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

被引：195

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?

引用

页码：111 / 121

页数：11

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