ArticleMolecular systems biology2018
Systematic characterization of pan-cancer mutation clusters.
Article in Molecular systems biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Global profiling of protein complex dynamics with an experimental library of protein interaction markers.Nature biotechnology · 2025Article
- Comprehensive Analysis of Human Colorectal Cancers Harboring Polymerase Epsilon Mutations.International journal of molecular sciences · 2025Article
- A series of reviews in familial cancer: genetic cancer risk in context variants of uncertain significance in MMR genes: which procedures should be followed?Familial cancer · 2025Review
- Neurogenic locus notch homolog protein 1 (NOTCH 1) SNP informatics coupled with intrinsically disordered regions and post-translational modifications reveals the complex structural crosstalk of Lung Adenocarcinoma (LUAD).Frontiers in bioinformatics · 2025Article
- Protein structural context of cancer mutations reveals molecular mechanisms and candidate driver genes.Cell reports · 2024Article
- Integrating Clinical Cancer and PTM Proteomics Data Identifies a Mechanism of ACK1 Kinase Activation.Molecular cancer research : MCR · 2024Article
- Quantitative proteomics and phosphoproteomics of urinary extracellular vesicles define putative diagnostic biosignatures for Parkinson's disease.Communications medicine · 2023Article
- Predicting the effects of rare genetic variants on oncogenic signaling pathways: A computational analysis of HRAS protein function.Frontiers in chemistry · 2023Article
- Analysis of missense variants in the human genome reveals widespread gene-specific clustering and improves prediction of pathogenicity.American journal of human genetics · 2022Article
- Known allosteric proteins have central roles in genetic disease.PLoS computational biology · 2022Article
- The role of BCL-2 family proteins in regulating apoptosis and cancer therapy.Frontiers in oncology · 2022Review
- The landscape and driver potential of site-specific hotspots across cancer genomes.NPJ genomic medicine · 2021Article
- Mutations of Intrinsically Disordered Protein Regions Can Drive Cancer but Lack Therapeutic Strategies.Biomolecules · 2021Article
- Mass spectrometry-based protein-protein interaction networks for the study of human diseases.Molecular systems biology · 2021Review
- Article
- Identification of new driver and passenger mutations within APOBEC-induced hotspot mutations in bladder cancer.Genome medicine · 2020Article
- Sphingosine kinase 1 contributes to doxorubicin resistance and glycolysis in osteosarcoma.Molecular medicine reports · 2020Article
- Kinase Interaction Network Expands Functional and Disease Roles of Human Kinases.Molecular cell · 2020Article
- Multi-layered proteomic analyses decode compositional and functional effects of cancer mutations on kinase complexes.Nature communications · 2020Article
- Genotype-phenotype analysis of LMNA-related diseases predicts phenotype-selective alterations in lamin phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cancer genome sequencing has shown that driver genes can often be distinguished not only by the elevated mutation frequency but also by specific nucleotide positions that accumulate changes at a high rate. However, properties associated with a residue's potential to drive tumorigenesis when mutated have not yet been systematically investigated. Here, using a novel methodological approach, we identify and characterize a compendium of 180 hotspot residues within 160 human proteins which occur with a significant frequency and are likely to have functionally relevant impact. We find that such mutations (i) are more prominent in proteins that can exist in the on and off state, (ii) reflect the identity of a tumor of origin, and (iii) often localize within interfaces which mediate interactions with other proteins or ligands. Following, we further examine structural data for human protein complexes and identify a number of additional protein interfaces that accumulate cancer mutations at a high rate. Jointly, these analyses suggest that disruption and dysregulation of protein interactions can be instrumental in switching functions of cancer proteins and activating downstream changes.
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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.