Familial and sporadic pancreatic cancer share the same molecular pathogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-03

AUTHORS

Alexis L. Norris, Nicholas J. Roberts, Siân Jones, Sarah J. Wheelan, Nickolas Papadopoulos, Bert Vogelstein, Kenneth W. Kinzler, Ralph H. Hruban, Alison P. Klein, James R. Eshleman

ABSTRACT

Pancreatic ductal adenocarcinoma (PDAC) is nearly uniformly lethal, with a median overall survival in 2014 of only 6 months. The genetic progression of sporadic PDAC (SPC) is well established, with common somatic alterations in KRAS, p16/CDKN2A, TP53, and SMAD4/DPC4. Up to 10 % of all PDAC cases occur in families with two or more affected first-degree relatives (familial pancreatic cancer, FPC), but these cases do not appear to present at an obviously earlier age of onset. This is unusual because most familial cancer syndrome patients present at a substantially younger age than that of corresponding sporadic cases. Here we collated the reported age of onset for FPC and SPC from the literature. We then used an integrated approach including whole exomic sequencing, whole genome sequencing, RNA sequencing, and high density SNP microarrays to study a cohort of FPC cell lines and corresponding germline samples. We show that the four major SPC driver genes are also consistently altered in FPC and that each of the four detection strategies was able to detect the mutations in these genes, with one exception. We conclude that FPC undergoes a similar somatic molecular pathogenesis as SPC, and that the same gene targets can be used for early detection and minimal residual disease testing in FPC patients. More... »

PAGES

95-103

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10689-014-9755-y

DOI

http://dx.doi.org/10.1007/s10689-014-9755-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036337964

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25240578


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