RT Journal Article
SR Electronic
T1 Colitic Cancer Develops Through Mutational Alteration Distinct from that in Sporadic Colorectal Cancer: A Comparative Analysis of Mutational Rates at Each Step
JF Cancer Genomics - Proteomics
JO Cancer Genomics Proteomics
FD International Institute of Anticancer Research
SP 341
OP 348
VO 14
IS 5
A1 TANAKA, TOSHIAKI
A1 KOBUNAI, TAKASHI
A1 YAMAMOTO, YOKO
A1 EMOTO, SHIGENOBU
A1 MURONO, KOJI
A1 KANEKO, MANABU
A1 SASAKI, KAZUHITO
A1 OTANI, KENSUKE
A1 NISHIKAWA, TAKESHI
A1 KAWAI, KAZUSHIGE
A1 HATA, KEISUKE
A1 NOZAWA, HIROAKI
A1 WATANABE, TOSHIAKI
YR 2017
UL http://cgp.iiarjournals.org/content/14/5/341.abstract
AB 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.