BACKGROUND: To clarify genetic changes in colorectal tumorigenesis, K-ras codon 12 point mutations were examined in 101 ordinary colorectal carcinomas and 6 that complicated ulcerative colitis (UC) with special attention to growth patterns. METHODS: The depths of invasion of ordinary carcinoma were submucosa (SMCa) in 39 cases, muscularis propria (PMCa) in 33, and far-advanced in 29. Growth patterns of SMCa and PMCa were classified into three types: polypoid-growth type without central depression (Type 1), polypoid-growth type with central depression (Type 2), and nonpolypoid-growth type. DNA samples were extracted from formalin fixed paraffin embedded sections, and K-ras codon 12 mutations were examined by two-step polymerase chain reaction-restriction fragment length polymorphism. RESULTS: K-ras mutation frequency was higher in Type 1 SMCa than in nonpolypoid SMCa, 56% (9/16) versus 6% (1/17), respectively, and in PMCa, 78% (7/9) versus 23% (3/13), respectively. In 6 UC carcinomas, a K-ras mutation was detected in only one polypoid carcinoma and none were detected in five nonpolypoid carcinomas. CONCLUSIONS: These results and the authors' previous study suggest that nonpolypoid carcinomas may be derived from flat adenomas, whose K-ras mutation incidence also was low, and this pathway is different from a genetic model based on the ordinary adenoma-carcinoma sequence through polypoid adenomas.
BACKGROUND: To clarify genetic changes in colorectal tumorigenesis, K-ras codon 12 point mutations were examined in 101 ordinary colorectal carcinomas and 6 that complicated ulcerative colitis (UC) with special attention to growth patterns. METHODS: The depths of invasion of ordinary carcinoma were submucosa (SMCa) in 39 cases, muscularis propria (PMCa) in 33, and far-advanced in 29. Growth patterns of SMCa and PMCa were classified into three types: polypoid-growth type without central depression (Type 1), polypoid-growth type with central depression (Type 2), and nonpolypoid-growth type. DNA samples were extracted from formalin fixed paraffin embedded sections, and K-ras codon 12 mutations were examined by two-step polymerase chain reaction-restriction fragment length polymorphism. RESULTS:K-ras mutation frequency was higher in Type 1 SMCa than in nonpolypoid SMCa, 56% (9/16) versus 6% (1/17), respectively, and in PMCa, 78% (7/9) versus 23% (3/13), respectively. In 6 UC carcinomas, a K-ras mutation was detected in only one polypoid carcinoma and none were detected in five nonpolypoid carcinomas. CONCLUSIONS: These results and the authors' previous study suggest that nonpolypoid carcinomas may be derived from flat adenomas, whose K-ras mutation incidence also was low, and this pathway is different from a genetic model based on the ordinary adenoma-carcinoma sequence through polypoid adenomas.
Authors: Janine G Einspahr; Maria Elena Martinez; Ruiyun Jiang; Chiu-Hsieh Hsu; Asif Rashid; Achyut K Bhattacharrya; Dennis J Ahnen; Elizabeth T Jacobs; P Scott Houlihan; C Renee Webb; David S Alberts; Stanley R Hamilton Journal: Cancer Epidemiol Biomarkers Prev Date: 2006-08 Impact factor: 4.254
Authors: S Fujii; T Fujimori; H Kawamata; J Takeda; K Kitajima; F Omotehara; T Kaihara; T Kusaka; K Ichikawa; Y Ohkura; Y Ono; J Imura; S Yamaoka; C Sakamoto; Y Ueda; T Chiba Journal: Gut Date: 2004-05 Impact factor: 23.059
Authors: Quirinus J M Voorham; Beatriz Carvalho; Angela J Spiertz; Bart Claes; Sandra Mongera; Nicole C T van Grieken; Heike Grabsch; Martin Kliment; Bjorn Rembacken; Mark A van de Wiel; Philip Quirke; Chris J J Mulder; Diether Lambrechts; Manon van Engeland; Gerrit A Meijer Journal: PLoS One Date: 2012-07-27 Impact factor: 3.240