Research Topics
| Vita M GolubovskayaSummaryAffiliation: Roswell Park Cancer Institute Country: USA Publications
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Detail Information
Publications
Focal adhesion kinase as a cancer therapy targetVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Anticancer Agents Med Chem 10:735-41. 2010..This review summarizes expression of FAK by immunohistochemical staining in different tumor types and presents several FAK inhibition therapy approaches...- FAK and Nanog Cross Talk with p53 in Cancer Stem CellsVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY, 14263, USA
Anticancer Agents Med Chem 13:576-80. 2013..The cross-linked signaling of FAK with p53 and Nanog signaling in cancer stem cell and function and targeted therapeutics approaches are discussed... - Mitoxantrone Targets the ATP-binding Site of FAK, Binds the FAK Kinase Domain and Decreases FAK, Pyk-2, c-Src, and IGF-1R In Vitro Kinase ActivitiesVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Anticancer Agents Med Chem 13:546-54. 2013..Thus, this novel function of the mitoxantrone drug can be critical for future development of anti-cancer agents and FAK-targeted therapy research... - A Small-molecule Inhibitor, 5'-O-Tritylthymidine, Targets FAK and Mdm-2 Interaction, and Blocks Breast and Colon Tumorigenesis in vivoVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Anticancer Agents Med Chem 13:532-45. 2013.... - A small molecule focal adhesion kinase (FAK) inhibitor, targeting Y397 site: 1-(2-hydroxyethyl)-3, 5, 7-triaza-1-azoniatricyclo [3.3.1.1(3,7)]decane; bromide effectively inhibits FAK autophosphorylation activity and decreases cancer cell viability, clonogVita M Golubovskaya
Department of Surgical Oncology, Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Carcinogenesis 33:1004-13. 2012..Thus, targeting the major autophosphorylation site of FAK with Y11 inhibitor is critical for development of cancer therapeutics and carcinogenesis field... - FAK overexpression and p53 mutations are highly correlated in human breast cancerVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Int J Cancer 125:1735-8. 2009..5, 95% CI 1.6-3.9]. This is the first analysis demonstrating a high correlation between FAK expression and p53 mutations in a population-based series of breast tumors... - FAK and p53 protein interactionsVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
Anticancer Agents Med Chem 11:617-9. 2011.... - Focal adhesion kinase and p53 signal transduction pathways in cancerVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Front Biosci 15:901-12. 2010..found that N-myc binds FAK promoter and induces FAK transcription in neuroblastoma cells. Thus, this review will be focused on FAK and p53 signal transduction pathways in cancer... - The direct effect of focal adhesion kinase (FAK), dominant-negative FAK, FAK-CD and FAK siRNA on gene expression and human MCF-7 breast cancer cell tumorigenesisVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY, USA
BMC Cancer 9:280. 2009..Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in survival signaling. FAK has been shown to be overexpressed in breast cancer tumors at early stages of tumorigenesis... 
A novel small molecule inhibitor of FAK decreases growth of human pancreatic cancerSteven N Hochwald
Department of Surgery, Roswell Park Cancer Institute, Buffalo, NY, USA
Cell Cycle 8:2435-43. 2009..Thus, targeting the Y397 site of FAK in pancreatic cancer with the small molecule inhibitor, 1,2,4,5-Benzenetetraamine tetrahydrochloride, is a potentially effective treatment strategy in this deadly disease...- Vascular endothelial growth factor receptor-3 promotes breast cancer cell proliferation, motility and survival in vitro and tumor formation in vivoElena V Kurenova
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
Cell Cycle 8:2266-80. 2009..For the first time, we have demonstrated that VEGFR-3 overexpression promotes breast cancer cell proliferation, motility, survival, anchorage-independent growth and tumorogenicity in the absence of ligand expression... - Nanog increases focal adhesion kinase (FAK) promoter activity and expression and directly binds to FAK protein to be phosphorylatedBaotran Ho
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA
J Biol Chem 287:18656-73. 2012.... - Pharmacologic blockade of FAK autophosphorylation decreases human glioblastoma tumor growth and synergizes with temozolomideVita M Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA
Mol Cancer Ther 12:162-72. 2013.... - Inhibition of hyaluronan synthase-3 decreases subcutaneous colon cancer growth by increasing apoptosisBrian P Teng
Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263 USA
Anticancer Agents Med Chem 11:620-8. 2011..HAS3 inhibition decreases subcutaneous tumor growth by colon cancer cells and significantly increases apoptosis with less effect on proliferation. These data show that HAS3 and HA mediate colon cancer growth by inhibiting apoptosis... - Evolving therapies and FAK inhibitors for the treatment of cancerKelli Bullard Dunn
Roswell Park Cancer Institute, University at Buffalo, State University of New York, NY, USA
Anticancer Agents Med Chem 10:722-34. 2010..This review summarizes the history and current use of targeted molecular therapy for cancer, with a special emphasis on recently developed inhibitors of Focal Adhesion Kinase (FAK)...