Clinical assessment of the GNAS mutation status in patients with intraductal papillary mucinous neoplasm of the pancreas

Ohtsuka Takao, Takahiro Tomosugi, Ryuichiro Kimura, So Nakamura, Yoshihiro Miyasaka, Kohei Nakata, Yasuhisa Mori, Makiko Morita, Nobuhiro Torata, Koji Shindo, Kenoki Ouchida, Masafumi Nakamura

研究成果: ジャーナルへの寄稿評論記事

抄録

Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is characterized by cystic dilation of the pancreatic duct, caused by mucin hypersecretion, with slow progression via the adenoma–carcinoma sequence mechanism. Mutation of GNAS at codon 201 is found exclusively in IPMNs, occurring at a rate of 41–75%. Recent advances in molecular biological techniques have demonstrated that GNAS mutation might play a role in the transformation of IPMNs after the appearance of neoplastic cells, rather than in the tumorigenesis of IPMNs. GNAS mutation is observed frequently in the intestinal subtype of IPMNs with MUC2 expression, and less frequently in IPMNs with concomitant pancreatic ductal adenocarcinoma (PDAC). Research has focused on assessing GNAS mutation status in clinical practice using various samples. In this review, we discuss the clinical application of GNAS mutation assessment to differentiate invasive IPMNs from concomitant PDAC, examine the clonality of recurrent IPMNs in the remnant pancreas using resected specimens, and differentiate pancreatic cystic lesions using cystic fluid collected by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA), duodenal fluid, and serum liquid biopsy samples.

元の言語英語
ジャーナルSurgery today
DOI
出版物ステータス出版済み - 1 1 2019

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Pancreatic Neoplasms
Mutation
Adenocarcinoma
Endoscopic Ultrasound-Guided Fine Needle Aspiration
Pancreatic Ducts
Mucins
Codon
Dilatation
Pancreas
Carcinogenesis
Biopsy
Serum
Research

All Science Journal Classification (ASJC) codes

  • Surgery

これを引用

Clinical assessment of the GNAS mutation status in patients with intraductal papillary mucinous neoplasm of the pancreas. / Takao, Ohtsuka; Tomosugi, Takahiro; Kimura, Ryuichiro; Nakamura, So; Miyasaka, Yoshihiro; Nakata, Kohei; Mori, Yasuhisa; Morita, Makiko; Torata, Nobuhiro; Shindo, Koji; Ouchida, Kenoki; Nakamura, Masafumi.

:: Surgery today, 01.01.2019.

研究成果: ジャーナルへの寄稿評論記事

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abstract = "Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is characterized by cystic dilation of the pancreatic duct, caused by mucin hypersecretion, with slow progression via the adenoma–carcinoma sequence mechanism. Mutation of GNAS at codon 201 is found exclusively in IPMNs, occurring at a rate of 41–75{\%}. Recent advances in molecular biological techniques have demonstrated that GNAS mutation might play a role in the transformation of IPMNs after the appearance of neoplastic cells, rather than in the tumorigenesis of IPMNs. GNAS mutation is observed frequently in the intestinal subtype of IPMNs with MUC2 expression, and less frequently in IPMNs with concomitant pancreatic ductal adenocarcinoma (PDAC). Research has focused on assessing GNAS mutation status in clinical practice using various samples. In this review, we discuss the clinical application of GNAS mutation assessment to differentiate invasive IPMNs from concomitant PDAC, examine the clonality of recurrent IPMNs in the remnant pancreas using resected specimens, and differentiate pancreatic cystic lesions using cystic fluid collected by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA), duodenal fluid, and serum liquid biopsy samples.",
author = "Ohtsuka Takao and Takahiro Tomosugi and Ryuichiro Kimura and So Nakamura and Yoshihiro Miyasaka and Kohei Nakata and Yasuhisa Mori and Makiko Morita and Nobuhiro Torata and Koji Shindo and Kenoki Ouchida and Masafumi Nakamura",
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AU - Takao, Ohtsuka

AU - Tomosugi, Takahiro

AU - Kimura, Ryuichiro

AU - Nakamura, So

AU - Miyasaka, Yoshihiro

AU - Nakata, Kohei

AU - Mori, Yasuhisa

AU - Morita, Makiko

AU - Torata, Nobuhiro

AU - Shindo, Koji

AU - Ouchida, Kenoki

AU - Nakamura, Masafumi

PY - 2019/1/1

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N2 - Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is characterized by cystic dilation of the pancreatic duct, caused by mucin hypersecretion, with slow progression via the adenoma–carcinoma sequence mechanism. Mutation of GNAS at codon 201 is found exclusively in IPMNs, occurring at a rate of 41–75%. Recent advances in molecular biological techniques have demonstrated that GNAS mutation might play a role in the transformation of IPMNs after the appearance of neoplastic cells, rather than in the tumorigenesis of IPMNs. GNAS mutation is observed frequently in the intestinal subtype of IPMNs with MUC2 expression, and less frequently in IPMNs with concomitant pancreatic ductal adenocarcinoma (PDAC). Research has focused on assessing GNAS mutation status in clinical practice using various samples. In this review, we discuss the clinical application of GNAS mutation assessment to differentiate invasive IPMNs from concomitant PDAC, examine the clonality of recurrent IPMNs in the remnant pancreas using resected specimens, and differentiate pancreatic cystic lesions using cystic fluid collected by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA), duodenal fluid, and serum liquid biopsy samples.

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