Hakem R, Mak T W
Amgen Institute, Ontario Cancer Institute and the University of Toronto, Toronto, Ontario, Canada M5G 2C1.
Annu Rev Genet. 2001;35:209-41. doi: 10.1146/annurev.genet.35.102401.090432.
The development of cancer requires multiple genetic alterations perturbing distinct cellular pathways. In human cancers, these alterations often arise owing to mutations in tumor-suppressor genes whose normal function is to either inhibit the proliferation, apoptosis, or differentiation of cells, or maintain their genomic integrity. Mouse models for tumor suppressors frequently provide definitive evidence for the antitumorigenic functions of these genes. In addition, animal models permit the identification of previously unsuspected roles of these genes in development and differentiation. The availability of null and tissue-specific mouse mutants for tumor-suppressor genes has greatly facilitated our understanding of the mechanisms leading to cancer. In this review, we describe mouse models for tumor-suppressor genes.
癌症的发展需要多个基因改变扰乱不同的细胞通路。在人类癌症中,这些改变通常是由于肿瘤抑制基因的突变引起的,这些基因的正常功能是抑制细胞增殖、凋亡或分化,或维持其基因组完整性。肿瘤抑制基因的小鼠模型经常为这些基因的抗肿瘤功能提供确凿证据。此外,动物模型有助于识别这些基因在发育和分化中以前未被怀疑的作用。肿瘤抑制基因的无效和组织特异性小鼠突变体的可用性极大地促进了我们对导致癌症的机制的理解。在这篇综述中,我们描述了肿瘤抑制基因的小鼠模型。