title: Pathological features and genetic alterations in colorectal carcinomas with characteristics of nonpolypoid growth.
abstract: We sought to clarify pathological features and genetic alterations in colorectal carcinomas with characteristics of nonpolypoid growth. Colorectal carcinomas resected at Showa University Hospital in Tokyo included 86 with characteristics of polypoid growth (PG) and 21 with those of nonpolypoid growth (NPG). Mutations of APC, Ki-ras, and p53 genes, as well as microsatellite instability (MSI), were analysed using fluorescence-based polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP). Carcinomas with an NPG pattern were smaller than PG tumours (P<0.0001). Carcinomas with a PG pattern were more likely to harbour Ki-ras mutations (36%) than NPG tumours (0%; P<0.0001). Mutation types in the APC gene differed significantly between PG and NPG carcinomas (P=0.0189), including frameshift mutations in 66% of PG carcinomas but no NPG carcinomas. Presence of a p53 mutation at a 'hot spot' also was more likely in PG carcinomas (37%) than in NPG carcinomas (0%; P=0.0124). No significant difference in presence of MSI was evident between carcinomas with PG and NPG patterns. In conclusion, significant genetic differences were evident between carcinomas with PG and NPG patterns. Genetic changes in NPG carcinomas differed from those of the conventional adenoma-carcinoma sequence. Assuming that some nonpolypoid growth lesions transform rapidly into advanced carcinomas, 20% of all colorectal carcinomas may progress in this manner.
authors.affiliation: Second Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. gikaneko@med.showa-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Kurahashi
authors.forename: R
authors.initials: R
authors.lastname: Makino
authors.forename: K
authors.initials: K
authors.lastname: Konishi
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: A
authors.initials: A
authors.lastname: Katagiri
authors.forename: Y
authors.initials: Y
authors.lastname: Kumekawa
authors.forename: Y
authors.initials: Y
authors.lastname: Hirayama
authors.forename: K
authors.initials: K
authors.lastname: Yoneyama
authors.forename: M
authors.initials: M
authors.lastname: Kushima
authors.forename: M
authors.initials: M
authors.lastname: Kusano
authors.forename: H
authors.initials: H
authors.lastname: Tajiri
authors.forename: B J
authors.initials: BJ
authors.lastname: Rembacken
authors.forename: K
authors.initials: K
authors.lastname: Mitamura
authors.forename: M
authors.initials: M
authors.lastname: Imawari
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002454:Cell Differentiation; D003111:Colonic Polyps / Q000235:genetics* / Q000473:pathology*; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology*; D003123:Colorectal Neoplasms, Hereditary Nonpolyposis / Q000235:genetics / Q000473:pathology; D005260:Female; D017491:Genes, APC; D016158:Genes, p53; D011905:Genes, ras; D042822:Genomic Instability; D006801:Humans; D008297:Male; D018895:Microsatellite Repeats; D008875:Middle Aged; D009154:Mutation