Literature DB >> 16330940

The prevalence of pancreatic intraepithelial neoplasia in pancreata with uncommon types of primary neoplasms.

Edward B Stelow1, Reid B Adams, Christopher A Moskaluk.   

Abstract

Pancreatic ductal adenocarcinoma is thought to develop through a series of genetic events through its purported precursor lesion, pancreatic intraepithelial neoplasia (PanIN). Little, however, is known regarding the role of possible precursor lesions in the development of other primary neoplasms of the pancreas. This study investigated the prevalence of PanIN, as defined by recent consensus statements, in pancreata with uncommon types of primary neoplasms. All pancreata resected at the University of Virginia from June 1, 1991 to March 1, 2005 for neoplasia not diagnosed as conventional ductal adenocarcinoma were reviewed and classified according to the World Health Organization's classification schema for tumors of the exocrine and endocrine pancreas. All slides from these cases were then assessed for PanIN, which was classified according to the criteria of the most recent consensus statement. Three acinar cell carcinomas (ACCs), 18 mucinous cystic neoplasms (MCNs), 24 pancreatic endocrine tumors (PETs), 12 serous cystadenomas (SCs), and 3 solid-pseudopapillary tumors (SPTs) were identified. PanIN was identified in the pancreata of 3 of 3 ACCs, 17 of 18 MCNs, 16 of 24 PETs, 10 of 12 SCs, and 2 of 3 SPTs. The degree of PanIN was noted to trend with patient age. Although the high prevalence of PanIN in pancreata concomitantly harboring certain uncommon neoplasms of the pancreas could signify its role as a precursor lesion for those neoplasms, its high prevalence throughout our series may simply be the result of a coincidental, prevalent finding seen in all pancreata, especially with aging. Because of the ubiquitous nature of PanIN, it should not be used histologically to assist in the diagnosis and subclassification of pancreatic neoplasia.

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Year:  2006        PMID: 16330940     DOI: 10.1097/01.pas.0000180440.41280.a5

Source DB:  PubMed          Journal:  Am J Surg Pathol        ISSN: 0147-5185            Impact factor:   6.394


  6 in total

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Authors:  Alec J Beaney; Paul J R Banim; Robert Luben; Marleen A H Lentjes; Kay-Tee Khaw; Andrew R Hart
Journal:  Pancreas       Date:  2017 May/Jun       Impact factor: 3.327

Review 2.  Precursors to pancreatic cancer.

Authors:  Ralph H Hruban; Anirban Maitra; Scott E Kern; Michael Goggins
Journal:  Gastroenterol Clin North Am       Date:  2007-12       Impact factor: 3.806

3.  Precursor lesions of early onset pancreatic cancer.

Authors:  Lukasz Liszka; Jacek Pająk; Sławomir Mrowiec; Ewa Zielińska-Pająk; Dariusz Gołka; Paweł Lampe
Journal:  Virchows Arch       Date:  2011-03-03       Impact factor: 4.064

4.  Duct- and Acinar-Derived Pancreatic Ductal Adenocarcinomas Show Distinct Tumor Progression and Marker Expression.

Authors:  Rute M M Ferreira; Rocio Sancho; Hendrik A Messal; Emma Nye; Bradley Spencer-Dene; Richard K Stone; Gordon Stamp; Ian Rosewell; Alberto Quaglia; Axel Behrens
Journal:  Cell Rep       Date:  2017-10-24       Impact factor: 9.423

5.  Comment on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:2595-2604.

Authors:  Robert J Heine; Haoda Fu; David M Kendall; David E Moller
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Review 6.  Carcinogenesis of pancreatic adenocarcinoma: precursor lesions.

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  6 in total

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