Non-conventional mucosal lesions (serrated epithelial change, villous hypermucinous change) are frequent in patients with inflammatory bowel disease-results of molecular and immunohistochemical single institutional study
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
00179906
Teaching Hospital Hradec Králové
LM2015089
Charles University
EF16 013/0001674
Charles University
PubMed
31375911
DOI
10.1007/s00428-019-02627-4
PII: 10.1007/s00428-019-02627-4
Knihovny.cz E-zdroje
- Klíčová slova
- Colitis, ulcerative, Colorectal carcinoma, Crohn disease, Dysplasia, Inflammatory bowel diseases, Serrated epithelial change, Villous hypermucinous change,
- MeSH
- adenokarcinom patologie MeSH
- adenom diagnóza patologie MeSH
- dítě MeSH
- dospělí MeSH
- idiopatické střevní záněty diagnóza patologie MeSH
- kolorektální nádory diagnóza patologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mutace genetika MeSH
- nádorové biomarkery analýza MeSH
- polypy tlustého střeva diagnóza patologie MeSH
- protoonkogenní proteiny B-Raf genetika MeSH
- retrospektivní studie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- Check Tag
- dítě MeSH
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- nádorové biomarkery MeSH
- protoonkogenní proteiny B-Raf MeSH
Chronically inflamed mucosa in inflammatory bowel disease (IBD) is associated with an increased risk of cancer. Besides IBD-associated dysplasia, there are non-conventional mucosal changes that may act as potential precursors. The aim of the study was to retrospectively review samples from IBD patients focusing on detection of such lesions with evaluation of their immunohistochemical and molecular properties. Surgical specimens and/or endoscopical biopsy samples of IBD patients examined during a 10-year period were reviewed. Detected mucosal lesions were divided into three groups-group 1 (non-conventional or putative precursor lesions - PPLs) with serrated or villous hypermucinous morphology, group 2 (true serrated polyps fulfilling valid criteria), and group 3 (IBD-associated neoplasia). Lesions from all groups were analyzed with antibodies against MLH1, p53, and MGMT and by molecular testing of KRAS, NRAS, and BRAF mutation. Samples from 309 IBD patients were reviewed. A total of 88 mucosal lesions were found in 51 patients. Most common were lesions from group 1 with superficial serrated epithelial change seen in 41 samples (46.6%) and villous hypermucinous change in 6 (6.8%). Group 2 consisted of 15 true serrated polyps. Six conventional IBD-dysplasia cases and 11 carcinomas were seen in group 3. Six lesions from group 1 were associated with invasive carcinoma whereas two shared the same mutation in KRAS or BRAF. Lesions from group 1 were characterized by loss of MGMT expression in 44.6%, aberrant p53 expression, and by mutations in KRAS gene in 42.9% of cases. This study proves the existence of mucosal changes other than conventional IBD-dysplasia and extends the knowledge about their immunohistochemical and molecular properties and relation to carcinoma further supporting their potential role in IBD-related carcinogenesis.
Zobrazit více v PubMed
Cell J. 2017 Spring;19(Suppl 1):113-117 PubMed
J Crohns Colitis. 2017 Jan;11(1):3-25 PubMed
Dig Dis Sci. 2015 Aug;60(8):2251-63 PubMed
Hum Pathol. 2015 Oct;46(10):1548-56 PubMed
Am J Pathol. 1994 Apr;144(4):767-75 PubMed
Gastrointest Endosc. 2015 Mar;81(3):489-501.e26 PubMed
Mod Pathol. 2000 Jul;13(7):797-801 PubMed
Pathol Res Pract. 2019 Apr;215(4):730-737 PubMed
World J Gastroenterol. 2011 Jul 21;17(27):3184-91 PubMed
J Gastroenterol Hepatol. 2007 Jul;22(7):1024-31 PubMed
Gastroenterology. 2016 Apr;150(4):931-43 PubMed
Hum Pathol. 1983 Nov;14(11):931-68 PubMed
Anticancer Res. 2000 Nov-Dec;20(6C):4761-4 PubMed
Gastroenterology Res. 2018 Oct;11(5):355-360 PubMed
J Cancer. 2013;4(4):320-2 PubMed
Mod Pathol. 2015 Dec;28(12):1584-93 PubMed
Asian Pac J Cancer Prev. 2015;16(5):1945-52 PubMed
Gastroenterol Hepatol (N Y). 2018 Jan;14(1):19-25 PubMed
Gastrointest Endosc. 2016 Jul;84(1):87-95.e1 PubMed
Oncol Rep. 2007 Nov;18(5):1093-7 PubMed
Saudi J Gastroenterol. 2009 Oct-Dec;15(4):244-52 PubMed
Aliment Pharmacol Ther. 2014 Jun;39(12):1408-17 PubMed
Best Pract Res Clin Gastroenterol. 2013 Apr;27(2):257-67 PubMed
J Crohns Colitis. 2017 Jun 1;11(6):649-670 PubMed
Inflamm Bowel Dis. 2009 Apr;15(4):630-8 PubMed
Dis Colon Rectum. 1984 May;27(5):283-7 PubMed
Can J Gastroenterol Hepatol. 2014 Dec;28(11):589-94 PubMed
J Clin Oncol. 2011 May 20;29(15):2011-9 PubMed
Can J Gastroenterol Hepatol. 2017;2017:5490803 PubMed
World J Gastroenterol. 2014 Mar 28;20(12):3164-72 PubMed
J Crohns Colitis. 2013 Nov;7(10):827-51 PubMed
Gut. 1999 Nov;45(5):686-92 PubMed
Dig Liver Dis. 2017 Apr;49(4):326-330 PubMed
Oncotarget. 2017 Mar 28;8(13):22175-22186 PubMed
Gut. 2010 Nov;59(11):1516-26 PubMed
Ann Oncol. 2009 Jul;20(7):1216-22 PubMed
Clin Cancer Res. 2018 Oct 15;24(20):4997-5011 PubMed
J Crohns Colitis. 2014 Dec;8(12):1735-9 PubMed
Mod Pathol. 2017 Dec;30(12):1728-1738 PubMed
Am J Surg Pathol. 2008 Feb;32(2):296-303 PubMed
