TP53, EGFR, and KRAS mutations in relation to VHL inactivation and lifestyle risk factors in renal-cell carcinoma from central and eastern Europe

被引：23

作者：

Szymanska, K. ^{[1
]}

Moore, L. E. ^{[2
]}

Rothman, N. ^{[2
]}

Chow, W. H. ^{[2
]}

Waldman, F. ^{[3
]}

Jaeger, E. ^{[3
]}

Waterboer, T. ^{[4
]}

Foretova, L. ^{[5
]}

Navratilova, M. ^{[5
]}

Janout, V. ^{[6
]}

Kollarova, H. ^{[6
]}

Zaridze, D. ^{[7
]}

Matveev, V. ^{[7
]}

Mates, D. ^{[8
]}

Szeszenia-Dabrowska, N. ^{[9
]}

Holcatova, I. ^{[10
]}

Bencko, V. ^{[10
]}

Le Calvez-Kelm, F. ^{[1
]}

Villar, S. ^{[1
]}

Pawlita, M.

Boffetta, P. ^{[1
]}

Hainaut, P. ^{[1
]}

Brennan, P. ^{[1
]}

机构：

[1] Int Agcy Res Canc, F-69008 Lyon, France

[2] NCI, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA

[3] Univ Calif San Francisco, UCSF Comprehens Canc Ctr, San Francisco, CA 94143 USA

[4] German Canc Res Ctr, Infect & Canc Program, Heidelberg, Germany

[5] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic

[6] Palacky Univ, Fac Med, Dept Prevent Med, CR-77147 Olomouc, Czech Republic

[7] Russian Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia

[8] Inst Publ Hlth, Bucharest, Romania

[9] Inst Occupat Med, Dept Epidemiol, Lodz, Poland

[10] Charles Univ Prague, Fac Med 1, Inst Hyg & Epidemiol, Prague, Czech Republic

来源：

CANCER LETTERS | 2010年 / 293卷 / 01期

关键词：

TP53; mutations; VHL; EGFR; Cancer; Renal carcinoma; TUMOR-SUPPRESSOR GENE; P53; EXPRESSION; CANCER; PVHL; RNA;

D O I：

10.1016/j.canlet.2009.11.024

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Renal-cell carcinomas (RCC) are frequent in central and eastern Europe and the reasons remain unclear. Molecular mechanisms, except for VHL, have not been much investigated. We analysed 361 RCCs (334 clear-cell carcinomas) from a multi-centre case-control study for mutations in TP53 (exons 5-9 in the whole series and exons 4 and 10 in a pilot subset of 60 tumours) and a pilot 50 tumours for mutations in EGFR (exons 18-21) or KRAS (codon 12) in relation to VHL status. TP53 mutations were detected in 4% of clear-cell cases, independently of VHL mutations. In non-clear-cell carcinomas, they were detected in 11% of VHL-wild-type tumours and in 0% of tumours with VHL functional mutations. No mutations were found in EGFR or KRAS. We conclude that mutations in TP53, KRAS, or EGFR are not major contributors to the RCC development even in the absence of VHL inactivation. The prevalence of TP53 mutations in relation to VHL status may differ between clear-cell and other renal carcinomas. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

引用

页码：92 / 98

页数：7