Kyoto University · 의학
Akihisa Fukuda 교수의 연구실은 췌장 발달 및 췌장암 발생 메커니즘을 중심으로, 전사 조절 인자(Ptf1a, Pdx1), 에피제네틱 조절 복합체(SWI/SNF, BRG1), 및 세포외기질 조절 단백질(RECK)의 기능을 규명하고 있습니다. 특히 췌장 줄기세포의 분화 이상, 아세틸기세포에서의 간선세포 전환, 그리고 암 미세환경 형성과 관련된 분자 기전에 초점을 맞추고 있습니다. 이들의 연구는 췌장암의 조기 진단 및 표적 치료 전략 개발에 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
