Evidence map›Paper›PMID 25537518›Full record

SynthesisOncotarget2015

Genetic alterations of histone lysine methyltransferases and their significance in breast cancer.

Lanxin Liu, Sarah Kimball, Hui Liu, Andreana Holowatyj, Zeng-Quan Yang

Open access · diamondAbstract readMeta-Analysis
In one paragraph

Synthesis in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

93 citing papers in PubMed, 167 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Loss-of-function mutations of microRNA-142-3p promoteWorld journal of gastroenterology · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. NovelCancers · 2023
    Article
  18. Article
  19. Review
  20. Article

33 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Lanxin LiuDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Sarah KimballDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Hui LiuDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Andreana HolowatyjDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Zeng-Quan YangDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

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

Histone lysine methyltransferases (HMTs), a large class of enzymes that catalyze site-specific methylation of lysine residues on histones and other proteins, play critical roles in controlling transcription, chromatin architecture, and cellular differentiation. However, the genomic landscape and clinical significance of HMTs in breast cancer remain poorly characterized. Here, we conducted a meta-analysis of approximately 50 HMTs in breast cancer and identified associations among recurrent copy number alterations, mutations, gene expression, and clinical outcome. We identified 12 HMTs with the highest frequency of genetic alterations, including 8 with high-level amplification, 2 with putative homozygous deletion, and 2 with somatic mutation. Different subtypes of breast cancer have different patterns of copy number and expression for each HMT gene. In addition, chromosome 1q contains four HMTs that are concurrently or independently amplified or overexpressed in breast cancer. Copy number or mRNA expression of several HMTs was significantly associated with basal-like breast cancer and shorter patient survival. Integrative analysis identified 8 HMTs (SETDB1, SMYD3, ASH1L, SMYD2, WHSC1L1, SUV420H1, SETDB2, and KMT2C) that are dysregulated by genetic alterations, classifying them as candidate therapeutic targets. Together, our findings provide a strong foundation for further mechanistic research and therapeutic options using HMTs to treat breast cancer.

Indexed as

DNA Copy Number VariationsGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticBreast NeoplasmsCell Line, TumorFemaleGene FrequencyHistone-Lysine N-MethyltransferaseHumansIsoenzymesKaplan-Meier EstimateMutationPhylogenyPrognosisReverse Transcriptase Polymerase Chain ReactionHistone-Lysine N-MethyltransferaseIsoenzymes

Identifiers

PMID25537518
PMCPMC4385864
OpenAlexW1573937463

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.