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Guinney, J.

Publications and source records attributed to Guinney, J..

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Probing the chemical-biological relationship space with the Drug Target Explorer

Modern phenotypic high-throughput screens (HTS) present several challenges including identifying the target(s) that mediate the effect seen in the screen, characterizing hits with a polypharmacologic target profile, and contextualizing screen data within the large potential space of drugs and biological screening model combinations. To address these challenges, we developed an interactive web application that enables exploration of the chemical-biological interaction space. Compound-target interaction data from public resources were quantified for over 280,000 molecules. Each molecule was annotated with a name and chemical structure, and every target was annotated with gene identifiers. The Drug-Target Explorer allows users to query molecules within this database of experimentally-derived and curated compound-target interactions and identify structurally similar molecules. It also enables network-based visualizations of the compound-target interaction space, and incorporates comparisons to publicly-available in vitro HTS datasets. Users can also identify compounds given one or more targets of interest. The Drug Target Explorer is a multifunctional platform for exploring chemical space as it relates to biological targets, and may be useful at several steps along the drug development pipeline including target discovery, structure-activity relationship, and lead compound identification studies.

pharmacology and toxicology

Combining accurate tumour genome simulation with crowd sourcing to benchmark somatic structural variant detection

BackgroundThe phenotypes of cancer cells are driven in part by somatic structural variants. Structural variants can initiate tumors, enhance their aggressiveness and provide unique therapeutic opportunities. Whole-genome sequencing of tumors can allow exhaustive identification of the specific structural variants present in an individual cancer, facilitating both clinical diagnostics and the discovery of novel mutagenic mechanisms. A plethora of somatic structural variant detection algorithms have been created to enable these discoveries, however there are no systematic benchmarks of them. Rigorous performance evaluation of somatic structural variant detection methods has been challenged by the lack of gold-standards, extensive resource requirements and difficulties arising from the need to share personal genomic information.\n\nResultsTo facilitate structural variant detection algorithm evaluations, we create a robust simulation framework for somatic structural variants by extending the BAMSurgeon algorithm. We then organize and enable a crowd-sourced benchmarking within the ICGC-TCGA DREAM Somatic Mutation Calling Challenge (SMC-DNA). We report here the results of structural variant benchmarking on three different tumors, comprising 204 submissions from 15 teams. In addition to ranking methods, we identify characteristic error-profiles of individual algorithms and general trends across them. Surprisingly, we find that ensembles of analysis pipelines do not always outperform the best individual method, indicating a need for new ways to aggregate somatic structural variant detection approaches.\n\nConclusionsThe synthetic tumors and somatic structural variant detection leaderboards remain available as a community benchmarking resource, and BAMSurgeon is available at https://github.com/adamewing/bamsurgeon.

bioinformatics

Community assessment of cancer drug combination screens identifies strategies for synergy prediction

The effectiveness of most cancer targeted therapies is short lived since tumors evolve and develop resistance. Combinations of drugs offer the potential to overcome resistance, however the number of possible combinations is vast necessitating data-driven approaches to find optimal treatments tailored to a patients tumor. AstraZeneca carried out 11,576 experiments on 910 drug combinations across 85 cancer cell lines, recapitulating in vivo response profiles. These data, the largest openly available screen, were hosted by DREAM alongside deep molecular characterization from the Sanger Institute for a Challenge to computationally predict synergistic drug pairs and associated biomarkers. 160 teams participated to provide the most comprehensive methodological development and subsequent benchmarking to date. Winning methods incorporated prior knowledge of putative drug target interactions. For >60% of drug combinations synergy was reproducibly predicted with an accuracy matching biological replicate experiments, however 20% of drug combinations were poorly predicted by all methods. Genomic rationale for synergy predictions were identified, including antagonism unique to combined PIK3CB/D inhibition with the ADAM17 inhibitor where synergy is seen with other PI3K pathway inhibitors. All data, methods and code are freely available as a resource to the community.

bioinformatics

Genomic determinants of protein abundance variation in colorectal cancer cells

Assessing the extent to which genomic alterations compromise the integrity of the proteome is fundamental in identifying the mechanisms that shape cancer heterogeneity. We have used isobaric labelling and tribrid mass spectrometry to characterize the proteomic landscapes of 50 colorectal cancer cell lines and to decipher the relationships between genomic and proteomic variation. The robust quantification of 12,000 proteins and 27,000 phosphopeptides revealed how protein symbiosis translates to a co-variome which is subjected to a hierarchical order and exposes the collateral effects of somatic mutations on protein complexes. Targeted depletion of key chromatin modifiers confirmed the transmission of variation and the directionality as characteristics of protein interactions. Protein level variation was leveraged to build drug response predictive models towards a better understanding of pharmacoproteomic interactions in colorectal cancer. Overall, we provide a deep integrative view of the molecular structure underlying the variation of colorectal cancer cells.\n\nHighlightsO_LIThe cancer cell functional \"co-variome\" is a strong attribute of the proteome.\nC_LIO_LIMutations can have a direct impact on protein levels of chromatin modifiers.\nC_LIO_LITransmission of genomic variation is a characteristic of protein interactions.\nC_LIO_LIPharmacoproteomic models are strong predictors of response to DNA damaging agents.\nC_LI\n\nAbbreviations

systems biology

A community-based collaboration to build prediction models for short-term discontinuation of docetaxel in metastatic castration-resistant prostate cancer patients

BackgroundDocetaxel has a demonstrated survival benefit for metastatic castration-resistant prostate cancer (mCRPC). However, 10-20% of patients discontinue docetaxel prematurely because of toxicity-induced adverse events, and managing risk factors for toxicity remains an ongoing challenge for health care providers and patients. Prospective identification of high-risk patients for early discontinuation has the potential to assist clinical decision-making and can improve the design of more efficient clinical trials. In partnership with Project Data Sphere (PDS), a non-profit initiative facilitating clinical trial data-sharing, we designed an open-data, crowdsourced DREAM (Dialogue for Reverse Engineering Assessments and Methods) Challenge for developing models to predict early discontinuation of docetaxel\n\nMethodsData from the comparator arms of four phase III clinical trials in first-line mCRPC were obtained from PDS, including 476 patients treated with docetaxel and prednisone from the ASCENT2 trial, 598 patients treated with docetaxel, prednisone/prednisolone, and placebo in the VENICE trial, 526 patients treated with docetaxel, prednisone, and placebo in the MAINSAIL trial, and 528 patients treated with docetaxel and placebo in the ENTHUSE 33 trial. Early discontinuation was defined as treatment stoppage within three months due to adverse treatment effects. Over 150 clinical features including laboratory values, medical history, lesion measures, prior treatment, and demographic variables were curated and made freely available for model building for all four trials. The ASCENT2, VENICE, and MAINSAIL trial data sets formed the training set that also included patient discontinuation status. The ENTHUSE 33 trial, with patient discontinuation status hidden, was used as an independent validation set to evaluate model performance. Prediction performance was assessed using area under the precision-recall curve (AUPRC) and the Bayes factor was used to compare the performance between prediction models.\n\nResultsThe frequency of early discontinuation was similar between training (ASCENT2, VENICE, and MAINSAIL) and validation (ENTHUSE 33) sets, 12.3% versus 10.4% of docetaxel-treated patients, respectively. In total, 34 independent teams submitted predictions from 61 different models. AUPRC ranged from 0.088 to 0.178 across submissions with a random model performance of 0.104. Seven models with comparable AUPRC scores (Bayes factor [&le;]; 3) were observed to outperform all other models. A post-challenge analysis of risk predictions generated by these seven models revealed three distinct patient subgroups: patients consistently predicted to be at high-risk or low-risk for early discontinuation and those with discordant risk predictions. Early discontinuation events were two-times higher in the high-versus low-risk subgroup and baseline clinical features such as presence/absence of metastatic liver lesions, and prior treatment with analgesics and ACE inhibitors exhibited statistically significant differences between the high- and low-risk subgroups (adjusted P < 0.05). An ensemble-based model constructed from a post-Challenge community collaboration resulted in the best overall prediction performance (AUPRC = 0.230) and represented a marked improvement over any individual Challenge submission. A\n\nFindingsOur results demonstrate that routinely collected clinical features can be used to prospectively inform clinicians of mCRPC patients risk to discontinue docetaxel treatment early due to adverse events and to the best of our knowledge is the first to establish performance benchmarks in this area. This work also underscores the \"wisdom of crowds\" approach by demonstrating that improved prediction of patient outcomes is obtainable by combining methods across an extended community. These findings were made possible because data from separate trials were made publicly available and centrally compiled through PDS.

bioinformatics