Evidence map›Paper›PMID 31950163›Full record

ArticleNucleic acids research2020

Prevalence and architecture of posttranscriptionally impaired synonymous mutations in 8,320 genomes across 22 cancer types.

Huajing Teng, Wenqing Wei, Qinglan Li, Meiying Xue, Xiaohui Shi, Xianfeng Li, Fengbiao Mao, Zhongsheng Sun

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Nucleotide Substitution Biases in Related Cancer Driver Genes.International journal of molecular sciences · 2025
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  13. Pan-cancer analyses of synonymous mutations based on tissue-specific codon optimality.Computational and structural biotechnology journal · 2022
    Article
  14. Article
  15. Article
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  18. Genomic Variation Prediction: A Summary From Different Views.Frontiers in cell and developmental biology · 2021
    Review
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  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

8 authors at 2 institutions in 1 country.

Huajing TengBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Wenqing WeiBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Qinglan LiBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Meiying XueBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Xiaohui ShiSino-Danish college, University of Chinese Academy of Sciences, Beijing 100049, China.
Xianfeng LiBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Fengbiao MaoBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Zhongsheng SunBeijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China.
Chinese Academy of Sciences · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic synonymous mutations are one of the most frequent genetic variants occurring in the coding region of cancer genomes, while their contributions to cancer development remain largely unknown. To assess whether synonymous mutations involved in post-transcriptional regulation contribute to the genetic etiology of cancers, we collected whole exome data from 8,320 patients across 22 cancer types. By employing our developed algorithm, PIVar, we identified a total of 22,948 posttranscriptionally impaired synonymous SNVs (pisSNVs) spanning 2,042 genes. In addition, 35 RNA binding proteins impacted by these identified pisSNVs were significantly enriched. Remarkably, we discovered markedly elevated ratio of somatic pisSNVs across all 22 cancer types, and a high pisSNV ratio was associated with worse patient survival in five cancer types. Intriguing, several well-established cancer genes, including PTEN, RB1 and PIK3CA, appeared to contribute to tumorigenesis at both protein function and posttranscriptional regulation levels, whereas some pisSNV-hosted genes, including UBR4, EP400 and INTS1, exerted their function during carcinogenesis mainly via posttranscriptional mechanisms. Moreover, we predicted three drugs associated with two pisSNVs, and numerous compounds associated with expression signature of pisSNV-hosted genes. Our study reveals the prevalence and clinical relevance of pisSNVs in cancers, and emphasizes the importance of considering posttranscriptional impaired synonymous mutations in cancer biology.

Indexed as

AdultAgedCalmodulin-Binding ProteinsCarcinogenesisClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsDNA HelicasesExomeFemaleGene Expression Regulation, NeoplasticGenome, HumanHumansKaplan-Meier EstimateMaleMiddle AgedNeoplasmsCalmodulin-Binding ProteinsClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsDNA HelicasesEP400 protein, humanPIK3CA protein, humanPTEN PhosphohydrolasePTEN protein, humanRB1 protein, humanRetinoblastoma Binding ProteinsUbiquitin-Protein LigasesUBR4 protein, humanWnt1 ProteinWNT1 protein, human

Identifiers

PMID31950163
PMCPMC7026592
OpenAlexW3000249748

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.