|1.||Christensen, James G: 9 articles (02/2011 - 11/2003)|
|2.||Medová, Michaela: 3 articles (02/2013 - 10/2010)|
|3.||Zimmer, Yitzhak: 3 articles (02/2013 - 10/2010)|
|4.||Al-Dayel, Fouad: 3 articles (01/2012 - 01/2011)|
|5.||Al-Kuraya, Khawla S: 3 articles (01/2012 - 01/2011)|
|6.||Ahmed, Maqbool: 3 articles (01/2012 - 01/2011)|
|7.||Uddin, Shahab: 3 articles (01/2012 - 01/2011)|
|8.||Hussain, Azhar R: 3 articles (01/2012 - 01/2011)|
|9.||Bavi, Prashant: 3 articles (01/2012 - 01/2011)|
|10.||You, Hanning: 2 articles (01/2015 - 09/2011)|
07/01/2013 - "Studies in vivo revealed that PHA665752 inhibited 3T3- RON160 and Du4475 cell-mediated tumor growth in mouse mammary fat pad. "
11/01/2003 - "In cellular studies, PHA-665752 potently inhibited HGF-stimulated and constitutive c-Met phosphorylation, as well as HGF and c-Met-driven phenotypes such as cell growth (proliferation and survival), cell motility, invasion, and/or morphology of a variety of tumor cells. "
09/01/2015 - "Tumor uptake of [99mTc]-Met peptide was significantly decreased as early as 1 week after PHA 665752 treatment, corresponding to decreases in tumor volumes. "
01/01/2015 - "We have previously demonstrated that treatment of MHCC97-H cells with a c-Met inhibitor, PHA665752, results in stasis of tumor growth in vivo. "
12/15/2013 - "Treatment of GEO-CR and SW48-CR cells with PHA665752, a selective MET inhibitor, inhibited cell growth, proliferation, and survival signals and impaired cancer cell migration. "
10/01/2012 - "In the present study, we analyzed the antitumor efficacy of EGFR inhibitors erlotinib and gefitinib and c-Met inhibitor PHA-665752, along with their respective small hairpin RNAs (shRNAs) alone or in combination with human umbilical cord blood stem cells (hUCBSCs), in glioma cell lines and in animal xenograft models. "
09/01/2010 - "Molecular predictors of sensitivity to the MET inhibitor PHA665752 in lung carcinoma cells."
09/01/2010 - "We examined the efficacy of the MET inhibitor PHA665752 in 41 cell lines of non-small lung carcinoma to determine whether sensitivity to the MET inhibitor is correlated with the (1) genetic statuses of MET, epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2, and KRAS, (2) MET phosphorylation and its downstream signaling pathways, or (3) epithelial-mesenchymal transition. "
02/01/2011 - "We utilized the highly sensitive gastric carcinoma cell line, SNU638, and two related MET inhibitors PHA-665752 and PF-2341066. "
01/01/2010 - "We examined the in vitro efficacy of targeting the MET receptor using the highly specific small molecule inhibitor PHA665752 as a novel treatment strategy in medulloblastoma. "
01/01/2010 - "MET inhibition using PHA665752 was effective at reducing the proliferative capacity of the D283, ONS76, and MED8A medulloblastoma cell lines as assessed by MTS assay. "
|5.||Lung Neoplasms (Lung Cancer)
02/01/2014 - "We used ALK fusion-positive and -negative lung cancer cell lines; crizotinib, PHA-665752, and saracatinib, and stable transfection with shMET. "
04/15/2007 - "A selective small molecule inhibitor of c-Met, PHA665752, inhibits tumorigenicity and angiogenesis in mouse lung cancer xenografts."
04/15/2007 - "These studies show the feasibility of selectively targeting c-Met with ATP competitive small molecule inhibitors and suggest that PHA665752 may provide a novel therapeutic approach to lung cancer."
01/01/2015 - "It worked synergistically with PHA665752 and SU11274, HGF receptor inhibitors on the lung cancer cells both on HGF receptor activation and on cell functions. "
|1.||erlotinib (CP 358,774)
|3.||Cyclooxygenase 2 (Cyclooxygenase-2)
|4.||Epidermal Growth Factor Receptor (EGF Receptor)
|6.||Adenosine Triphosphate (ATP)
|8.||Protein-Tyrosine Kinases (Tyrosine Kinase)
|9.||Proto-Oncogene Proteins c-met
|10.||Hepatocyte Growth Factor (Growth Factor, Hepatocyte)
|1.||Heterologous Transplantation (Xenotransplantation)
|2.||Drug Therapy (Chemotherapy)