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Christoph A. Ritter
Researcher at University of Greifswald
Publications - 79
Citations - 4733
Christoph A. Ritter is an academic researcher from University of Greifswald. The author has contributed to research in topics: Epidermal growth factor receptor & Growth factor receptor. The author has an hindex of 27, co-authored 76 publications receiving 4366 citations. Previous affiliations of Christoph A. Ritter include Vanderbilt University & Greifswald University Hospital.
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Journal Article
Herceptin-induced Inhibition of Phosphatidylinositol-3 Kinase and Akt Is Required for Antibody-mediated Effects on p27, Cyclin D1, and Antitumor Action
F. Michael Yakes,Wichai Chinratanalab,Christoph A. Ritter,Walter King,Steven A. Seelig,Carlos L. Arteaga +5 more
TL;DR: Data suggest that changes in cell cycle- and apoptosis-regulatory molecules after HER2 blockade with Herceptin result, at least in part, from the inhibition of Akt, and disabling PI3K and Akt is required for the antitumor effect of HER2 inhibitors.
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Blockade of TGF-β inhibits mammary tumor cell viability, migration, and metastases
Rebecca S. Muraoka,Nancy Dumont,Christoph A. Ritter,Teresa C. Dugger,Dana M. Brantley,Jin Chen,Evangeline Easterly,L. Renee Roebuck,Sarah Ryan,Philip Gotwals,Victor Koteliansky,Carlos L. Arteaga +11 more
TL;DR: Blockade of TGF-β signaling may reduce tumor cell viability and migratory potential and represents a testable therapeutic approach against metastatic carcinomas.
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Human breast cancer cells selected for resistance to trastuzumab in vivo overexpress epidermal growth factor receptor and ErbB ligands and remain dependent on the ErbB receptor network.
Christoph A. Ritter,Marianela Perez-Torres,Cammie Rinehart,Marta Guix,Teresa C. Dugger,Jeffrey A. Engelman,Carlos L. Arteaga +6 more
TL;DR: The results are consistent with the inability of trastuzumab to block the heterodimerization of HER2 and suggest that amplification of ligand-induced activation of ErbB receptors is a plausible mechanism of acquired resistance to trastzumab that should be investigated in primary mammary cancers.
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Loss of PTEN/MMAC1/TEP in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors.
Roberto Bianco,Incheol Shin,Christoph A. Ritter,F. Michael Yakes,Andrea D. Basso,Neal Rosen,Junji Tsurutani,Phillip A. Dennis,Gordon B. Mills,Carlos L. Arteaga +9 more
TL;DR: Combined blockade of the EGFR tyrosine kinase and Akt should be considered as a therapeutic approach in EGFR-expressing tumor cells with concomitant amplification(s) of PI3K-Akt signaling.
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The epidermal growth factor receptor–tyrosine kinase: A promising therapeutic target in solid tumors
TL;DR: ZD1839 (Iressa; AstraZeneca Pharmaceuticals LP, Wilmington, DE) is the EGFR-TK inhibitor furthest along in clinical development, and it is currently being investigated in a variety of solid tumors, including non-small-cell lung cancer.