Pathology · 2011
Adenocarcinomas associated with perianal fistulae in Crohn's disease have a rectal, not an anal, immunophenotype.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Nishigami Takashi, Kataoka Tatsuki R, Ikeuchi Hiroki, Torii Ikuko, Sato Ayuko, Tomita Naohiro, Tsujimura Tohru
Аннотация
AIMS: Perianal fistulae are often observed in patients with Crohn's disease (CD), although the development of associated adenocarcinomas is very rare. The origin of adenocarcinomas in perianal fistulae associated with CD remains controversial and includes adjacent anal glands or rectal mucosa. Here, we attempted to determine the origin.
METHODS: We performed immunohistochemical analysis on seven cases of adenocarcinomas in perianal fistulae associated with CD using antibodies against mucins (MUCs), cytokeratins (CKs) and the intestine-specific transcription factor CDX2.
RESULTS: MUC2 and CK20 were expressed in all seven adenocarcinomas examined. MUC5AC/CLH2, MUC5AC/HGM and CDX2 were positive in four (57%), five (71%), and five (71%) adenocarcinomas, respectively. These proteins were positive in rectal mucosa, and negative in the anal glands. Six of seven adenocarcinomas (86%) were negative for CK7. CK7 was expressed in the anal glands, but not in rectal mucosa.
CONCLUSIONS: Adenocarcinomas in perianal fistulae associated with CD showed immunohistochemical phenotypes similar to those of rectal-type mucosa, rather than the anal glands. The adenocarcinomas might originate from cells migrating from the adjacent rectal mucosa to the CD-associated perianal fistulae.
METHODS: We performed immunohistochemical analysis on seven cases of adenocarcinomas in perianal fistulae associated with CD using antibodies against mucins (MUCs), cytokeratins (CKs) and the intestine-specific transcription factor CDX2.
RESULTS: MUC2 and CK20 were expressed in all seven adenocarcinomas examined. MUC5AC/CLH2, MUC5AC/HGM and CDX2 were positive in four (57%), five (71%), and five (71%) adenocarcinomas, respectively. These proteins were positive in rectal mucosa, and negative in the anal glands. Six of seven adenocarcinomas (86%) were negative for CK7. CK7 was expressed in the anal glands, but not in rectal mucosa.
CONCLUSIONS: Adenocarcinomas in perianal fistulae associated with CD showed immunohistochemical phenotypes similar to those of rectal-type mucosa, rather than the anal glands. The adenocarcinomas might originate from cells migrating from the adjacent rectal mucosa to the CD-associated perianal fistulae.