Transcription factors as targets for cancer therapy

By James E. Darnell. Nature Reviews. Cancer, 2002

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How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

A census of human transcription factors: function, expression and evolution (2009, background): “TFs and human diseases Transcriptional misregulation has been associated with a diverse set of diseases, including cancer and developmental syndrome”
The STATs of cancer — new molecular targets come of age (2004, background): “For example, a number of oncogenic signalling pathways all seem to converge on a limited set of nuclear transcription factor”
Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “Once activated in malignant or immune cells, STAT3 can induce the expression of a subset of genes whose products are important for further STAT3 activation, including IL-6, IL-22, EGF, IL-23 and IL-10 [52,53] as well as STAT3-dependent induction of cell surface growth factor and cytokine receptors (”
BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, neutral): “Your story matters.”
Reactive oxygen species in tumor progression. (2005, background): “NF-κB almost always drives transcription in association with other transcription factors (156).”
Axis of evil: molecular mechanisms of cancer metastasis (2003, background): “Target genes of TCF/b-catenin that could be relevant for tumor progression include the protooncogenes c-Myc and cyclin D1 (Polakis, 2000; Barth and Nelson, 2002; Darnell, 2002).”