Evidence map›Paper›PMID 35672401›Full record

ArticleCommunications biology2022

Somatic point mutations are enriched in non-coding RNAs with possible regulatory function in breast cancer.

Narges Rezaie, Masroor Bayati, Mehrab Hamidi, Maedeh Sadat Tahaei, Sadegh Khorasani, Nigel H Lovell, James Breen, Hamid R Rabiee, Hamid Alinejad-Rokny

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
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  4. Review
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

9 authors at 4 institutions in 3 countries.

Narges Rezaie *Center for Complex Biological Systems, University of California Irvine, Irvine, CA, 92697, USA.ORCID 0000-0001-9326-9954
Masroor Bayati *Bioinformatics and Computational Biology Lab, Department of Computer Engineering, Sharif University of Technology, Tehran, 11365, Iran.
Mehrab HamidiBioinformatics and Computational Biology Lab, Department of Computer Engineering, Sharif University of Technology, Tehran, 11365, Iran.
Maedeh Sadat TahaeiBioinformatics and Computational Biology Lab, Department of Computer Engineering, Sharif University of Technology, Tehran, 11365, Iran.
Sadegh KhorasaniBioinformatics and Computational Biology Lab, Department of Computer Engineering, Sharif University of Technology, Tehran, 11365, Iran.
Nigel H LovellTyree Institute of Health Engineering and The Graduate School of Biomedical Engineering, UNSW Sydney, Sydney, NSW, 2052, Australia.
James BreenSouth Australian Health & Medical Research Institute, Adelaide, SA, 5000, Australia.
Hamid R RabieeBioinformatics and Computational Biology Lab, Department of Computer Engineering, Sharif University of Technology, Tehran, 11365, Iran. rabiee@sharif.edu.ORCID 0000-0002-9835-4493
Hamid Alinejad-RoknyBioMedical Machine Learning Lab (BML), The Graduate School of Biomedical Engineering, UNSW Sydney, Sydney, NSW, 2052, Australia. h.alinejad@unsw.edu.au.ORCID 0000-0002-8999-7702
Sharif University of Technology · IRUNSW Sydney · AUSouth Australian Health and Medical Research Institute · AUUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-coding RNAs (ncRNAs) form a large portion of the mammalian genome. However, their biological functions are poorly characterized in cancers. In this study, using a newly developed tool, SomaGene, we analyze de novo somatic point mutations from the International Cancer Genome Consortium (ICGC) whole-genome sequencing data of 1,855 breast cancer samples. We identify 1030 candidates of ncRNAs that are significantly and explicitly mutated in breast cancer samples. By integrating data from the ENCODE regulatory features and FANTOM5 expression atlas, we show that the candidate ncRNAs significantly enrich active chromatin histone marks (1.9 times), CTCF binding sites (2.45 times), DNase accessibility (1.76 times), HMM predicted enhancers (2.26 times) and eQTL polymorphisms (1.77 times). Importantly, we show that the 1030 ncRNAs contain a much higher level (3.64 times) of breast cancer-associated genome-wide association (GWAS) single nucleotide polymorphisms (SNPs) than genome-wide expectation. Such enrichment has not been seen with GWAS SNPs from other cancers. Using breast cell line related Hi-C data, we then show that 82% of our candidate ncRNAs (1.9 times) significantly interact with the promoter of protein-coding genes, including previously known cancer-associated genes, suggesting the critical role of candidate ncRNA genes in the activation of essential regulators of development and differentiation in breast cancer. We provide an extensive web-based resource ( https://www.ihealthe.unsw.edu.au/research ) to communicate our results with the research community. Our list of breast cancer-specific ncRNA genes has the potential to provide a better understanding of the underlying genetic causes of breast cancer. Lastly, the tool developed in this study can be used to analyze somatic mutations in all cancers.

Indexed as

Breast NeoplasmsGenome-Wide Association StudyFemaleHumansPoint MutationPolymorphism, Single NucleotideRNA, UntranslatedRNA, Untranslated

Identifiers

PMID35672401
PMCPMC9174258
OpenAlexW4281613752

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.