997 resultados para 10121102 TM-41


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Vorbesitzer: Bartholomaeusstift Frankfurt am Main;

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Vorbesitzer: Hartwin von Ergerßheim

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Vorbesitzer: Georg von Breidenbach; Dominikanerkloster Frankfurt am Main

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Vorbesitzer: Antonius Ediger; Elisabeth Ruprechtin; Anna Elisabetha Johannisin zu Leiselsheim; Johann Nicolaus Johannes

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Verlorener Brief an Stoltze, Der wahre Jakob, Bitte um Übertragung einiger Texte ins Frankfurterische,für eine "Comoedia politica", Hermann Presber

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Transliterationsvarianten: Mišne Tōrā. Mischne Tora.

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Vorbesitzer: Eduard Rüppell

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"Problem der neueren Philosophie", Vorlesung Wintersemester 1950/51 und Sommersemester 1951, 1) Heft, 78 Blatt und 20 zusätzliche Blätter, eigenhändige Notizen (GS 14, S. 145, 151-152), 2) Friedrich Pollock: Notizen zur Volesung Max Horkheimers, Wintersemester 1950/51), eigenhändige Notizen, 9 Blatt; "Philosophie im 17. Jahrhundert (insbes. Spinoza)", Vorlesung Winteremester 1951/52, 1) Heft 1, 17 Blatt und 2 zusätzliche Blätter, eigenhändige Notizen, 2) Heft 2, 46 Blatt, davon 3 leer, und 15 zusätzliche Blätter, eigenhändige Notizen; "Philosophie im 18. Jahrhundert", Vorlesung Sommersemester 1952, 1 Heft mit eigenhändigen Notizen, 64 Blatt, davon 30 leer, und 44 zusätzliche Blätter;

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46 Briefe zwischen Max Horkheimer und Frederick Wild; 1 Brief von Frederick Pollock an Leo Löwenthal, 22.04.1948; 5 Empfehlungsschreiben für Max Horkheimer von Frederick Pollock, 16. u. 17.04.1948; 1 Telegramm von Frederick Pollock an Max Horkheimer, 28.06.1943; 1 Brief an Max Horkheimer von Julius Schwietering, 18.02.1948; 10 Briefe zwischen der National City Bank of New York und Max Horkheimer, 1943-1944; 1 Brief von Frederick Wild an H. P. Edelman, 27.01.1944; 1 Brief von Hilda Kahn an Frederick Wild, 02.12.1943; 1 Brief von Frederick Wild an Jane Reinheimer, 30.11.1943;

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Vorbesitzer: Johann Nikolaus Rücker; Karl Konstanz Victor Rücker

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Trägerband: Ms. Barth. 29; Vorbesitzer: Bartholomaeusstift Frankfurt am Main

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Vorbesitzer: Johann Maximilian Zum Jungen

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The epidermal growth factor receptor (EGFR) and its ligands are overexpressed in many human tumors, including bladder and pancreas, correlating with a more aggressive tumor phenotype and poor patient prognosis. We initiated the present study to characterize the heterogeneity of gefitinib responsiveness in a panel of human bladder and pancreatic cancer cell lines in order to identify the biological characteristics of EGFR-dependent proliferation that could be used to prospectively identify drug-sensitive tumors. A second objective was to elucidate how to best exploit these results by utilizing gefitinib in combination therapy. To these ends, we examined the effects of the EGFR antagonist gefitinib on proliferation and apoptosis in a panel of 18 human bladder cancer cell lines and 9 human pancreatic cancer cell lines. Our data confirmed the existence of marked heterogeneity in Iressa responsiveness with less than half of the cell lines displaying significant growth inhibition by clinically relevant concentrations of the drug. Gefitinib responsiveness was found to be p27 kip1 dependent as DNA synthesis was restored following exposure to p27siRNA. Unfortunately, Iressa responsiveness was not closely linked to surface EGFR or TGF-α expression in the bladder cancer cells, however, cellular TGF-α expression correlated directly with Iressa sensitivity in the pancreatic cancer cell lines. These findings provide the potential for prospectively identifying patients with drug-sensitive tumors. ^ Further studies aimed at exploiting gefitinib-mediated cell cycle effects led us to investigate if gefitinib-mediated TRAIL sensitization correlated with increased p27kip1 accumulation. We observed that increased TRAIL sensitivity following gefitinib exposure was not dependent on p27 kip1 expression. Additional studies initiated to examine the role(s) of Akt and Erk signaling demonstrated that exposure to PI3K or MEK inhibitors significantly enhanced TRAIL-induced apoptosis at concentrations that block target phosphorylation. Furthermore, combinations of TRAIL and the PI3K or MEK inhibitors increased procaspase-8 processing above levels observed with TRAIL alone, indicating that the effects were exerted at the level of caspase-8 activation, considered the earliest step in the TRAIL pathway. ^