Does focal overexpression of CEACAM6 contribute to enhanced tumourigenesis in head and neck cancer via suppression of apoptosis?
We report that CEACAM6 is focally overexpressed in a large fraction of human HNSCCs in situ. We also show that over-expression of CEACAM6 increases tumour growth and tumour initiating activity by suppressing PI3K/AKT-dependent apoptosis of HNSCC in a xenotransplant model of HNSCC. Finally, our studies indicate that foci of CEACAM6 expressing cells are selectively ablated by treatment of xenotransplant tumours with pharmacological inhibitors of PI3K/AKT in vivo.
Postoperative immobilization supports recovery of biomechanical properties after shrinkage. Despite immobilization, biomechanical properties of shrunken tissue did not completely reach levels of normal tissue.