TGF-β and cancer

被引:122
作者
Reiss, M
机构
[1] Yale Univ, Sch Med, Dept Med Med Oncol, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Yale Canc Ctr, New Haven, CT 06520 USA
关键词
TGF-beta; cancer; Smad;
D O I
10.1016/S1286-4579(99)00251-8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The relationships between transforming growth factor-beta (TGF-beta) and cancer are varied and complex. The paradigm that is emerging from the experimental evidence accumulated over the past decade or so is that TGF-beta can play two different and opposite roles with respect to the process of malignant progression. During early stages of carcinogenesis, TGF-beta acts predominantly as a potent tumor suppressor and may mediate the actions of chemopreventive agents such as retinoids and nonsteroidal anti-estrogens. However, at some point during the development and progression of malignant neoplasms, bioactive TGF-beta s make their appearance in the tumor microenvironment and the tumor cells escape from TGF-beta-dependent growth arrest. In many cases, this resistance to TGF-beta is the consequence of loss or mutational inactivation of the genes that encode signaling intermediates. These include the types I and II TGF-beta receptors, as well as receptor-associated and common-mediator Smads. The stage of tumor development or progression at which TGF-beta-resistant clones come to dominate the tumor cell population in different types of neoplasm remains to be defined. The phenotypic switch from TGF-beta-sensitivity to TGF-beta-resistance that occurs during carcinogenesis has several important implications for cancer prevention and treatment. (C) 1999 Editions scientifiques et medicales Elsevier SAS.
引用
收藏
页码:1327 / 1347
页数:21
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