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- W2059192510 endingPage "377" @default.
- W2059192510 startingPage "368" @default.
- W2059192510 abstract "Several advances in recent years have focused increasing attention on the role of the RAF-MEK-ERK1/2 pathway in promoting cell survival. The demonstration that BRAF is a human oncogene mutated at high frequency in melanoma, thyroid and colon cancer has provided a pathophysiological context, whilst the description of potent and highly selective inhibitors of BRAF or MEK has allowed a more informed and rational intervention in both normal and tumour cells. In addition, separate studies have uncovered new mechanisms by which the ERK1/2 pathway can control the activity or abundance of members of the BCL-2 protein family to promote cell survival. It is now apparent that various oncogenes co-opt ERK1/2 signalling to de-regulate these BCL-2 proteins and this contributes to, and even underpins, survival signalling in some tumours. New oncogene-targeted therapies allow direct or indirect inhibition of ERK1/2 signalling and can cause quite striking tumour cell death. In other cases, inhibition of the ERK1/2 pathway may be more effective in combination with other conventional and novel therapeutics. Here, we review recent advances in our understanding of how the ERK1/2 pathway regulates BCL-2 proteins to promote survival, how this is de-regulated in tumour cells and the opportunities this might afford with the use of new targeted therapies." @default.
- W2059192510 created "2016-06-24" @default.
- W2059192510 creator A5025815250 @default.
- W2059192510 creator A5056826438 @default.
- W2059192510 date "2008-10-10" @default.
- W2059192510 modified "2023-10-06" @default.
- W2059192510 title "Tumour cell survival signalling by the ERK1/2 pathway" @default.
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- W2059192510 doi "https://doi.org/10.1038/cdd.2008.148" @default.
- W2059192510 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18846109" @default.
- W2059192510 hasPublicationYear "2008" @default.
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