TY - JOUR
T1 - From somatic mutation to early detection
T2 - insights from molecular characterization of pancreatic cancer precursor lesions
AU - Fischer, Catherine G.
AU - Wood, Laura D.
N1 - Funding Information:
The authors acknowledge the following sources of funding: NIH/NCI P50 CA62924; NIH/NIDDK K08 DK107781; Sol Goldman Pancreatic Cancer Research Center; Buffone Family Gastrointestinal Cancer Research Fund; Kaya Tuncer Career Development Award in Gastrointestinal Cancer Prevention; AGA-Bernard Lee Schwartz Foundation Research Scholar Award in Pancreatic Cancer; Sidney Kimmel Foundation for Cancer Research Kimmel Scholar Award; AACR-Incyte Corporation Career Development Award for Pancreatic Cancer Research; Rolfe Pancreatic Cancer Foundation; Joseph C Monastra Foundation; and The Gerald O Mann Charitable Foundation (Harriet and Allan Wulfstat, Trustees).
Publisher Copyright:
Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
PY - 2018/12
Y1 - 2018/12
N2 - Pancreatic cancer arises from noninvasive precursor lesions, including pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasm (MCN), which are curable if detected early enough. Recently, these types of precursor lesions have been extensively characterized at the molecular level, defining the timing of critical genetic alterations in tumorigenesis pathways. The results of these studies deepen our understanding of tumorigenesis in the pancreas, providing novel insights into tumor initiation and progression. Perhaps more importantly, they also provide a rational foundation for early detection approaches that could allow clinical intervention prior to malignant transformation. In this review, we summarize the results of comprehensive molecular characterization of PanINs, IPMNs, and MCNs and discuss the implications for cancer biology as well as early detection.
AB - Pancreatic cancer arises from noninvasive precursor lesions, including pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasm (MCN), which are curable if detected early enough. Recently, these types of precursor lesions have been extensively characterized at the molecular level, defining the timing of critical genetic alterations in tumorigenesis pathways. The results of these studies deepen our understanding of tumorigenesis in the pancreas, providing novel insights into tumor initiation and progression. Perhaps more importantly, they also provide a rational foundation for early detection approaches that could allow clinical intervention prior to malignant transformation. In this review, we summarize the results of comprehensive molecular characterization of PanINs, IPMNs, and MCNs and discuss the implications for cancer biology as well as early detection.
KW - cancer genomics
KW - driver gene
KW - intraductal papillary mucinous neoplasm
KW - mucinous cystic neoplasm
KW - pancreatic cancer precursor lesion
KW - pancreatic intraepithelial neoplasia
KW - somatic mutation
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U2 - 10.1002/path.5154
DO - 10.1002/path.5154
M3 - Review article
C2 - 30105857
AN - SCOPUS:85056640333
VL - 246
SP - 395
EP - 404
JO - Investigative and Cell Pathology
JF - Investigative and Cell Pathology
SN - 0022-3417
IS - 4
ER -