| Theme | Mystery concerning the lower rectum | |
|---|---|---|
| Title | Clinicopathological and molecular differences between rectal and colonic serrated neoplasias | |
| Publish Date | 2010/11 | |
| Author | Kazuo Konishi | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| Author | Atsushi Katagiri | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| Author | Toshiko Yamochi | Second Department of Pathology, Showa University School of Medicine |
| Author | Yuichiro Yano | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| Author | Yutaro Kubota | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| Author | Takashi Muramoto | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| Author | Nozomi Yoshikawa | Endoscopic Center, Showa University Hospital |
| Author | Hidekazu Ota | Second Department of Pathology, Showa University School of Medicine |
| Author | Michio Imawari | Division of Gastroenterology, Department of Medicine, Showa University School of Medicine |
| [ Summary ] | Recently, it has been reported that some hyperplastic polyps may develop from serrated neoplasias into cancer. However, it remains unclear whether there are different mechanisms related to progression of cancer in the colon versus the rectum. We examined a total of 86 serrated neoplasias (SNs) (56 traditional serrated adenomas [TSAs], 15 sessile serrated adenomas [SSAs] and 15 mixed polyps [MPs]). Of these, 22 tumors were located in the rectum (R-group), 30 were in the distal colon (D-group) and 34 were in the proximal colon (P-group). We evaluated clinicopathological and molecular findings in the three groups. Approximately 80 % of R and D-group tumors were TSAs, whereas a half of P-group tumors were SSAs or MPs. The incidence of KRAS mutations was significantly higher in the R-group lesions than in other groups. However, we observed a significantly higher incidence of CpG island methylator phenotype (CIMP) in P-group tumors than other groups. These findings suggest that the development of proximal and distal SNs, especially rectal SNs, may occur through the sessile and traditional serrated pathways. | |