| Theme |
Molecular pathology of colorectal cancer for clinicians |
| Title |
Colitic cancer -- Clinicopathological and molecular aspects |
| Author |
Yoichi Ajioka |
1st Department of Pathology, Niigata University School of Medicine |
| Author |
Hidenobu Watanabe |
1st Department of Pathology, Niigata University School of Medicine |
| Author |
Hideya Takaku |
1st Department of Surgery, Niigata University School of Medicine |
| Author |
Ken Nishikura |
1st Department of Pathology, Niigata University School of Medicine |
| Author |
Hideki Hashidate |
1st Department of Pathology, Niigata University School of Medicine |
| [ Summary ] |
Long-standing and extensive ulcerative colitis(UC) increases one's risk for developing colorectal cancer, colitis-associated colorectal cancer or colitic cancer. It usually develops in the form of multiple lesions and more frequent is poorly differentiated, mucinous or displays signet ring cell type histology, compared to sporadic colorectal carcinomas. Most, if not at all, colitic cancers originate from unequivocal neoplastic changes in the mucosa, known as dysplasia. Macroscopically, around 50% of dysplasias are flat lesions which are difficult to detect endoscopically. The kind of genetic alterations playing roles in the pathogenesis of dysplasia and colitic cancer are similar to those of sporadic colorectal carcinoma. The difference is the frequencies and timing of genetic events in those special types of neoplasias, compared to the sporadic type. It has been revealed that the frequency of APC and K-ras alterations plays less of a role in this type of development, compared to sporadic colorectal adenoma or carcinoma, while p53 alteration is regarded as an earlier event. The significance of microsatellite instability, caused by the alteration of mismatch repair genes has not been yet established. A set of colitic cancer may develop through the ordinary adenoma - carcinoma sequence, which would follow a genetic alteration pathway similar to sporadic colorectal carcinoma. Therefore, it is necessary to distinguish these types of carcinomas in order to establish the molecular mechanism of carcinogenesis, caused by long standing inflammatory processes. |