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Cold Spring Harb Perspect Med. 2015 Apr 1;5(4). pii: a006098. doi: 10.1101/cshperspect.a006098.

Signal transduction in cancer.

Author information

1
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724.
2
Harvard Medical School, Department of Cell Biology, Boston, Massachusetts 02115.

Abstract

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 hyperactivation 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.

PMID:
25833940
PMCID:
PMC4382731
DOI:
10.1101/cshperspect.a006098
[Indexed for MEDLINE]
Free PMC Article

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