Since the 1970s, it has been well known that long-standing
ulcerative colitis (UC) disposes to the development of
colorectal adenocarcinoma (CRC). To date, CRC associated with UC is thought to arise along a pathway of
dysplasia, however, primary factors for developing of UC-related
dysplasia and cancer are unclear.
Vitamin D, which works through binding the
vitamin D receptor (VDR) has an important role in cancer progression and
immune response. In this study, we investigated the impact of VDR expression on UC as well as
colon cancer. We examined retrospectively the expression of VDR in extraction specimens of UC (n=124) patients by
immunohistochemistry. We counted VDR positive cells in at least 10 fields in each case to evaluate the
frequency of VDR positive cells in
ductal epithelium. In addition, effect of VDR expression on
inflammation was analyzed. On a normal
mucosa, the expression of VDR was recognized in 58.8% of
ductal cells. In UC patient, the expression of VDR was considerably decreased compared to normal
mucosa, VDR positive rate was only 3.4+/-9.0%. Importantly,
dysplasia and UC-CRC patients showed lower rate of VDR expression compared to non-colon
cancer patients, whose expression rates were 0.6+/-1.3% and 3.8+/-10%, respectively. Moreover, long-term UC patients (more than ten years) who were at high-risk of developing CRC showed significantly lower VDR expression than short-term patients. We did not detect direct association of VDR expression with
inflammation and clinical stage of UC. These findings suggested that
correlation seems to exist between the level of VDR expression and
carcinogenesis in UC. VDR could be a possible marker to detect
dysplasia and cancer in
ulcerative colitis.
