Familial adenomatous polyposis‐associated and sporadic pyloric gland adenomas of the upper gastrointestinal tract share common genetic features. Issue 5 (14th May 2015)

• Record Type: Journal Article
• Authors: Hashimoto, Taiki; Ogawa, Reiko; Matsubara, Akiko; Taniguchi, Hirokazu; Sugano, Kokichi; Ushiama, Mineko; Yoshida, Teruhiko; Kanai, Yae; Sekine, Shigeki
• Is Part Of: Histopathology. Volume 67:Issue 5(2015)
• Page Start: 689
• Page End: 698
• Publication Date: 2015-05-14
• Subjects: Histology, Pathological -- Periodicals; 611.018
• DOI: 10.1111/his.12705
• Languages: English
• ISSNs: 0309-0167

Abstract

<abstract abstract-type="main" id="his12705-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="his12705-sec-0001" sec-type="section"> <title>Aims</title> <p>Familial adenomatous polyposis (FAP) is a hereditary cancer predisposition syndrome caused by a germline <italic>APC</italic> mutation. A recent study showed the enrichment of pyloric gland adenomas (PGAs) of the stomach, in addition to fundic gland polyps (FGPs) and foveolar‐type adenomas (FAs), in patients with FAP. In the present study, we analysed the genetic alterations in these FAP‐associated gastric lesions.</p> </sec> <sec id="his12705-sec-0002" sec-type="section"> <title>Methods and results</title> <p>Mutational statuses of <italic>GNAS</italic> and <italic>KRAS</italic>, which are frequently mutated in sporadic PGAs, as well as those of <italic>APC</italic>, were examined in PGAs, FAs and FGPs in patients with FAP using Sanger sequencing. Our analysis identified <italic>GNAS</italic> mutations in five of six PGAs (83%), but in none of the three FAs or the 40 FGPs examined. <italic>KRAS</italic> mutations were identified in four PGAs (67%), one FA (33%) and one FGP (3%). Somatic truncating <italic>APC</italic> mutations were found in all PGAs (100%), two FAs (67%) and 14 FGPs (47%). We additionally analysed sporadic PGAs of the stomach and duodenum and identified truncating <italic>APC</italic> mutations in 11 of 25 lesions (44%).</p> </sec> <sec id="his12705-sec-0003" sec-type="section"> <title>Conclusions</title> <p>FAP‐associated and sporadic PGAs not only show similar morphologies, but also share common genetic aberrations, including mutations of <italic>GNAS</italic>, <italic> KRAS</italic> and <italic>APC</italic>.</p> </sec> </abstract>