الفهرس 
Introduction
Management of Pancreatic cancerOnly 14 pages are availabe for public view
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Abstract
In this dissertation, we demonstrated that PSC-mediated ß1-Integrin radiation-protection occurs through FAK-AKT activation. FAK is a prognostic factor with impairment of local control and survival in patients with alterations of PTK2. FAK-tyrosine kinase domain Y397 inhibition would block the downstream singling AKT and inhibit the anti-apoptosis signals after radiation in vitro, it blocks DNA-repair and induces cell cycle arrest in the radio-sensitive G2 phase. FAK-inhibition in PSCs contributes also in radiation-modulation by inhibiting the ECM production. The effect of FAK inhibition was even stronger and obvious as expected in tumor spheroids. FAK is essential in radiation-resistance of PDAC through two mechanisms: In cancer cells, propagates the survival signals from ß1-Integrin and other growth factors to the nucleus through PI3K-AKT.