oa Editorial [Hot Topic : Targeting Focal Ahhesion Kinase in Cancer-Part I (Guest Editor: Vita M. Golubovskaya)]

I would like to thank you all authors for their excellent contribution to the Focal Kinase Adhesion issue. I would like to thank the journal editorial staff for their professional help in preparation of the issue. Focal Adhesion Kinase (FAK) is a 125 kDa protein that is localized at the focal adhesions. It plays a significant role in motility, adhesion, survival, proliferation, metastasis, angiogenesis and lymphangiogenesis. FAK has three domains: N-terminal with y397 autophosphorylation site, Kinase domain with ATP binding site and Y576/Y577 tyrosines, critical for protein activation and kinase function and also C-terminal domain with Y925 tyrosine and others sites, including many focal adhesion protein binding sites, such as paxillin, Grb-2, talin. Focal Adhesion Kinase is overexpressed in many types of tumors and recently has been proposed to be a therapeutic target. The authors summarize most of the known, published inhibitors of FAK that have been used in different cancer types. This issue contains several reviews that are focused on the role of FAK in different types of cancers. The review of Dr. Vita Golubovskaya summarizes data on expression of FAK in different tumor types and highlights different inhibitors of FAK. It includes data on immunohistochemical staining of FAK in different types of tumors and correlation with the patient prognostic factors. The review of Dr. Deniz A. Ucar and Steven N. Hochwald describes FAK expression and its role in pancreatic cancer. The authors describe association of FAK and IGFR-1 and extracellular matrix in pancreatic cancer. The authors show the data on the effect of FAK inhibitors on pancreatic cancer. The review of Dr. Gillory and Beierle is focused on the role of Focal Adhesion Kinase in neuroblastoma. It shows that inhibition of FAK can be a novel therapeutic approach in neuroblastoma. The authors demonstrate the effective inhibition of neuroblastoma cell growth with Y15 autophosphorylation inhibitor in contrast to the normal cells. The authors show the link of FAK and VEGFR signaling in neurobalstoma cells and demonstrate the anti-tumor effect of the inhibitor targeting FAK and VEGFR signaling. The review of Dr. Ko et al. “Focal Adhesion Kinase as a therapeutic Target of bortezomib” is focused on the novel effect of bortezomib on Focal Adhesion expression. The authors have excellent data on transcriptional repression of FAK by bortezomib through inhibiting NFkappaB binding to the FAK promoter. The authors suggest a potential targeting of FAK with bortezomib as a strategy to prevent tumor growth and metastasis. The review of Dr. Bullard Dunn et al. summarizes different therapeutic approaches in surgical oncology. The authors describe different cell cycle inhibitors, inducers of apoptosis, angiogenesis and FAK inhibitors and present mechanism and rational of using these inhibitors. The authors describe novel FAK inhibitors that are tested or presently evaluated in the ongoing clinical trials (http://www.clinicaltrials.gov/). In conclusion, these reviews summarize the importance of FAK in cancer cell survival and present evidence on the FAK as a therapeutic target. Future, clinical studies and clinical trials will present more data on FAK inhibitors as a first step for its clinical use. I would like to thank again all authors who contributed to this issue.