Katherine R. Singleton
Duke University
22 Papers
84 Citations
Katherine R. Singleton is an academic researcher from Duke University. The author has contributed to research in topics: Epidermal growth factor receptor & Biology. The author has an hindex of 10, co-authored 18 publications. Previous affiliations of Katherine R. Singleton include Anschutz Medical Campus & University of Colorado Boulder.
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Papers
Systematic identification of signaling pathways with potential to confer anticancer drug resistance.
Colin A. Martz,Kathleen A. Ottina,Katherine R. Singleton,J. Jasper,Suzanne E. Wardell,Ashley Peraza-Penton,Grace R. Anderson,Peter S. Winter,Timothy C. Wang,Timothy C. Wang,Holly M. Alley,Lawrence N. Kwong,Zachary A. Cooper,Michael T. Tetzlaff,Pei Ling Chen,Jeffrey C. Rathmell,Keith T. Flaherty,Jennifer A. Wargo,Donald P. McDonnell,David M. Sabatini,David M. Sabatini,Kris C. Wood +21 more
TL;DR: In this article, a library of barcoded pathway-activating mutant complementary DNAs was used to identify those that enhanced the survival of cancer cells in the presence of 13 clinically relevant, targeted therapies.
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Fibroblast Growth Factor Receptors Are Components of Autocrine Signaling Networks in Head and Neck Squamous Cell Carcinoma Cells
Marianne E. Marshall,Trista K. Hinz,Scott A. Kono,Katherine R. Singleton,Brady Bichon,Kathryn E. Ware,Lindsay Marek,Barbara Frederick,David Raben,Lynn E. Heasley +9 more
TL;DR: The HNSCC cell lines can be divided into subsets defined by sensitivity to EGFR and FGFR-specific TKIs, andFGFR inhibitors may represent novel therapeutics to deploy alone or in combination with EGFR inhibitors in H NSCC.
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Kinome RNAi Screens Reveal Synergistic Targeting of MTOR and FGFR1 Pathways for Treatment of Lung Cancer and HNSCC
Katherine R. Singleton,Trista K. Hinz,Emily K. Kleczko,Lindsay Marek,Jeff W. Kwak,Taylor Harp,Jihye Kim,Aik Choon Tan,Lynn E. Heasley +8 more
TL;DR: Findings support the existence of a signaling network wherein FGFR1-driven ERK and activated MTOR/AKT represent distinct arms required to induce full transformation and suggest that clinical efficacy of treatments for FGFR 1-driven lung cancers and HNSCC may be achieved by combining MTOR inhibitors and FGFR-specific TKIs.
A receptor tyrosine kinase network composed of fibroblast growth factor receptors, epidermal growth factor receptor, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, and hepatocyte growth factor receptor drives growth and survival of head and neck squamous carcinoma cell lines.
Katherine R. Singleton,Jihye Kim,Trista K. Hinz,Lindsay Marek,Matias Casás-Selves,Clark Hatheway,Aik Choon Tan,James DeGregori,Lynn E. Heasley +8 more
TL;DR: A whole-genome loss-of-function screen to identify genes whose knockdown potentiated the inhibitory effect of the FGFR inhibitor, AZ8010, found that multiple alternate receptors provided protection from FGFR inhibition, including receptor tyrosine kinases (RTKs), v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2), and hepatocyte growth factor receptor (MET).
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Elevated extracellular K+ inhibits apoptosis of corneal epithelial cells exposed to UV-B radiation
Katherine R. Singleton,David S. Will,Mark P. Schotanus,L. Haarsma,Leah R. Koetje,Susan L. Bardolph,John L. Ubels,John L. Ubels +7 more
TL;DR: In this article, the authors showed that the relatively high [K + ] o of tears, 20−25mM, serves to protect corneal epithelial cells from going into apoptosis after exposure to ambient UV-B radiation.
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