Metachronous pancreatic cancer originating from disseminated founder pancreatic intraductal neoplasias (PanINs)
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Author
Imai, Koji
Karasaki, Hidenori
Ono, Yusuke
Sasajima, Junpei
Chiba, Shin‐ichi
Funakoshi, Hiroshi
Muraki, Miho
Hanaoka, Hideki
Furukawa, Takahisa
Furukawa, Hiroyuki
Kono, Toru
Nagashima, Kazuo
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1002/cjp2.8Metadata
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Imai, K., H. Karasaki, Y. Ono, J. Sasajima, S. Chiba, H. Funakoshi, M. Muraki, et al. 2015. “Metachronous pancreatic cancer originating from disseminated founder pancreatic intraductal neoplasias (PanINs).” The Journal of Pathology: Clinical Research 1 (2): 76-82. doi:10.1002/cjp2.8. http://dx.doi.org/10.1002/cjp2.8.Abstract
Abstract Clonal populations originated from benign‐looking ‘founder cells' may spread widely within pancreas instead of being localized in situ before frank pancreatic ductal adenocarcinoma (PDA) can be detected. Metachronous PDA is not common event, and we here sought to define potent origin of multiple PDAs developed in a woman using advanced genetics technologies. Curative resection of pancreatic head tumour was performed; however, ‘recurrent' lesions in the remnant pancreas were found 3.5 years later and total pancreatectomy was subsequently performed. The metachronous lesions were morphologically similar to the primary PDA. Using a next‐generation sequencing and digital PCR, all three PDAs were shown to possess rare somatic mutations in KRAS (p.T58I & p.Q61H). Curiously, identical KRAS mutations were found in low‐grade ‘intraepithelial' lesions, which localized in normal area of the pancreas and one of them possessed p53 mutation, which was also found in the PDAs. The footprint of the tumour evolution marked by mutational profiling supports a human correlate to the mouse models of ‘dissemination' occurring at the earliest stages of pancreatic neoplasia.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858137/pdf/Terms of Use
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