ArticleMolecular & cellular proteomics : MCP2016
Systematic Prioritization of Druggable Mutations in ∼5000 Genomes Across 16 Cancer Types Using a Structural Genomics-based Approach.
Article in Molecular & cellular proteomics : MCP, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- SLAYER: a computational framework for identifying synthetic lethal interactions through integrated analysis of cancer dependencies.NAR genomics and bioinformatics · 2025Article
- Artificial Intelligence and Precision Medicine: A New Frontier for the Treatment of Brain Tumors.Life (Basel, Switzerland) · 2022Review
- Identifying candidate genes and drug targets for Alzheimer's disease by an integrative network approach using genetic and brain region-specific proteomic data.Human molecular genetics · 2022Article
- Drug repositioning: A bibliometric analysis.Frontiers in pharmacology · 2022Review
- Landscape of drug-resistance mutations in kinase regulatory hotspots.Briefings in bioinformatics · 2021Article
- My personal mutanome: a computational genomic medicine platform for searching network perturbing alleles linking genotype to phenotype.Genome biology · 2021Article
- KinaseMD: kinase mutations and drug response database.Nucleic acids research · 2021Article
- Computational methods for cancer driver discovery: A survey.Theranostics · 2021Review
- 3D spatial organization and network-guided comparison of mutation profiles in Glioblastoma reveals similarities across patients.PLoS computational biology · 2019Article
- Non-invasive analysis of tumor mutation profiles and druggable mutations by sequencing of cell free DNA of Chinese metastatic breast cancer patients.Thoracic cancer · 2019Article
- Review: Precision medicine and driver mutations: Computational methods, functional assays and conformational principles for interpreting cancer drivers.PLoS computational biology · 2019Review
- Personal Mutanomes Meet Modern Oncology Drug Discovery and Precision Health.Pharmacological reviews · 2019Review
- Integrative omics analyses broaden treatment targets in human cancer.Genome medicine · 2018Article
- SOX2-mediated inhibition of miR-223 contributes to STIM1 activation in phenylephrine-induced hypertrophic cardiomyocytes.Molecular and cellular biochemistry · 2018Article
- An integrative functional genomics framework for effective identification of novel regulatory variants in genome-phenome studies.Genome medicine · 2018Article
- Osmolyte Induced Tumorigenesis and Metastasis: Interactions With Intrinsically Disordered Proteins.Frontiers in oncology · 2018Article
- Breakthroughs in modern cancer therapy and elusive cardiotoxicity: Critical research-practice gaps, challenges, and insights.Medicinal research reviews · 2018Review
- Functional variomics and network perturbation: connecting genotype to phenotype in cancer.Nature reviews. Genetics · 2017Review
- Tissue-Specific Signaling Networks Rewired by Major Somatic Mutations in Human Cancer Revealed by Proteome-Wide Discovery.Cancer research · 2017Article
- Identification of driver modules in pan-cancer via coordinating coverage and exclusivity.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
A massive amount of somatic mutations has been cataloged in large-scale projects such as The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium projects. The majority of the somatic mutations found in tumor genomes are neutral 'passenger' rather than damaging "driver" mutations. Now, understanding their biological consequences and prioritizing them for druggable targets are urgently needed. Thanks to the rapid advances in structural genomics technologies (e.g. X-ray), large-scale protein structural data has now been made available, providing critical information for deciphering functional roles of mutations in cancer and prioritizing those alterations that may mediate drug binding at the atom resolution and, as such, be druggable targets. We hypothesized that mutations at protein-ligand binding-site residues are likely to be druggable targets. Thus, to prioritize druggable mutations, we developed SGDriver, a structural genomics-based method incorporating the somatic missense mutations into protein-ligand binding-site residues using a Bayes inference statistical framework. We applied SGDriver to 746,631 missense mutations observed in 4997 tumor-normal pairs across 16 cancer types from The Cancer Genome Atlas. SGDriver detected 14,471 potential druggable mutations in 2091 proteins (including 1,516 recurrently mutated proteins) across 3558 cancer genomes (71.2%), and further identified 298 proteins harboring mutations that were significantly enriched at protein-ligand binding-site residues (adjusted p value < 0.05). The identified proteins are significantly enriched in both oncoproteins and tumor suppressors. The follow-up drug-target network analysis suggested 98 known and 126 repurposed druggable anticancer targets (e.g. SPOP and NR3C1). Furthermore, our integrative analysis indicated that 13% of patients might benefit from current targeted therapy, and this -proportion would increase to 31% when considering drug repositioning. This study provides a testable strategy for prioritizing druggable mutations in precision cancer medicine.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.