathogenesis and therapeutic response. Their work also extends to rare cardiac manifestations of metastatic disease, highlighting translational insights from clinical case studies.
Figures are computed from collected data and may differ slightly.
Reduced Ptf1a dosage resulted in pancreatic hypoplasia and glucose intolerance with insufficient insulin secretion in a dosage-dependent manner. In hypomorphic mutant mice, pancreatic bud size was small and substantial proportions of pancreatic progenitors were misspecified to the common bile duct and duodenal cells. Growth with branching morphogenesis and subsequent exocrine cytodifferentiation was reduced and delayed. Total beta-cell number was decreased, proportion of non-beta islet cells was
Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar c
RECK is downregulated in various human cancers; however, how RECK inactivation affects carcinogenesis remains unclear. We addressed this issue in a pancreatic ductal adenocarcinoma (PDAC) mouse model and found that pancreatic Reck deletion dramatically augmented the spontaneous development of PDAC with a mesenchymal phenotype, which was accompanied by increased liver metastases and decreased survival. Lineage tracing revealed that pancreatic Reck deletion induced epithelial-mesenchymal transitio
The new endoscopic classification of internal hemorrhoids proved to be closely correlated to symptoms, particularly bleeding, and thus highly useful in evaluating the effectiveness of the treatment.
ATP-dependent chromatin remodeling complexes are a group of epigenetic regulators that can alter the assembly of nucleosomes and regulate the accessibility of transcription factors to DNA in order to modulate gene expression. One of these complexes, the SWI/SNF chromatin remodeling complex is mutated in more than 20% of human cancers. We have investigated the roles of the SWI/SNF complex in pancreatic ductal adenocarcinoma (PDA), which is the most lethal type of cancer. Here, we reviewed the rec
A 62-year-old man with a history of surgical therapy for papillary thyroid carcinoma was admitted because of chest pain, dyspnea on effort, pretibial edema, and slight fever. An electrocardiogram showed ST segment elevation in the precordial leads and low voltage in the limb leads. A large solid mass was demonstrated in both ventricles, with pericardial effusion, by echocardiography, thoracic computed tomography scan, transesophageal echocardiography, and angiography. A punch biopsy of the tumor
Tumor cells capable of self-renewal and continuous production of progeny cells are called tumor stem cells (TSCs) and are considered to be potential therapeutic targets. However, the mechanisms underlying the survival and function of TSCs are not fully understood. We previously reported that chromatin remodeling regulator Brg1 is essential for intestinal stem cells in mice and Dclk1 is an intestinal TSC marker. In this study, we investigated the role of Brg1 in Dclk1<sup>+</sup> intestinal tumor
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