| Theme | Aiming at the future of depressed type of lesion in early colorectal cancer | |
|---|---|---|
| Title | Genetic abnormalities in flat and depressed type colorectal cancer | |
| Publish Date | 2008/11 | |
| Author | Ho Min Kim | Department of Surgery, Graduate School of Medicine, Osaka University |
| Author | Hirofumi Yamamoto | Department of Surgery, Graduate School of Medicine, Osaka University |
| Author | Mitsugu Sekimoto | Department of Surgery, Graduate School of Medicine, Osaka University |
| Author | Yuichiro Doki | Department of Surgery, Graduate School of Medicine, Osaka University |
| Author | Masaki Mori | Department of Surgery, Graduate School of Medicine, Osaka University |
| [ Summary ] | Flat and depressed type colorectal early cancer is considered to be generated via de novo cancer pathways. In the adenoma carcinoma sequence (ACS), several genes such as APC, K-ras and p53, are responsible for the development of early polypoid cancer. However, the underlying genetic mechanisms in regard to flat and depressed type cancer are still unknown. In addition to the above putative genes, studies were done on beta-catenin, BRAF, microsatellite instability (MSI), and 17p LOH to assess flat and depressed lesions. For instance, beta-catenin gene mutations of exon 3 were reported in 23.5 % of flat and depressed lesions, while the protruded type had mutation rates of 5.1 %. Likewise, BRAF mutations were found in 11.1 % of flat and depressed type colon cancers and 0 % in polypoid colon cancer cases. It has also been shown that de novo early cancers have a tendency to exhibit MSI-H when compared to early cancers with adenoma (4 / 25 versus 0 / 25, p = 0.055). In this review, we introduce related articles as well as our study on diminutive flat depressed lesions with diameters under 5 mm. Although this link has not been conclusively established, some gene alterations may be associated with flat and depressed early colorectal cancer. | |