Evidence map›Paper›PMID 26657081›Full record

ArticleMolecular & cellular proteomics : MCP2016

Systematic Prioritization of Druggable Mutations in ∼5000 Genomes Across 16 Cancer Types Using a Structural Genomics-based Approach.

Junfei Zhao, Feixiong Cheng, Yuanyuan Wang, Carlos L Arteaga, Zhongming Zhao

Open access · hybridAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Drug repositioning: A bibliometric analysis.Frontiers in pharmacology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Junfei ZhaoFrom the ‡Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203;
Feixiong ChengFrom the ‡Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203;
Yuanyuan WangFrom the ‡Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203;
Carlos L Arteaga§Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; ¶Breast Cancer Program, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; ‖Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232;
Zhongming ZhaoFrom the ‡Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203; ‖Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; **Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; ¶¶School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, Texas 77030 zhongming.zhao@vanderbilt.edu.
Vanderbilt University · USBreast Cancer Research Foundation · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
Understanding and Controlling p120 Dysfunction in CRCP50CA095103 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI COFFEY, ROBERT J. · 2002 to 2017
$33.6M
Mapping the Genetic Architecture of Complex Disease via RNA-seq and GWAS DataR01LM011177 · NLM · VANDERBILT UNIVERSITY · PI WANG, LILY, ZHAO, ZHONGMING · 2012 to 2014
$1.0M
NCI NIH HHS P30 CA068485NCI NIH HHS P30CA068485NCI NIH HHS P50 CA095103NCI NIH HHS P50CA095103NCI NIH HHS P50 CA098131NCI NIH HHS P50CA098131NLM NIH HHS R01 LM011177NLM NIH HHS R01LM011177
6 · The paper itself

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

GenomicsBayes TheoremComputational BiologyGene Expression Regulation, NeoplasticGenome, HumanHumansMutation, MissenseNeoplasms

Identifiers

PMID26657081
PMCPMC4739678
OpenAlexW2195653324

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.