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Signal Transduction in Cancer
Author(s) -
Richard Sever,
Joan S. Brugge
Publication year - 2015
Publication title -
cold spring harbor perspectives in medicine
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 3.853
H-Index - 105
eISSN - 2472-5412
pISSN - 2157-1422
DOI - 10.1101/cshperspect.a006098
Subject(s) - signal transduction , biology , epigenetics , microbiology and biotechnology , cancer cell , angiogenesis , tumor microenvironment , cell signaling , pi3k/akt/mtor pathway , protein kinase b , cancer research , context (archaeology) , cancer , cell growth , hyperactivation , genetics , paleontology , gene
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.

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