Signal Transduction in Cancer

被引:607
|
作者
Sever, Richard [1 ]
Brugge, Joan S. [2 ]
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
来源
关键词
PYRUVATE-KINASE M2; EPITHELIAL-MESENCHYMAL TRANSITIONS; ACUTE MYELOID-LEUKEMIA; PAR3 POLARITY PROTEIN; BREAST-CANCER; C-MYC; CELL-MIGRATION; TUMOR-GROWTH; DEPENDENT PHOSPHORYLATION; NASOPHARYNGEAL CARCINOMA;
D O I
10.1101/cshperspect.a006098
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Cancer is driven by genetic and epigenetic alterations that allow cells to overproliferate and escape mechanisms that normally control their survival and migration. Many of these alterations map to signaling pathways that control cell growth and division, cell death, cell fate, and cell motility, and can be placed in the context of distortions of wider signaling networks that fuel cancer progression, such as changes in the tumor microenvironment, angiogenesis, and inflammation. Mutations that convert cellular proto-oncogenes to oncogenes can cause hyper-activation of these signaling pathways, whereas inactivation of tumor suppressors eliminates critical negative regulators of signaling. An examination of the PI3K-Akt and Ras-ERK pathways illustrates how such alterations dysregulate signaling in cancer and produce many of the characteristic features of tumor cells.
引用
收藏
页数:21
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