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Analysis of the origin of anaplastic pancreatic cancer and the mechanism of its dedifferentiation
Author(s) -
Miura Kotaro,
Kimura Kenjiro,
Amano Ryosuke,
Yamazoe Sadaaki,
Ohira Go,
Nishio Kohei,
Kametani Naoki,
Hirakawa Kosei,
Ohira Masaichi
Publication year - 2017
Publication title -
journal of hepato‐biliary‐pancreatic sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 1868-6974
DOI - 10.1002/jhbp.429
Subject(s) - pancreatic cancer , immunohistochemistry , cancer research , vimentin , epithelial–mesenchymal transition , cancer stem cell , cd44 , pathology , pancreatic duct , cancer , biology , pancreas , medicine , metastasis , cell , genetics
Background We researched the origin and progression of anaplastic pancreatic cancer ( APC ) from the viewpoints of cell lineage, epithelial‐mesenchymal transition ( EMT ) and cancer stem‐like cells ( CSC ). Methods Using specimens from patients with APC and differentiated pancreatic ductal adenocarcinoma ( PDAC ), expression of sex‐determining region Y‐box 9 ( SOX 9), E‐cadherin, vimentin, ZEB1, Snail, N‐cadherin, CD 24 and CD 44 was estimated using immunohistochemistry. Results Almost all cases were positive for SOX 9 expression. APC cases were negative, but many PDAC cases were positive for the expression of E‐cadherin. A much higher number of APC cases than PDAC cases were positive for the expression of other EMT related proteins and for the expression of CSC related proteins. The ductal cancerous component of APC accounted for an average of 12% of the cancerous lesion and the expression of each marker in this component was similar to that of PDAC cases. Conclusions Anaplastic pancreatic cancer had pancreatic duct cell like features and might gain dedifferentiate components through EMT and the acquisition of CSC properties.