Evidence map›Paper›PMID 38303701›Full record

ArticleiScience2024

Identification of somatic mutation-driven enhancers and their clinical utility in breast cancer.

Hongying Zhao, Ke Feng, Junjie Lei, Yaopeng Shu, Lin Bo, Ying Liu, Lixia Wang, Wangyang Liu, Shangwei Ning, Li Wang

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

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Bioinformatics analysis and clinical validation identifyTranslational andrology and urology · 2026
    Article
  3. 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

10 authors at 2 institutions in 1 country.

Hongying ZhaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Ke FengCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Junjie LeiCollege of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
Yaopeng ShuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Lin BoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Ying LiuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Lixia WangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Wangyang LiuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Shangwei NingCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Li WangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Harbin Medical University · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic mutations contribute to cancer development by altering the activity of enhancers. In the study, a total of 135 mutation-driven enhancers, which displayed significant chromatin accessibility changes, were identified as candidate risk factors for breast cancer (BRCA). Furthermore, we identified four mutation-driven enhancers as independent prognostic factors for BRCA subtypes. In Her2 subtype, enhancer G > C mutation was associated with poorer prognosis through influencing its potential target genes FBXW9, TRIR, and WDR83. We identified aminoglutethimide and quinpirole as candidate drugs targeting the mutated enhancer. In normal subtype, enhancer G > A mutation was associated with poorer prognosis through influencing its target genes ALOX15B, LINC00324, and MPDU1. We identified eight candidate drugs such as erastin, colforsin, and STOCK1N-35874 targeting the mutated enhancer. Our findings suggest that somatic mutations contribute to breast cancer subtype progression by altering enhancer activity, which could be potential candidates for cancer therapy.

Indexed as

GeneticsMedical biochemistry

Identifiers

PMID38303701
PMCPMC10831879
OpenAlexW4390611175

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.