Gene expression patterns in mismatch repair-deficient colorectal cancers highlight the potential therapeutic role of inhibitors of the phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin pathway.

Publication Type:

Journal Article

Source:

Clinical cancer research : an official journal of the American Association for Cancer Research, Volume 15, Issue 8, p.2829-39 (2009)

Keywords:

2009, Algorithms, Antineoplastic Agents, Benzoquinones, cell cycle, Cell Line, Tumor, Chromones, Colorectal Neoplasms, Computational Biology, DNA Mismatch Repair, Drug Evaluation, Preclinical, Enzyme Inhibitors, Gene Expression Profiling, Humans, Hydroxamic Acids, Immunosuppressive Agents, Lactams, Macrocyclic, Microsatellite Instability, Morpholines, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Public Health Sciences Division, Shared Resources, Sirolimus

Abstract:

High-frequency microsatellite-instable (MSI-H) tumors account for approximately 15% of colorectal cancers. Therapeutic decisions for colorectal cancer are empirically based and currently do not emphasize molecular subclassification despite an increasing collection of gene expression information. Our objective was to identify low molecular weight compounds with preferential activity against MSI colorectal cancers using combined gene expression data sets.