Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours

Masashi Mikami; Katsuhiko Nosho; Hiroyuki Yamamoto; Taiga Takahashi; Tadateru Maehata; Hiroaki Taniguchi; Yasushi Adachi; Akimichi Imamura; Masahiro Fujita; Masao Hosokawa; Fumio Itoh; Kohzoh Imai; Yasuhisa Shinomura

doi:10.1016/j.ejca.2006.06.029

Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours

Masashi Mikami, Katsuhiko Nosho, Hiroyuki Yamamoto, Taiga Takahashi, Tadateru Maehata, Hiroaki Taniguchi, Yasushi Adachi, Akimichi Imamura, Masahiro Fujita, Masao Hosokawa, Fumio Itoh, Kohzoh Imai, Yasuhisa Shinomura

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	3065-3072
Number of pages	8
Journal	European Journal of Cancer
Volume	42
Issue number	17
DOIs	https://doi.org/10.1016/j.ejca.2006.06.029
Publication status	Published - 2006 Nov 1
Externally published	Yes

Keywords

BRAF
Flat-type colorectal tumours
KRAS
PIK3CA
RAS-RAF signalling pathway
β-catenin

ASJC Scopus subject areas

Oncology
Cancer Research

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Mikami, M., Nosho, K., Yamamoto, H., Takahashi, T., Maehata, T., Taniguchi, H., Adachi, Y., Imamura, A., Fujita, M., Hosokawa, M., Itoh, F., Imai, K., & Shinomura, Y. (2006). Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours. European Journal of Cancer, 42(17), 3065-3072. https://doi.org/10.1016/j.ejca.2006.06.029

Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours. / Mikami, Masashi; Nosho, Katsuhiko; Yamamoto, Hiroyuki; Takahashi, Taiga; Maehata, Tadateru; Taniguchi, Hiroaki; Adachi, Yasushi; Imamura, Akimichi; Fujita, Masahiro; Hosokawa, Masao; Itoh, Fumio; Imai, Kohzoh; Shinomura, Yasuhisa.

In: European Journal of Cancer, Vol. 42, No. 17, 01.11.2006, p. 3065-3072.

Research output: Contribution to journal › Article › peer-review

Mikami, M, Nosho, K, Yamamoto, H, Takahashi, T, Maehata, T, Taniguchi, H, Adachi, Y, Imamura, A, Fujita, M, Hosokawa, M, Itoh, F, Imai, K & Shinomura, Y 2006, 'Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours', European Journal of Cancer, vol. 42, no. 17, pp. 3065-3072. https://doi.org/10.1016/j.ejca.2006.06.029

Mikami, Masashi ; Nosho, Katsuhiko ; Yamamoto, Hiroyuki ; Takahashi, Taiga ; Maehata, Tadateru ; Taniguchi, Hiroaki ; Adachi, Yasushi ; Imamura, Akimichi ; Fujita, Masahiro ; Hosokawa, Masao ; Itoh, Fumio ; Imai, Kohzoh ; Shinomura, Yasuhisa. / Mutational analysis of β-catenin and the RAS-RAF signalling pathway in early flat-type colorectal tumours. In: European Journal of Cancer. 2006 ; Vol. 42, No. 17. pp. 3065-3072.

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abstract = "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.",

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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

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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.

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