BACKGROUND: Patients with ulcerative colitis (UC) are at risk of UC-associated colorectal cancer (CRC); however, little is known about genetic alterations occurring during UC carcinogenesis. We examined mutational changes in patients with colitic cancer and the features that differed between the carcinogenesis of UC and sporadic CRC. MATERIAL AND METHODS: Specimens were obtained from the non-neoplastic mucosa and cancer cells of 12 patients with colitic cancer. The mutational rate of oncogenes in colitic cancer was analyzed and compared to that of oncogenes in sporadic CRC. RESULTS: We observed a lower mutation rate in adenomatous polyposis coli (APC) (16.7%(2/12) vs. 75.9%(161/212), respectively, p=0.0001) and KRAS (16.7%(2/12) vs. 42% (89/212), respectively, p=0.04) in colitic cancer than in sporadic CRC. With respect to cadherin 1 (CDH1) and fibroblast growth factor receptor 2 (FGFR2), the mutational rates for non-neoplastic colorectal mucosa were similar to those in sporadic CRC. CONCLUSION: We demonstrated that mutational rates for APC and KRAS differ between colitic cancer and sporadic CRC. Furthermore, we revealed that CDH1 and FGFR2 become mutated at an earlier stage in colitic carcinogenesis than in sporadic CRC. Copyright
BACKGROUND:Patients with ulcerative colitis (UC) are at risk of UC-associated colorectal cancer (CRC); however, little is known about genetic alterations occurring during UC carcinogenesis. We examined mutational changes in patients with colitic cancer and the features that differed between the carcinogenesis of UC and sporadic CRC. MATERIAL AND METHODS: Specimens were obtained from the non-neoplastic mucosa and cancer cells of 12 patients with colitic cancer. The mutational rate of oncogenes in colitic cancer was analyzed and compared to that of oncogenes in sporadic CRC. RESULTS: We observed a lower mutation rate in adenomatous polyposis coli (APC) (16.7%(2/12) vs. 75.9%(161/212), respectively, p=0.0001) and KRAS (16.7%(2/12) vs. 42% (89/212), respectively, p=0.04) in colitic cancer than in sporadic CRC. With respect to cadherin 1 (CDH1) and fibroblast growth factor receptor 2 (FGFR2), the mutational rates for non-neoplastic colorectal mucosa were similar to those in sporadic CRC. CONCLUSION: We demonstrated that mutational rates for APC and KRAS differ between colitic cancer and sporadic CRC. Furthermore, we revealed that CDH1 and FGFR2 become mutated at an earlier stage in colitic carcinogenesis than in sporadic CRC. Copyright
Authors: S M Powell; N Zilz; Y Beazer-Barclay; T M Bryan; S R Hamilton; S N Thibodeau; B Vogelstein; K W Kinzler Journal: Nature Date: 1992-09-17 Impact factor: 49.962
Authors: K Hata; T Watanabe; S Kazama; K Suzuki; M Shinozaki; T Yokoyama; K Matsuda; T Muto; H Nagawa Journal: Br J Cancer Date: 2003-10-06 Impact factor: 7.640
Authors: Manon de Krijger; Beatriz Carvalho; Christian Rausch; Anne S Bolijn; Pien M Delis-van Diemen; Marianne Tijssen; Manon van Engeland; Nahid Mostafavi; Roel M M Bogie; Evelien Dekker; Ad A M Masclee; Joanne Verheij; Gerrit A Meijer; Cyriel Y Ponsioen Journal: Inflamm Bowel Dis Date: 2022-09-01 Impact factor: 7.290