Inconsistency in large pharmacogenomic studies
By Benjamin Haibe-Kains, N. El-Hachem, Nicolai J. Birkbak, Andrew C. Jin, Andrew H. Beck, Hugo J. W. L. Aerts, John Quackenbush. Nature, 2013
486 citations recorded by the source corpus.
Two large-scale pharmacogenomic studies were published recently in this journal. Genomic data are well correlated between studies; however, the measured drug response data are highly discordant. Although the source of inconsistencies remains uncertain, it has potential implications for using these outcome measures to assess gene–drug associations or select potential anticancer drugs on the basis of their reported results.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/eb9b5eda01c33051acc7ba3898782d71702f27dd
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Citations in the corpus
- Reproducibility in Science: Improving the Standard for Basic and Preclinical Research (2015, unknown): “standardization of the experimental assays and methods of analysis.(29)”
- Harnessing Connectivity in a Large-Scale Small-Molecule Sensitivity Dataset (2015, unknown): “For example, one report recently highlighted inconsistencies in drug-response measurements within and between two reported sensitivity profiling studies (10).”
- An open investigation of the reproducibility of cancer biology research (2014, unknown): “…of appropriate controls, lack of equipment calibration, or unrecognized experimental variables ( Ioannidis, 2005 ; Nieuwenhuis et al., 2011 ; Loscalzo, 2012 ; Haibe-Kains et al., 2013 ; Pusztai et al., 2013 ; Vasilevsky et al., 2013 ; Hines et al., 2014 ; Ioannidis et al., 2014 ; Perrin, 2014 ).”
- The harmonizome: a collection of processed datasets gathered to serve and mine knowledge about genes and proteins (2016, background): “Integration with the recently published cancer cell-line sensitivity data is an alternative (27,30, 31,134).”
- pRRophetic: An R Package for Prediction of Clinical Chemotherapeutic Response from Tumor Gene Expression Levels (2014, result): “These represent similar correlations to those observed when drug sensitivity was compared for cell lines that overlap both CGP and CCLE [4].”
- Large-scale integration of small molecule-induced genome-wide transcriptional responses, Kinome-wide binding affinities and cell-growth inhibition profiles reveal global trends characterizing systems-level drug action (2014, result): “It may therefore be the case that such results are in fact more robust in terms of reproducibility as oppose to comparing just two different assay methods or assay conditions, which can sometimes give considerably different outcomes (Haibe-Kains et al., 2013).”
- Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, unknown): “Whilst we acknowledge the limitations of cell lines and IC 50 as a drug assay (Haibe-Kains et al , 2013), we believe our results give a bird’s-eye view of EMT and drug resistance.”
- Drug-induced death signaling strategy rapidly predicts cancer response to chemotherapy (2015, unknown): “Moreover, it is likely that many tumors have unrecognized sensitivity to agents for which there is simply no useful predictive biomarker to inform therapy decisions (Garraway and Jä nne, 2012; Haibe-Kains et al., 2013).”