Discovery of Precision Oncology Drugs
NTRC provides fee-for-services to pharmaceutical and biotech companies and academic institutions worldwide. Oncolines™ is the most important service product of NTRC, consisting of the parallel profiling of drug candidates on a panel of 102 human cancer cell lines. The cancer cell lines are from diverse tumor tissue origin and have been characterized with regard to the mutation status of cancer genes and by gene expression analysis. Clients of NTRC order full panel profiling studies or cherry pick cell lines from the panel based on specific characteristics, such as tumor origin, gene mutations, or expression of certain cancer genes.
Identification of Patient Selection Markers
The drug sensitivity of the Oncolines™ cancer cell lines is determined in cell proliferation assays and correlated to the cancer gene mutation status of the cell lines. This yields novel candidate drug sensitivity biomarkers (Uitdehaag et al., 2019 and 2014) These biomarkers are used as selection markers for patient stratification (Zaman et al., 2017), while the drug sensitivity fingerprint of compounds in Oncolines™ is used for comparative analyses with other anti-cancer agents (Uitdehaag et al., 2016) and for mechanism-of-action studies (Libouban et al., 2017). The Oncolines™ cell lines are also the basis of drug combination screens (Uitdehaag et al, 2015).
Deliverables For You
We deliver reproducible results that are adapted to your specific needs with a short delivery time. Direct contacts between our staff and sponsors result in efficient scientific and technical support. We provide cost-free consultation on next steps in research if desired by the sponsor.
Uitdehaag et al. (2019) Combined cellular and biochemical profiling to identify predictive drug response biomarkers for kinase inhibitors approved for clinical use between 2013 and 2017, Molecular Cancer Therapeutics, 18 (2), 470-481.
Uitdehaag et al. (2014) Comparison of the cancer gene targeting and biochemical selectivities of all targeted kinase inhibitors approved for clinical use, PLOS ONE, 9 (3) e92146.
Zaman et al. (2017) TTK inhibitors as a targeted therapy for CTNNB1(β-catenin) mutant cancers, Molecular Cancer Therapeutics, 16 (11), 2609-2617.
Uitdehaag et al. (2016) Cell panel profiling reveals conserved therapeutic clusters and differentiates the mechanism of action of different PI3K/mTOR, Aurora kinase and EZH2 inhibitors, Molecular Cancer Therapeutics, 15 (12), 3097-3109.
Libouban et al. (2017) Stable aneuploid tumor cells are more sensitive to TTK inhibition than chromosomally unstable cell lines, Oncotarget 8 (24), 38309-38325.
Uitdehaag et al. (2015) Selective Targeting of CTNNB1-, KRAS- or MYC-Driven Cell Growth by Combinations of Existing Drugs, PLoS ONE, 10 (5): e0125021.