Wilms' tumours: about tumour suppressor genes, an oncogene and a chameleon gene

被引：190
作者：
Huff, Vicki [1 ,2 ,3 ]
机构：
[1] Univ Texas MD Anderson Canc Ctr, Dept Genet, Unit 1010, Houston, TX 77030 USA
[2] UT Houston Grad Sch Biomed Sci, Grad Program Genes & Dev, Houston, TX 77025 USA
[3] UT Houston Grad Sch Biomed Sci, Grad Program Human Mol Genet, Houston, TX 77025 USA
来源：
NATURE REVIEWS CANCER | 2011年 / 11卷 / 02期
关键词：
ACUTE MYELOID-LEUKEMIA; BECKWITH-WIEDEMANN-SYNDROME; HEMATOPOIETIC PROGENITOR CELLS; MINIMAL RESIDUAL DISEASE; EARLY KIDNEY DEVELOPMENT; WT1; MESSENGER-RNA; BETA-CATENIN; NEPHROGENIC RESTS; PROGNOSTIC-SIGNIFICANCE; WILMS-TUMOR-1; GENE;
D O I：
10.1038/nrc3002
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Genes identified as being mutated in Wilms' tumour include TP53, a classic tumour suppressor gene (TSG); CTNNB1 (encoding beta-catenin), a classic oncogene; WTX, which accumulating data indicate is a TSG; and WT1, which is inactivated in some Wilms' tumours, similar to a TSG. However, WT1 does not always conform to the TSG label, and some data indicate that WT1 enhances cell survival and proliferation, like an oncogene. Is WT1 a chameleon, functioning as either a TSG or an oncogene, depending on cellular context? Are these labels even appropriate for describing and understanding the function of WT1?
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收藏
页码：111 / 121
页数：11
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