TY - JOUR
T1 - Clinical assessment of the GNAS mutation status in patients with intraductal papillary mucinous neoplasm of the pancreas
AU - Ohtsuka, Takao
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 - Ohuchida, Kenoki
AU - Nakamura, Masafumi
N1 - Funding Information:
This study was supported by a Grant-in-Aid from the Japan Society for the Promotion of Sciences for Scientific Research (B) (Grant no 16H05417).
Publisher Copyright:
© 2019, Springer Nature Singapore Pte Ltd.
PY - 2019/11/1
Y1 - 2019/11/1
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.
AB - 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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U2 - 10.1007/s00595-019-01797-7
DO - 10.1007/s00595-019-01797-7
M3 - Review article
C2 - 30879148
AN - SCOPUS:85063028426
SN - 0941-1291
VL - 49
SP - 887
EP - 893
JO - Surgery today
JF - Surgery today
IS - 11
ER -