Deregulation of cell signaling in cancer Journal Article


Author: Giancotti, F. G.
Article Title: Deregulation of cell signaling in cancer
Abstract: Oncogenic mutations disrupt the regulatory circuits that govern cell function, enabling tumor cells to undergo de-regulated mitogenesis, to resist to pro-apoptotic insults, and to invade through tissue boundaries. Cancer cell biology has played a crucial role in elucidating the signaling mechanisms by which oncogenic mutations sustain these malignant behaviors and thereby in identifying rational targets for cancer drugs. The efficacy of such targeted therapies illustrate the power of a reductionist approach to the study of cancer. © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Keywords: signal transduction; protein phosphorylation; review; liver cell carcinoma; endometrium carcinoma; colorectal cancer; cell proliferation; cell survival; cell cycle s phase; complex formation; melanoma; metastasis; apoptosis; breast cancer; cell growth; smad2 protein; smad3 protein; transforming growth factor beta; protein metabolism; lung non small cell cancer; sonic hedgehog protein; mitogenesis; notch receptor; enzyme activation; protein tyrosine kinase; protein p53; tumorigenesis; colorectal carcinoma; sarcoma; lung adenocarcinoma; glioblastoma; cancer stem cell; cell migration; rna translation; pancreas adenocarcinoma; tumor necrosis factor receptor; gene silencing; senescence; negative feedback; autophagy; colon carcinoma; retinoblastoma protein; cadherin; wnt protein; loss of function mutation; focal adhesion kinase; cell invasion; ligand binding; lipogenesis; integrin; cell cycle g1 phase; oligomerization; targeted therapies; contact inhibition; cell signaling; cell dedifferentiation; epithelial mesenchymal transition; mammalian target of rapamycin complex 1; mammalian target of rapamycin complex 2; notch signaling; wnt signaling pathway; human; priority journal; cancer cell biology; gastrointestinal sarcoma; hh pathway
Journal Title: FEBS Letters
Volume: 588
Issue: 16
ISSN: 0014-5793
Publisher: Wiley Blackwell  
Date Published: 2014-08-19
Start Page: 2558
End Page: 2570
Language: English
DOI: 10.1016/j.febslet.2014.02.005
PROVIDER: scopus
PMCID: PMC4111980
PUBMED: 24561200
DOI/URL:
Notes: Export Date: 2 September 2014 -- CODEN: FEBLA -- Source: Scopus
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