Der serratierte Polyp – morphologische Kriterien und klinische Konsequenzen

Zusammenfassung

Die serratierte Route des kolorektalen Karzinoms stellt einen wichtigen Karzinogeneseweg dar, der in den letzten Jahren aufgrund seiner klinischen Relevanz verstärkt Beachtung findet und dank zahlreicher molekularer, histologischer und kli­nischer Untersuchungen inzwischen sehr gut ­charakterisiert ist. Zur Gruppe der serratierten Läsionen gehören der hyperplastische Polyp, das sessile serratierte Adenom, das traditionelle serratierte Adenom und das serratierte Adenokarzinom. Die Läsionen unterscheiden sich hinsichtlich ihrer Größe, Morphologie, Lokalisation, molekularen Veränderungen sowie ihres malignen Potenzials. Während hyperplastische Polypen meist kleine harmlose Veränderungen sind, besitzen sessile und traditionelle serratierte Adenome ein erhöhtes Entartungsrisiko. Auf molekularer Ebene spielen initial vor allem Mutationen des BRAF- und KRAS-Onkogens eine entscheidende Rolle. Im Rahmen der Tumorprogression tritt zudem eine Hypermethylierung zahlreicher Genpromotoren auf, von denen vor allem der daraus resultierende Ausfall des Reparaturenzyms MLH1 und des Zellzyklusinhibitors p16^Ink4a für die weitere Progression verantwortlich zu sein scheinen. Aufgrund des unterschiedlichen Entartungs­potenzials ist es wichtig die einzelnen Läsionen zu charakterisieren und das klinische Vorgehen darauf abzustimmen. 

Abstract

The serrated route to colorectal carcinoma is an important way of carcinogenesis which has ­gained more attention in recent years due to is clinical relevance and has meanwhile been char­ac­terized very well through molecular, histo­logical and clinical investigations. The group of ser­rated le­sions comprises hyperplastic polyps, sessile ser­rated adenomas, traditional serrated adenomas and serrated adenocarcinomas. The le­sions differ in size, morphology, localisation, molecular changes, and their malignant potential. Hyperplastic polyps are mostly small innocent lesions whereas sessile and serrated adenomas have an increased malignant potential. Initially mutations of the BRAF and KRAS oncogene play a curcial role on the molecular level. Tumor progression is accompanied by hypermethylation of various gene promoters. Especially the resulting loss of the repair enzyme MLH1 and the cell cyclus inhibitor p16^Ink4a seem to be responsible for further tumor progression. Because of their di­verse malignant potential it is important to characterize the individual lesions and to define the clinical procedure accordingly. 

Schlüsselwörter

serratierte Route - hyperplastischer Polyp - sessiles serratiertes Adenom - traditionelles serratiertes Adenom - serratiertes Adenokarzinom

Key words

serrated route - hyperplastic polyp - sessile serrated adenoma - traditional serrated adenoma - serrated adenocarcinoma

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