Journal
ONCOGENE
Volume 22, Issue 20, Pages 3152-3161Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1206456
Keywords
melanoma; apoptosis; death receptors; Fas; TNFR-1; TRAIL
Funding
- NCI NIH HHS [CA55995, CA559908] Funding Source: Medline
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Impaired ability to undergo programmed cell death in response to a wide range of external stimuli acquires melanomas a selective advantage for progression and metastasis as well as their notorious resistance to therapy. Better understanding of mechanisms that govern apoptosis has enabled identification of diverse routes by which melanomas manage to escape stimuli of apoptosis. Changes at genomic, transcriptional and post-translational levels of G-proteins and protein kinases (Ras, B-Raf) and their transcription factor effectors (c-Jun, ATF2, Stat3 and NF-kappaB) affects TNF, Fas and TRAIL receptors, which play important roles in acquiring melanoma's resistance to apoptosis. Here, we summarize our current understanding of changes that alters the regulation of death receptors during melanoma development.
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