Gene expression profiling of multiple histone deacetylase (HDAC) inhibitors: defining a common gene set produced by HDAC inhibition in T24 and MDA carcinoma cell lines.
- K. Glaser, M. Staver, J. Waring, J. Stender, R. Ulrich, S. Davidsen
- Biology, ChemistryMolecular Cancer Therapeutics
- 1 February 2003
Researchers studied the gene expression profiles of T24 bladder and MDA breast carcinoma cells treated with three HDAC inhibitors to understand the genomic effects of HDAC inhibition on gene transcription, which may be responsible for antitumor effects.
The odyssey of marine pharmaceuticals: a current pipeline perspective.
- A. Mayer, K. Glaser, D. Shuster
- BiologyTIPS - Trends in Pharmacological Sciences
- 1 June 2010
HDAC inhibitors: clinical update and mechanism-based potential.
- K. Glaser
- BiologyBiochemical Pharmacology
- 1 September 2007
Preclinical activity of ABT-869, a multitargeted receptor tyrosine kinase inhibitor
- D. Albert, P. Tapang, S. Davidsen
- Biology, MedicineMolecular Cancer Therapeutics
- 1 May 2005
In tumor growth studies, ABT-869 exhibits efficacy in human fibrosarcoma and breast, colon, and small cell lung carcinoma xenograft models and is also effective in orthotopic breast and glioma models.
Enhanced activation of STAT pathways and overexpression of survivin confer resistance to FLT3 inhibitors and could be therapeutic targets in AML.
- Jianbiao Zhou, C. Bi, C. Chen
- 16 November 2007
Results demonstrate that enhanced activation ofSTAT pathways and overexpression of survivin are important mechanisms of resistance to ABT-869, suggesting that the STAT pathways and survivin could be potential targets for reducing resistance developed in patients receiving FLT3 inhibitors.
ABT-869, a multitargeted receptor tyrosine kinase inhibitor: inhibition of FLT3 phosphorylation and signaling in acute myeloid leukemia.
- D. Shankar, Junling Li, K. Glaser
- 15 April 2007
In tumors, ABT-869 inhibited FLT3 phosphorylation, induced apoptosis (transferase-mediated dUTP nick-end labeling [TUNEL]) and decreased proliferation (Ki67).
1-Benzyl-3-cetyl-2-methylimidazolium iodide (NH125) Induces Phosphorylation of Eukaryotic Elongation Factor-2 (eEF2)
- Zehan Chen, S. Gopalakrishnan, K. Glaser
- Biology, ChemistryJournal of Biological Chemistry
- 21 October 2011
NH125-induced peEF2 corrects a misconception and provides an opportunity for a new multipathway approach to anticancer therapies, as it was reported to correlate with inhibition of cancer cell growth.
Etodolac selectively inhibits human prostaglandin G/H synthase 2 (PGHS-2) versus human PGHS-1.
- K. Glaser, M. Sung, B. Weichman
- Medicine, BiologyEuropean Journal of Pharmacology
- 25 July 1995
Role of class I and class II histone deacetylases in carcinoma cells using siRNA.
- K. Glaser, Junling Li, M. Staver, R. Wei, D. Albert, S. Davidsen
- Biology, ChemistryBiochemical and Biophysical Research…
- 17 October 2003
Fluorescence assay of SIRT protein deacetylases using an acetylated peptide substrate and a secondary trypsin reaction.
- P. Marcotte, P. Richardson, K. Glaser
- Biology, ChemistryAnalytical Biochemistry
- 1 September 2004