|1.||Wells, Alan: 2 articles (11/2012 - 01/2012)|
|2.||Rocco, Silvana A: 2 articles (01/2010 - 12/2009)|
|3.||Rittner, Roberto: 2 articles (01/2010 - 12/2009)|
|4.||Franchini, Kleber G: 2 articles (01/2010 - 12/2009)|
|5.||Wan, Yinsheng: 2 articles (08/2008 - 09/2005)|
|6.||Di, Wen: 2 articles (08/2008 - 09/2005)|
|7.||Grunt, Thomas W: 2 articles (11/2007 - 04/2005)|
|8.||Tomek, Katharina: 2 articles (11/2007 - 04/2005)|
|9.||Puckmair, Klaudia: 2 articles (11/2007 - 04/2005)|
|10.||Piché, Alain: 1 article (07/2015)|
01/01/2010 - "The aim of the present study was to evaluate the protective effects of the 4-anilinoquinazoline derivative PD153035 on cardiac ischemia/reperfusion and mitochondrial function. "
01/01/2010 - "Nanomolar doses of PD153035 strongly protect against heart and cardiomyocyte damage induced by ischemia/reperfusion and cyanide/aglycemia. "
01/15/2012 - "The anti-apoptotic effect is maintained in the presence of tyrosine kinase inhibitor genistein and the epidermal growth factor receptor inhibitor PD153035, but is suppressed by the PI3K inhibitor Ly294002 and the Akt inhibitor Akti-1/2.The unique PI3K regulatory subunit p55γ was upregulated by berberine during ischemia-reperfusion and was not blocked by these inhibitors. "
10/01/2013 - "The aim of this study was to investigate the in vivo metabolism of [(11)C]PD153035 to determine whether alterations in metabolite formation are accompanied by changes in biodistribution and tumor uptake. "
04/08/2007 - "In conclusion, this study demonstrated that both PD153035 and ANAPD inhibit tumor cell growth in HCC through inhibition of EGFR signaling pathway, and ANAPD is a more potent inhibitor than PD153035. "
10/01/2013 - "We suggest that the metabolism of [(11)C]PD153035 should be taken into consideration when this tracer is used to quantify EGFR expression, as our results indicated that the distribution of radioactivity to EGFR-overexpressing tumors was affected by the rate of metabolism and the route of administration."
10/01/2013 - "Local administration of [(11)C]PD153035 greatly increased radioactivity levels in the adjacent tumor compared with levels typically found after intravenous administration. "
04/01/2010 - "In vitro, F84 and PD153035 significantly inhibited the growth of four different human gynecologic cancer cell lines in a dose-dependent manner. "
05/01/2005 - "The purpose of this study is to evaluate the ability of the epidermal growth factor receptor tyrosine kinase inhibitor PD153035 to abrogate the expression of prometastasis phenotypes in malignant pleural mesothelioma cells in vitro. "
05/01/2005 - "Epidermal growth factor receptor tyrosine kinase inhibitor PD153035 significantly inhibited motility and invasion in malignant pleural mesothelioma cells in vitro, regardless of their epidermal growth factor receptor expression levels. "
05/01/2005 - "The selective epidermal growth factor receptor tyrosine kinase inhibitor PD153035 suppresses expression of prometastasis phenotypes in malignant pleural mesothelioma cells in vitro."
|4.||Prostatic Neoplasms (Prostate Cancer)
09/01/2010 - "(123)I-PD153035 was synthesized by a non-isotopic [(123)I]iodo-debromination of PD153035 in 50-60% radiochemical yield in a total synthesis time including HPLC separation of 70 min. In vitro (123)I-mAb425 and (123)I-PD153035 accumulated highly in human PC-3 and DU-145 prostate cancer cells. "
08/10/2003 - "Of particular interest, the combination of PD153035 and Rp-cAMPs also caused a more substantial apoptotic/necrotic death of these prostatic cancer cells as compared to drugs alone. "
08/10/2003 - "N-oleoylethanolamine (OE), an inhibitor of acidic ceramidase, consistently potentiated the apoptotic effects of PD153035 in all the prostatic cancer cell lines tested. "
01/01/2012 - "Similar results were obtained in DU-145 prostate cancer cells induced to re-express E-cadherin in hepatocyte coculture or following chemical induction by the GnRH agonist buserelin or the EGFR inhibitor PD153035. "
11/01/2012 - "We further found that epidermal growth factor (EGF) receptor up-regulates Kaiso at the RNA and protein levels in prostate cancer cell lines, but more interestingly causes a shift of cytoplasmic Kaiso to the nucleus that is reversed by the EGF receptor-specific kinase inhibitor, PD153035. "
04/22/2005 - "Western blotting, colorimetric in vitro cell proliferation assays, and reverse transcription-polymerase chain reaction demonstrated that the EGFR inhibitor PD153035 not only blocked activation of EGFR and inhibited cell growth, but also stimulated RAR-beta expression in MDA-MB-468 breast and OVCAR-3 ovarian carcinoma cells. "
04/01/2005 - "We used cDNA microarrays to examine alterations in gene expression after treatment of carcinoma cells with PD153035, a specific and reversible inhibitor of EGFR function. "
08/01/1998 - "Using the EGFR-overexpressing head and neck carcinoma cell line HN5, we have compared the biological consequences of treatment with an inhibitor of EGFR tyrosine kinase (PD153035) with anti-EGFR monoclonal antibodies (mAbs) ICR63 or ICR80. "
|1.||Epidermal Growth Factor Receptor (EGF Receptor)
|2.||Protein-Tyrosine Kinases (Tyrosine Kinase)
|3.||Epidermal Growth Factor (EGF)
|6.||2- (4- morpholinyl)- 8- phenyl- 4H- 1- benzopyran- 4- one
|7.||retinoic acid receptor beta
|9.||Cytochrome P-450 CYP3A
|10.||Protein Isoforms (Isoforms)
|1.||Heterologous Transplantation (Xenotransplantation)
|3.||Drug Therapy (Chemotherapy)