title: Disrupting the scaffold to improve focal adhesion kinase-targeted cancer therapeutics.
abstract: Focal adhesion kinase (FAK) is emerging as a promising cancer target because it is highly expressed at both the transcriptional and translational level in cancer and is involved in many aspects of tumor growth, invasion, and metastasis. Existing FAK-based therapeutics focus on inhibiting the kinase's catalytic function and not the large scaffold it creates that includes many oncogenic receptor tyrosine kinases and tumor suppressor proteins. Targeting the FAK scaffold is a feasible and promising approach for developing highly specific therapeutics that disrupt FAK signaling pathways in cancer.
authors.affiliation: Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
authors.forename: William G
authors.initials: WG
authors.lastname: Cance
authors.forename: Elena
authors.initials: E
authors.lastname: Kurenova
authors.forename: Timothy
authors.initials: T
authors.lastname: Marlowe
authors.forename: Vita
authors.initials: V
authors.lastname: Golubovskaya
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D016503:Drug Delivery Systems / Q000379:methods*; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism*; D011485:Protein Binding / Q000187:drug effects*; D017434:Protein Structure, Tertiary
chemical_list: D000970:Antineoplastic Agents; D051416:Focal Adhesion Protein-Tyrosine Kinases