Abstract
Pancreatic ductal adenocarcinoma is one of the most lethal human cancers. Its precursor lesions include pancreatic intra-epithelial neoplasia, mucinous cystic neoplasm, and intraductal papillary mucinous neoplasm (IPMN). IPMNs usually present as an incidental finding at imaging in 2.6% of the population and, according to the degree of dysplasia, they are classified as low- or high-grade lesions. Since the risk of malignant transformation is not accurately predictable, the management of these lesions is based on morphological and clinical parameters, such as presence of mural nodule, main pancreatic duct dilation, presence of symptoms, or high-grade dysplasia. Although the main genetic alterations associated to IPMNs have been elucidated, they are still not helpful for disease risk stratification. The growing body of genomic and epigenomic studies along with the more recent development of organotypic cultures provide the opportunity to improve our understanding of the malignant transformation process, which will likely deliver biomarkers to help discriminate between low- and high-risk lesions. Recent insights on the topic are herein summarized.
Highlights
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers, with a 5 year-overall survival of 9% [1]
Efforts are being made towards elucidating mechanisms of carcinogenesis through the study of pancreatic cancer precursor lesions, which include pancreatic intra-epithelial neoplasia (PanIN), being the most common, mucinous cystic neoplasm (MCN), and intra-ductal papillary mucinous neoplasm (IPMN)
The PanIN to pancreatic cancer progression model has been well investigated and the associated genetic events identified; being microscopic lesions, they cannot be detected by imaging modalities [7]
Summary
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers, with a 5 year-overall survival of 9% [1]. Oncocytic IPMNs, previously classified as a fourth histological subtype, are recognized as a separate entity by the 2019 WHO classification [16], as histology shows complex papillae with cuboidal lining cells and have only focal expression of mucins; they are usually BD-IPMN and often present with HGD or invasive carcinoma [32]. When they progress into invasive cancer, they give rise to oncocytic or tubular carcinoma. Based on the degree of dysplasia, the 2015 Baltimore Consensus Meeting issued recommendations for pancreatic precursor lesions, leading to a two-tier system grouping low- and high-grade lesions, leaving behind the previous intermediate-grade dysplasia [5]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
