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 | |
| Publication status | Published - 2006 Nov |
| Externally published | Yes |
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Keywords
- β-catenin
- BRAF
- Flat-type colorectal tumours
- KRAS
- PIK3CA
- RAS-RAF signalling pathway
ASJC Scopus subject areas
- Cancer Research
- Hematology
- Oncology
Cite this
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, 11.2006, p. 3065-3072.Research output: Contribution to journal › Article
}
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
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 - β-catenin
KW - BRAF
KW - Flat-type colorectal tumours
KW - KRAS
KW - PIK3CA
KW - RAS-RAF signalling pathway
UR - http://www.scopus.com/inward/record.url?scp=33750514803&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33750514803&partnerID=8YFLogxK
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 -