Evidence map›Paper›PMID 35962343›Full record

ArticleJournal of translational medicine2022

Comprehensive characterization of clonality of driver genes revealing their clinical relevance in colorectal cancer.

Jian Shi, Li Wang, Xiangzhe Yin, Lixia Wang, Lin Bo, Kailai Liu, Ke Feng, Shihua Lin, Yanjun Xu, Shangwei Ning and 1 more

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

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. 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

11 authors at 1 institution in 1 country.

Jian Shi *College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Li Wang *College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. wangli@hrbmu.edu.cn.ORCID 0000-0002-1936-8513
Xiangzhe Yin *College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Lixia WangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Lin BoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Kailai LiuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Ke FengCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Shihua LinCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Yanjun XuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. xuyanjun@hrbmu.edu.cn.
Shangwei NingCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. ningsw@ems.hrbmu.edu.cn.
Hongying ZhaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. zhaohongying@hrbmu.edu.cn.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenomic studies of colorectal cancer have revealed the complex genomic heterogeneity of the tumor. The acquisition and selection of genomic alterations may be critical to understanding the initiation and progression of this disease.

methodsIn this study, we have systematically characterized the clonal architecture of 97 driver genes in 536 colorectal cancer patients from TCGA.

resultsA high proportion of clonal mutations in 93 driver genes were observed. 40 genes showed significant associations between their clonality and multiple clinicopathologic factors. Kaplan-Meier analysis suggested that the mutation clonality of ANK1, CASP8, SMAD2, and ARID1A had a significant impact on the CRC patients' outcomes. Multivariable analysis revealed that subclonal ANK1 mutations, clonal CASP8 mutations, and clonal SMAD2 mutations independently predicted for shorter overall survival after adjusting for clinicopathological factors. The poor outcome of the subclonal ANK1 mutation may be caused by upregulation of IL4I1, IDO1, IFNG and MAPK12 which showed potential roles in tumor immune evasion through accumulation of immunosuppressive cells such as regulatory T cells and myeloid derived suppressor cells.

conclusionThese results suggested that the clonality of driver genes could act as prognostic markers and potential therapeutic targets in human colorectal cancer.

Indexed as

Colorectal NeoplasmsGenomicsHumansKaplan-Meier EstimateL-Amino Acid OxidaseMutationIL4I1 protein, humanL-Amino Acid OxidaseClonal mutationColorectal cancerDriver genesImmune evasionPrognostic biomarkersSubclonal mutation

Identifiers

PMID35962343
PMCPMC9373375
OpenAlexW4291161758

What OpenQuestion holds

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LicenceCC BY
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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.