| Theme |
Aiming at the future of depressed type of lesion in early colorectal cancer |
| Title |
Genetic instability of non-polypoid colorectal carcinomas |
| Author |
Taishi Ogawa |
Endoscopy Division, Cancer Institute Hospital, Japanese Foundation For Cancer Research |
| Author |
Isao Okayasu |
Department of Pathology, Kitasato University School of Medicine |
| Author |
Masami Arai |
Clinical Genetic Oncolory, Cancer Institute Hospital, Japanese Foundation For Cancer Research |
| Author |
Naoyuki Uragami |
Department of Gastroenterology, Cancer Institute Hospital, Japanese Foundation For Cancer Research |
| Author |
Masahiro Igarashi |
Endoscopy Division, Cancer Institute Hospital, Japanese Foundation For Cancer Research |
| [ Summary ] |
Early colorectal carcinomas (submucosal invasive adenocarcinomas ; SM-Cas) can be classified into the categories of polypoid growth carcinoma (PG-Ca) and nonpolypoid growth carcinoma (NPG-Ca), the latter transforming more rapidly into advanced carcinomas. Previously, we indicated that stromal genetic instability might contribute to tumorigenesis associated with both sporadic and ulcerative colitis-associated colorectal adenocarcinomas. In the present study, we analyzed the genetic instability of both epithelial and surrounding stromal components in PG-Cas and NPG-Cas. In colorectal SM-Cas, epithelial and stromal genetic instability was analyzed using National Cancer Institute-standard microsatellite markers, chromosome 17 (Chr. 17) markers and tumor suppressor gene-related markers, using a combination of laser-captured microdissection and GeneScan approaches. Immunohistochemical analysis was performed for hMLH1. In addition, we investigated methylation of the hMLH1 promoters. The frequency of epithelial microsatellite instability (MSI) with Chr. 17 markers was significantly higher in NPG-Cas, as compared to PG-Cas. Stromal MSI was observed in PG-Cas and NPG-Cas. These results suggest that epithelial MSI with Chr. 17 markers contributes markedly to carcinogenesis in NPG-Cas, while stromal genetic instability may be necessary for the development of both types of colorectal carcinoma. |