Frameshift mutations in TGFβRII, IGFIIR, BAX, hMSH3 and hMSH6 are absent in lung cancers

被引:17
作者
Gotoh, K
Yatabe, Y
Sugiura, T
Takagi, K
Ogawa, M
Takahashi, T
Mitsudomi, T [1 ]
机构
[1] Aichi Canc Ctr Hosp, Dept Internal Med & Pulmon Med, Chikusa Ku, Nagoya, Aichi 4648681, Japan
[2] Aichi Canc Ctr Hosp, Dept Pathol & Clin Labs, Chikusa Ku, Nagoya, Aichi, Japan
[3] Aichi Canc Ctr Hosp, Dept Thorac Surg, Chikusa Ku, Nagoya, Aichi, Japan
[4] Aichi Canc Ctr Res Inst, Lab Ultrastructure Res, Chikusa Ku, Nagoya, Aichi, Japan
[5] Nagoya Univ, Sch Med, Dept Internal Med 2, Showa Ku, Nagoya, Aichi 466, Japan
关键词
D O I
10.1093/carcin/20.3.499
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A genome-wide instability at simple repeat sequences characterizes gastrointestinal and endometrial cancers of the microsatellite mutator phenotype (MMP). The genes encoding transforming growth factor-beta receptor type II (TGF beta RII), insulin-like growth factor II receptor (IGFIIR), Bcl-2 associated X protein (BAX), hMSH3 and hMSH6 have simple repeat sequences in their coding regions. Consequently, mutations in the single repeat sequences in these genes provide one major route for carcinogenesis in these cancers. We examined 43 non-small cell lung carcinomas and 16 small cell carcinomas for frameshift mutations in simple repeat sequences of TGF beta RII, IGFIIR, BAX, hMSH3 and hMSH6. In addition, MMP was assessed using a primer set for BAT-26, None of 59 lung cancers exhibited frameshift mutations or MMP, It is concluded that somatic frameshift mutations in these genes and MMP do not constitute important mechanisms in lung carcinogenesis. The possibility of some sort of genetic instability undetectable as a form of MMP cannot be precluded.
引用
收藏
页码:499 / 502
页数:4
相关论文
共 33 条
[1]   MICROSATELLITE INSTABILITY IN PRIMARY AND METASTATIC LUNG CARCINOMAS [J].
ADACHI, J ;
SHISEKI, M ;
OKAZAKI, T ;
ISHIMARU, G ;
NOGUCHI, M ;
HIROHASHI, S ;
YOKOTA, J .
GENES CHROMOSOMES & CANCER, 1995, 14 (04) :301-306
[2]   Mutations of mitotic checkpoint genes in human cancers [J].
Cahill, DP ;
Lengauer, C ;
Yu, J ;
Riggins, GJ ;
Willson, JKV ;
Markowitz, SD ;
Kinzler, KW ;
Vogelstein, B .
NATURE, 1998, 392 (6673) :300-303
[3]  
Dietmaier W, 1997, CANCER RES, V57, P4749
[4]  
FONG KM, 1995, CANCER RES, V55, P28
[5]  
Hoang JM, 1997, CANCER RES, V57, P300
[6]   UBIQUITOUS SOMATIC MUTATIONS IN SIMPLE REPEATED SEQUENCES REVEAL A NEW MECHANISM FOR COLONIC CARCINOGENESIS [J].
IONOV, Y ;
PEINADO, MA ;
MALKHOSYAN, S ;
SHIBATA, D ;
PERUCHO, M .
NATURE, 1993, 363 (6429) :558-561
[7]  
KIM HG, 1994, AM J PATHOL, V145, P148
[8]   Molecular nature of colon tumors in hereditary nonpolyposis colon cancer, familial polyposis, and sporadic colon cancer [J].
Konishi, M ;
KikuchiYanoshita, R ;
Tanaka, K ;
Muraoka, M ;
Onda, A ;
Okumura, Y ;
Kishi, N ;
Iwama, T ;
Mori, T ;
Koike, M ;
Ushio, K ;
Chiba, M ;
Nomizu, S ;
Konishi, F ;
Utsunomiya, J ;
Miyaki, M .
GASTROENTEROLOGY, 1996, 111 (02) :307-317
[9]   Genetic instability in colorectal cancers [J].
Lengauer, C ;
Kinzler, KW ;
Vogelstein, B .
NATURE, 1997, 386 (6625) :623-627
[10]  
Lynch HT, 1996, CANCER, V78, P1149, DOI 10.1002/(SICI)1097-0142(19960915)78:6<1149::AID-CNCR1>3.0.CO