Evidence map›Paper›PMID 27638352›Full record

ReviewCold Spring Harbor perspectives in medicine2016

MLL3/MLL4/COMPASS Family on Epigenetic Regulation of Enhancer Function and Cancer.

Christie C Sze, Ali Shilatifard

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. KMT2C and KMT2D amplify GRHL2-driven enhancer activation.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Biomolecules · 2025
    Article
  10. Review
  11. Mapping of the hSOX10 protein interactome in human melanoma.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Somatic mutations of MLL4/COMPASS induce cytoplasmic localization providing molecular insight into cancer prognosis and treatment.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article

46 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

2 authors at 1 institution in 1 country.

Christie C SzeDepartment of Biochemistry and Molecular Genetics and Robert H. Lurie NCI Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Ali ShilatifardDepartment of Biochemistry and Molecular Genetics and Robert H. Lurie NCI Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
UNC Lineberger Comprehensive Cancer Center

Funding

Mutations of Chromatin and its Modifying Machineries in MalignanciesR35CA197569 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Ali Shilatifard · 2015 to 2026
$10.7M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
NCI NIH HHS R35 CA197569NCI NIH HHS T32 CA009560
6 · The paper itself

Abstract

During development, precise spatiotemporal patterns of gene expression are coordinately controlled by cis-regulatory modules known as enhancers. Their crucial role in development helped spur numerous studies aiming to elucidate the functional properties of enhancers within their physiological and disease contexts. In recent years, the role of enhancer malfunction in tissue-specific tumorigenesis is increasingly investigated. Here, we direct our focus to two primary players in enhancer regulation and their role in cancer pathogenesis: MLL3 and MLL4, members of the COMPASS family of histone H3 lysine 4 (H3K4) methyltransferases, and their complex-specific subunit UTX, a histone H3 lysine 27 (H3K27) demethylase. We review the most recent evidence on the underlying roles of MLL3/MLL4 and UTX in cancer and highlight key outstanding questions to help drive future research and contribute to our fundamental understanding of cancer and facilitate identification of therapeutic opportunities.

Indexed as

Enhancer Elements, GeneticProtein Processing, Post-TranslationalAnimalsCell Transformation, NeoplasticDNA-Binding ProteinsEpigenesis, GeneticGene ExpressionHistone-Lysine N-MethyltransferaseHistonesHumansMethylationMiceNeoplasmsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHistonesKMT2C protein, humanMLL4 protein, human

Identifiers

PMID27638352
PMCPMC5088509
OpenAlexW2519986025

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.