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- W4361951576 abstract "<div>Abstract<p><b>Purpose:</b> Non–small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths worldwide due to the limited availability of effective therapeutic options. For instance, there are no effective strategies for NSCLCs that harbor mutant <i>KRAS</i>, the most commonly mutated oncogene in NSCLC. Thus, our purpose was to make progress toward the generation of a novel therapeutic strategy for NSCLC.</p><p><b>Experimental Design:</b> We characterized the effects of suppressing focal adhesion kinase (FAK) by RNA interference (RNAi), CRISPR/CAS9 gene editing or pharmacologic approaches in NSCLC cells and in tumor xenografts. In addition, we tested the effects of suppressing FAK in association with ionizing radiation (IR), a standard-of-care treatment modality.</p><p><b>Results:</b> FAK is a critical requirement of mutant <i>KRAS</i> NSCLC cells. With functional experiments, we also found that, in mutant KRAS NSCLC cells, FAK inhibition resulted in persistent DNA damage and susceptibility to exposure to IR. Accordingly, administration of IR to FAK-null tumor xenografts causes a profound antitumor effect <i>in vivo</i>.</p><p><b>Conclusions:</b> FAK is a novel regulator of DNA damage repair in mutant <i>KRAS</i> NSCLC and its pharmacologic inhibition leads to radiosensitizing effects that could be beneficial in cancer therapy. Our results provide a framework for the rationale clinical testing of FAK inhibitors in NSCLC patients. <i>Clin Cancer Res; 22(23); 5851–63. ©2016 AACR</i>.</p></div>" @default.
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- W4361951576 date "2023-03-31" @default.
- W4361951576 modified "2023-09-26" @default.
- W4361951576 title "Data from Focal Adhesion Kinase Regulates the DNA Damage Response and Its Inhibition Radiosensitizes Mutant <i>KRAS</i> Lung Cancer" @default.
- W4361951576 doi "https://doi.org/10.1158/1078-0432.c.6523946.v1" @default.
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