Phosphorylations of serines 21/9 in glycogen synthase kinase 3α/β are dispensable for V600EBRAF-driven premalignant tumour development in the mouse intestine.

Abstract excerpt

Valine to glutamate substitution at residue 600 of the BRAF oncogene (V600EBRAF mutation) is prevalent in human colorectal cancers with a serrated histopathology and is thought to be a founder mutation. Using a conditional knock-in mouse model we have previously demonstrated that V600EBraf drives crypt hyperplasia in the short term as well as shortened survival linked to increased tumour burden in the long-term....

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