Tohoku University · 의학
Michiaki Unno 교수의 연구실은 췌장암의 치료 전략 개선을 핵심 목표로 하며, 신규 항암 치료법의 임상적 유효성을 평가하는 다기관 무작위 대조 시험을 수행하고 있습니다. 특히 흡입성 항암치료(지미세이브린과 S-1 조합)를 통한 신도관 치료와 수술 시기 선정에 대한 연구를 중심으로 진행되고 있으며, 췌장암 환자의 생존율 향상에 기여하고자 합니다. 또한, 췌장 베타세포 재생과 관련된 Reg 단백질의 기능을 규명하는 분자생물학적 연구도 병행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
A randomized, controlled trial has begun to compare neoadjuvant chemotherapy using gemcitabine and S-1 with upfront surgery for patients planned resection of pancreatic cancer. Patients were enrolled after the diagnosis of resectable or borderline resectable by portal vein involvement pancreatic cancer with histological confirmation. They were randomly assigned to either neoadjuvant chemotherapy or upfront surgery. Adjuvant chemotherapy using S-1 was administered for 6 months to patients with cu
189 Background: Despite improvements of postoperative adjuvant therapy for resected pancreatic ductal adenocarcinoma (PDAC), its prognosis remains poor. A randomized controlled trial has begun to compare neoadjuvant chemotherapy using gemcitabine and S1 (NAC-GS) with upfront surgery (Up-S) for patients with PDAC planned resection. Methods: Patients were enrolled after the diagnosis of resectable PDAC with histological confirmation. They were randomly assigned as either NAC-GS or Up-S. In NAC-GS,
We previously identified a gene, reg (i.e. regenerating gene), in the screening of a regenerating islet-derived cDNA library of rat (Terazono, K., Yamamoto, H., Takasawa, S., Shiga, K., Yonemura, Y., Tochino, Y., and Okamoto, H. (1988) J. Biol. Chem. 263, 2111-2114), and isolated a human reg cDNA and gene (Watanabe, T., Yonekura, H., Terazono, K., Yamamoto, H., and Okamoto, H. (1990) J. Biol. Chem. 265, 7432-7439); the rat and human cDNAs encode 165- and 166-amino acid proteins, respectively. Un
Reg (regenerating gene) was isolated as a gene specifically expressed in regenerating islets. We have demonstrated in vitro and in vivo that the exogenous addition of rat and human Reg gene products, Reg/REG proteins, induced beta-cell replication via the Reg receptor and thereby ameliorated experimental diabetes. In the present study, we produced Reg knockout mice by homologous recombination. The Reg gene disruption resulted in a null mutation. Knockout mice developed normally. Islets from the