| Theme |
Prevalence of the IIc type colorectal neoplasm |
| Title |
Genetic alterations in colorectal de novo carcinoma |
| Author |
Shigehiko Fujii |
Department of Surgical and Molecular Pathology, Dokkyo University School of Medicine |
| Author |
Takahiro Fujimori |
Department of Surgical and Molecular Pathology, Dokkyo University School of Medicine |
| Author |
Hideki Mitooka |
Center for Digestive Diseases, Kobe Kaisei Hospital |
| Author |
Tsutomu Chiba |
Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine |
| [ Summary ] |
It is now widely accepted that sporadic colorectal cancers develop through the three pathways, the adenoma-carcinoma sequence (ACS), the hereditary nonpolyposis colorectal cancer pathway, and the de novo pathway. Although many studies have clarified genetic alterations related to sporadic colorectal cancer, genetic alterations of de novo colorectal cancer remain poorly understood to date. The alterations of APC and K-ras genes in de novo cancer are infrequent compared to those in ACS cancer. The rate of p53 gene alteration is high in de novo cancer and similar to ACS cancer, but its alteration may represent an early event in the development of de novo cancer. In adherens junction molecules, E-cadherin and beta-catenin, the rate of decreased E-cadherin expression were higher in de novo cancer than in ACS cancer, however, there is no significant difference in translocation of beta-catenin expression.
It remains unclear which genetic alterations are associated with the biological features of de novo cancers that these cancers had a tendency to more deeply invade the colonic wall at a smaller size. Further studies are needed to determine the potential genetic alterations of de novo cancer. |