モリヤ タクヤ   Takuya Moriya
  森谷 卓也
   所属   川崎医科大学  医学部
   職種   学長付特任教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Pancreatic ductal adenocarcinoma with acinar-to-ductal metaplasia-like cancer cells shows increased cellular proliferation.
掲載誌名 正式名:Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
略  称:Pancreatology
ISSNコード:14243911/14243903
掲載区分国外
巻・号・頁 23(7),pp.811-817
著者・共著者 Reiji Nishimon, Koji Yoshida, Fumiaki Sanuki, Yoshihiro Nakashima, Tomoo Miyake, Tatsuki Sato, Yasuyuki Tomiyama, Sohji Nishina, Takuya Moriya, Akiko Shiotani, Keisuke Hino
発行年月 2023/11
概要 BACKGROUND/OBJECTIVES:Acinar-to-ductal metaplasia (ADM) has been shown to contribute to the development of pancreatic ductal adenocarcinoma (PDAC) in genetically engineered mouse models, but little is known about whether acinar cell plasticity contributes to carcinogenesis in human PDAC. We aimed to assess whether cancer cells that stain positive for amylase and CK19 (ADM-like cancer cells) are present in human resected PDAC and to investigate their role in tumor progression.METHODS:We immunohistochemically investigated the presence of ADM-like cancer cells, and compared the clinical and histological parameters of PDAC patients with and without ADM-like cancer cells.RESULTS:ADM-like cancer cells were detected in 16 of 60 (26.7%) PDAC specimens. Positive staining for anterior gradient protein 2 (AGR2) was observed in 14 of 16 (87.5%) PDAC specimens with ADM-like cancer cells. On the other hand, the intensity of AGR2 expression (negative, low/moderate or high) was lower in PDAC with ADM-like cancer cells (9/7) than in PDAC without these cells (11/33) (P = 0.032). The presence of ADM-like cancer cells was significantly correlated with increased cell proliferation (P = 0.012) and tended to be associated with MUC1 expression (P = 0.067).CONCLUSIONS:These results indicated that acinar cells may act as the origin of human PDAC, and that their presence may be useful for the stratification of human PDAC to predict prognosis.
DOI 10.1016/j.pan.2023.08.007
PMID 37659916