Evidence map›Paper›PMID 28887438›Full record

ArticleThe Journal of cell biology2017

Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia.

Trinna L Cuellar, Anna-Maria Herzner, Xiaotian Zhang, Yogesh Goyal, Colin Watanabe, Brad A Friedman, Vasantharajan Janakiraman, Steffen Durinck, Jeremy Stinson, David Arnott and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

143 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

  1. Pooled it
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  8. Article
  9. mNature communications · 2026
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  16. Article
  17. Article
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  19. Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Trinna L CuellarDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA trinna.cuellar@princeton.edu.ORCID 0000-0002-9991-9505
Anna-Maria HerznerDepartment of Human Genetics, Genentech, Inc., South San Francisco, CA.ORCID 0000-0001-6746-0587
Xiaotian ZhangDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Yogesh GoyalDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Colin WatanabeDepartment of Bioinformatics and Computational Biology, Genentech, Inc., South San Francisco, CA.
Brad A FriedmanDepartment of Bioinformatics and Computational Biology, Genentech, Inc., South San Francisco, CA.ORCID 0000-0002-5864-5253
Vasantharajan JanakiramanDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Steffen DurinckDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Jeremy StinsonDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
David ArnottDepartment of Protein Chemistry, Genentech, Inc., South San Francisco, CA.
Tommy K CheungDepartment of Protein Chemistry, Genentech, Inc., South San Francisco, CA.
Subhra ChaudhuriDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Zora ModrusanDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.
Jonas Martin DoerrDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA.ORCID 0000-0003-3599-6023
Marie ClassonDepartment of Discovery Oncology, Genentech, Inc., South San Francisco, CA.
Benjamin HaleyDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA benjamih@gene.com.ORCID 0000-0002-0074-0020

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A propensity for rewiring genetic and epigenetic regulatory networks, thus enabling sustained cell proliferation, suppression of apoptosis, and the ability to evade the immune system, is vital to cancer cell propagation. An increased understanding of how this is achieved is critical for identifying or improving therapeutic interventions. In this study, using acute myeloid leukemia (AML) human cell lines and a custom CRISPR/Cas9 screening platform, we identify the H3K9 methyltransferase SETDB1 as a novel, negative regulator of innate immunity. SETDB1 is overexpressed in many cancers, and loss of this gene in AML cells triggers desilencing of retrotransposable elements that leads to the production of double-stranded RNAs (dsRNAs). This is coincident with induction of a type I interferon response and apoptosis through the dsRNA-sensing pathway. Collectively, our findings establish a unique gene regulatory axis that cancer cells can exploit to circumvent the immune system.

Indexed as

Gene SilencingRetroelementsApoptosisCell Line, TumorCell SurvivalCRISPR-Cas SystemsEpigenesis, GeneticGene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHumansImmunity, InnateInterferon Type ILeukemia, Myeloid, AcuteProtein MethyltransferasesRNA, Double-StrandedRNA InterferenceHistone-Lysine N-MethyltransferaseInterferon Type IProtein MethyltransferasesRetroelementsRNA, Double-StrandedSETDB1 protein, human

Identifiers

PMID28887438
PMCPMC5674883
OpenAlexW2752297066

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.