%0 Journal Article
%T Depressed-Type Colonic Lesions and ¡°De Novo¡± Cancer in Familial Adenomatous Polyposis: A Colonoscopist¡¯s Viewpoint
%A Shin-ei Kudo
%A Yuusaku Sugihara
%A Hiroyuki Kida
%A Fumio Ishida
%A Hideyuki Miyachi
%A Yuichi Mori
%A Masashi Misawa
%A Tomokazu Hisayuki
%A Kenta Kodama
%A Kunihiko Wakamura
%A Takemasa Hayashi
%A Yoshiki Wada
%A Shigeharu Hamatani
%J ISRN Gastroenterology
%D 2013
%R 10.1155/2013/838134
%X Familial adenomatous polyposis (FAP) is the most common inherited polyposis syndrome. Almost all patients with FAP will develop colorectal cancer if their FAP is not identified and treated at an early stage. Although there are many reports about polypoid lesions and colorectal cancers in FAP patients, little information is available concerning depressed lesions in FAP patients. Several reports suggested that depressed-type lesions are characteristic of FAP and important in the light of their rapid growth and high malignancy. Here, we describe the occurrence of depressed-type lesions in FAP patients treated at our institution. Between April 2001 and March 2010, eight of 18 FAP patients had colorectal cancers. Depressed-type colorectal cancer was found in three patients. It should be kept in mind that depressed-type lesions occur even in FAP. 1. Introduction In 1859, Half et al. [1] first described adenomatous polyposis in a 16-year-old female and a 21-year-old male. Later, familial adenomatous polyposis (FAP) was recognized as the most common inherited polyposis syndrome. FAP is an autosomal dominant disease that is classically characterized by the development of hundreds to thousands of adenomas in the rectum and colon during the second decade of life. Almost all FAP patients will develop colorectal cancer if the FAP is not identified and treated at an early stage. Cumulative evidence indicates that, under the umbrella of FAP, classic FAP (cFAP) and attenuated FAP (aFAP) might be very different identities both clinically and molecularly. aFAP is a milder form that is characterized by fewer adenomas and a later age of adenoma development and cancer diagnosis [1]. The genetic basis of FAP is a germline mutation of the adenomatous polyposis coli (APC) gene on chromosome 5 (5q21-q22) [2]. Only about 10%¨C15% of aFAP cases are secondary to APC. More frequently, in 20%¨C30% of cases, this condition has been correlated with a biallelic mutation of the MutY human homolog gene (MUTYH) located on chromosome 1 (1p34.3-p32.1). Two mutations account for most of the variations of the MUTYH gene: Y165C (exon7) and G382D (exon13) [3]. It is difficult to obtain accurate nationwide and global data about the incidence of FAP, although there are local FAP registries in many countries. A 1955 report calculated that the incidence of FAP at birth in the UK was 1£¿:£¿8,300 [4]. In classic FAP, the optimal surveillance interval is two years between sigmoidoscopies. If adenomas are detected, colonoscopic investigations should be performed annually until a colectomy is planned. In
%U http://www.hindawi.com/journals/isrn.gastroenterology/2013/838134/