English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Intraductal neoplasms are important precursors to invasive pancreatic cancer and provide an opportunity to detect and treat pancreatic neoplasia before an invasive carcinoma develops. The diagnostic evaluation of these lesions is challenging, as diagnostic imaging and cytological sampling do not provide accurate information on lesion classification, the grade of dysplasia or the presence of invasion. Moreover, the molecular driver gene mutations of these precursor lesions have yet to be fully characterized. Fifty‐two intraductal papillary neoplasms, including 48 intraductal papillary mucinous neoplasms ( IPMNs ) and four intraductal tubulopapillary neoplasms ( ITPNs ), were subjected to the mutation assessment in 51 cancer‐associated genes, using ion torrent semiconductor‐based next‐generation sequencing.  P16  and Smad4 immunohistochemistry was performed on 34  IPMNs  and 17  IPMN ‐associated carcinomas. At least one somatic mutation was observed in 46/48 (96%)  IPMNs ; 29 (60%) had multiple gene alterations.   GNAS   and/or   KRAS   mutations were found in 44/48 (92%) of  IPMNs .   GNAS   was mutated in 38/48 (79%)  IPMNs ,   KRAS   in 24/48 (50%) and these mutations coexisted in 18/48 (37.5%) of  IPMNs .   RNF43   was the third most commonly mutated gene and was always associated with   GNAS   and/or   KRAS   mutations, as were virtually all the low‐frequency mutations found in other genes. Mutations in   TP53   and   BRAF   genes (10% and 6%) were only observed in high‐grade  IPMNs .  P16  was lost in 7/34  IPMNs  and 9/17  IPMN ‐associated carcinomas; Smad4 was lost in 1/34  IPMNs  and 5/17  IPMN ‐associated carcinomas. In contrast to  IPMNs , only one of four  ITPNs  had detectable driver gene (  GNAS   and   NRAS  ) mutations. Deep sequencing  DNA  from seven cyst fluid aspirates identified 10 of the 13 mutations detected in their associated  IPMN . Using next‐generation sequencing to detect cyst fluid mutations has the potential to improve the diagnostic and prognostic stratification of pancreatic cystic neoplasms. © 2014 The Authors.  The Journal of Pathology  published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Targeted next‐generation sequencing of cancer genes dissects the molecular profiles of intraductal papillary neoplasms of the pancreas