Evidence map›Paper›PMID 33371192›Full record

ReviewCells2020

Targeting Chromatin Complexes in Myeloid Malignancies and Beyond: From Basic Mechanisms to Clinical Innovation.

Florian Perner, Scott A Armstrong

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Haematologica · 2025
    Review
  7. Review
  8. Review
  9. Distinct Responses to Menin Inhibition and Synergy with DOT1L Inhibition inInternational journal of molecular sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

2 authors at 1 institution in 2 countries.

Florian PernerDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Scott A ArmstrongDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Harvard University · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
Targeting SYK Kinase in AMLP50CA206963 · NCI · DANA-FARBER CANCER INST · PI GRAUBERT, TIMOTHY A · 2017 to 2021
$10.6M
Targeting to Epigenetic Modications in ALLR01CA176745 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ARMSTRONG, SCOTT A, QI, JUN · 2012 to 2022
$4.2M
Functional and Mechanistic Study of Histone Crotonylation in Hematological MalignanciesR01CA204639 · NCI · ROCKEFELLER UNIVERSITY · PI ALLIS, CHARLES DAVID, ARMSTRONG, SCOTT A · 2016 to 2020
$3.5M
NCI NIH HHS P01 CA066996NCI NIH HHS P50 CA206963NCI NIH HHS R01 CA176745NCI NIH HHS R01 CA204639
6 · The paper itself

Abstract

The aberrant function of chromatin regulatory networks (epigenetics) is a hallmark of cancer promoting oncogenic gene expression. A growing body of evidence suggests that the disruption of specific chromatin-associated protein complexes has therapeutic potential in malignant conditions, particularly those that are driven by aberrant chromatin modifiers. Of note, a number of enzymatic inhibitors that block the catalytic function of histone modifying enzymes have been established and entered clinical trials. Unfortunately, many of these molecules do not have potent single-agent activity. One potential explanation for this phenomenon is the fact that those drugs do not profoundly disrupt the integrity of the aberrant network of multiprotein complexes on chromatin. Recent advances in drug development have led to the establishment of novel inhibitors of protein-protein interactions as well as targeted protein degraders that may provide inroads to longstanding effort to physically disrupt oncogenic multiprotein complexes on chromatin. In this review, we summarize some of the current concepts on the role epigenetic modifiers in malignant chromatin states with a specific focus on myeloid malignancies and recent advances in early-phase clinical trials.

Indexed as

Gene Expression Regulation, LeukemicAcetylationAnimalsChromatinDNA MethylationEpigenesis, GeneticHistone CodeHistone DemethylasesHistone-Lysine N-MethyltransferaseHistonesHumansLeukemia, MyeloidModels, BiologicalMyeloid-Lymphoid Leukemia ProteinProtein DomainsProtein Interaction MappingChromatinHistone DemethylasesHistone-Lysine N-MethyltransferaseHistonesKDM1A protein, humanKMT2A protein, humanMEN1 protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene ProteinsacetylationBRD4BRD9chromatindegradationDOT1LepigeneticsEZH2KMT2ALSD1MeninmethylationMLL1PPIPROTACtranscription

Identifiers

PMID33371192
PMCPMC7767226
OpenAlexW3117964745

What Socratic 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 Socratic graph.