TY - JOUR
T1 - Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours
AU - Mikami, Masashi
AU - Nosho, Katsuhiko
AU - Yamamoto, Hiroyuki
AU - Takahashi, Taiga
AU - Maehata, Tadateru
AU - Taniguchi, Hiroaki
AU - Adachi, Yasushi
AU - Imamura, Akimichi
AU - Fujita, Masahiro
AU - Hosokawa, Masao
AU - Itoh, Fumio
AU - Imai, Kohzoh
AU - Shinomura, Yasuhisa
N1 - Funding Information:
This study was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (H.Y. and K.I.) and Grants-in-Aid for Cancer Research and for the Third Term Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan (H.Y. and K.I.).
PY - 2006/11
Y1 - 2006/11
N2 - Morphologically, early colorectal tumours can be divided into two groups, protruded-type and flat-type. However, little is known about genetic mechanisms of the latter. We investigated mutations of β-catenin, KRAS, BRAF, and PIK3CA in 310 early colorectal tumours. β-catenin mutation was detected in 7.1% of 310 tumours. β-catenin mutation was detected in a significantly higher percentage of flat-type tumours with depressed areas (4/17, 23.5%) than in other tumours (18/293, 6.1%; p = 0.0246). KRAS, BRAF, and PIK3CA mutations were detected in 21.6%, 5.4%, and 1.0% of 310 tumours, respectively. Concomitant mutations of β-catenin and KRAS or BRAF were detected in seven tumours. Mutation of at least one gene was detected in a significantly higher percentage of flat-type tumour tissues (75/193, 38.9%) than in protruded-type tumour tissues (25/117, 21.4%; p = 0.0014), and it was correlated significantly with size (p = 0.0001). In conclusion, β-catenin mutation seemed to play an important role in flat-type tumours, especially in those with depressed areas. The genetic abnormalities could arise and accumulate in the early stage of colorectal tumourigenesis, and seem to contribute to the development of flat-type tumour.
AB - Morphologically, early colorectal tumours can be divided into two groups, protruded-type and flat-type. However, little is known about genetic mechanisms of the latter. We investigated mutations of β-catenin, KRAS, BRAF, and PIK3CA in 310 early colorectal tumours. β-catenin mutation was detected in 7.1% of 310 tumours. β-catenin mutation was detected in a significantly higher percentage of flat-type tumours with depressed areas (4/17, 23.5%) than in other tumours (18/293, 6.1%; p = 0.0246). KRAS, BRAF, and PIK3CA mutations were detected in 21.6%, 5.4%, and 1.0% of 310 tumours, respectively. Concomitant mutations of β-catenin and KRAS or BRAF were detected in seven tumours. Mutation of at least one gene was detected in a significantly higher percentage of flat-type tumour tissues (75/193, 38.9%) than in protruded-type tumour tissues (25/117, 21.4%; p = 0.0014), and it was correlated significantly with size (p = 0.0001). In conclusion, β-catenin mutation seemed to play an important role in flat-type tumours, especially in those with depressed areas. The genetic abnormalities could arise and accumulate in the early stage of colorectal tumourigenesis, and seem to contribute to the development of flat-type tumour.
KW - BRAF
KW - Flat-type colorectal tumours
KW - KRAS
KW - PIK3CA
KW - RAS-RAF signalling pathway
KW - β-catenin
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U2 - 10.1016/j.ejca.2006.06.029
DO - 10.1016/j.ejca.2006.06.029
M3 - Article
C2 - 17011185
AN - SCOPUS:33750514803
VL - 42
SP - 3065
EP - 3072
JO - European Journal of Cancer
JF - European Journal of Cancer
SN - 0959-8049
IS - 17
ER -