Evidence map›Paper›PMID 28560068›Full record

ArticleAmerican journal of cancer research2017

HDAC2 overexpression correlates with aggressive clinicopathological features and DNA-damage response pathway of breast cancer.

Wenqi Shan, Yuanyuan Jiang, Huimei Yu, Qianhui Huang, Lanxin Liu, Xuhui Guo, Lei Li, Qingsheng Mi, Kezhong Zhang, Zengquan Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025
    Review
  10. Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  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

10 authors at 3 institutions in 2 countries.

Wenqi ShanDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Yuanyuan JiangDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Huimei YuDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Qianhui HuangDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Lanxin LiuDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Xuhui GuoDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Lei LiDepartment of Hygiene Analysis and Detection, School of Public Health, Nanjing Medical UniversityNanjing, China.
Qingsheng MiImmunology Program, Department of Dermatology, Henry Ford Health SystemDetroit, MI, USA.
Kezhong ZhangCenter for Molecular Medicine and Genetics, Department of Immunology and Microbiology, Wayne State University School of MedicineDetroit, MI, USA.
Zengquan YangDepartment of Oncology, Wayne State University School of MedicineDetroit, MI, USA.
Wayne State University · USHenry Ford Health System · USNanjing Medical University · CN

Funding

Molecular mechanism of oncogenic programming by histone demethylase GASC1R21CA175244 · NCI · WAYNE STATE UNIVERSITY · PI YANG, ZENG-QUAN · 2014 to 2015
$365k
NCI NIH HHS R21 CA175244
6 · The paper itself

Abstract

There are 18 lysine deacetylases, also known as histone deacetylases (HDACs), that remove acetyl groups from histone and non-histone proteins, thereby playing critical roles in numerous biological processes. In many human cancers, HDACs are dysregulated through mutation, altered expression, or inappropriate recruitment to certain loci. However, knowledge of the genomic and transcriptomic alterations and the clinical significance of most HDACs in breast cancer remain incomplete. We used TCGA and METABRIC datasets to perform comprehensive, integrated genomic and transcriptomic analyses of 18 HDAC genes in approximately 3000 primary breast cancers and identified associations among recurrent copy number alteration, gene expression, clinicopathological features, and patient survival. We found distinct patterns of copy number alteration and expression for each HDAC in breast cancer subtypes. We demonstrated that

Indexed as

Breast cancerhistone deacetylasemicroRNAmocetinostatRAD51

Identifiers

PMID28560068
PMCPMC5446485
OpenAlexW2981792677

What OpenQuestion holds

Textmetadata
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.