A study published in Cancer Cell by researchers of the Molecular Oncology Program at the Spanish National Cancer Research Centre (CNIO) shows how the elimination of the c-Raf kinase by genetic manipulation causes the regression of Kras oncogene-driven advanced lung tumours in a genetically designed mouse model that faithfully reproduces the natural history of this tumour. It has also been shown that the elimination of the c-Raf protein produces very tolerable toxic effects. This opens a new possibility for the development of therapies against tumours for which there are still no selective medicines and which therefore must be treated with cytotoxic drugs, that, as it is known, are not effective and produce abundant side effects.
One in four human solid tumours harbours mutations in KRAS, some, such as adenocarcinomas of the pancreas, lung and colon with very poor prognosis. The alteration of this gene directly and indirectly affects cell proliferation and differentiation through the activation of multiple signalling pathways, key phenomena in tumour development. However, there are no approved compounds in the clinic that selectively attack these pathways present in these carcinomas.
Blocking these oncogenic signalling pathways without affecting normal homeostasis is “one of the greatest challenges of precision
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