The NF-kappaB signalling pathway has a vital role in certain cancers, according to two Nature studies published. The results highlight potential targets for therapeutic design.
Mutated versions of the KRAS gene are found in many human tumours, most of which are aggressive and respond poorly to standard therapies. Cancerous cells containing mutated KRAS depend on a key component of the NF-kappaB signalling pathway, the enzyme TBK1, William Hahn and colleagues show. Suppressing TBK1 causes these cells to die in a tissue culture model.
Tyler Jacks and colleagues demonstrate that NF-kappaB signalling is actively involved in the development and maintenance of lung tumours in mice carrying mutated Kras and lacking the tumour suppressor protein p53. Together, the studies suggest that drugs that inhibit NF-kappaB or TBK1 could prove useful targeted therapies for the treatment of cancer patients with defined Kras mutations.
William Hahn (Dana-Farber Cancer Institute, Boston, MA, USA) Author paper 
Tyler Jacks (Massachusetts Institute of Technology, Cambridge, MA, USA) Author paper 
(C) Nature press release.
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