Evidence map›Paper›PMID 33827917›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Epigenetic reprogramming of tumor cell-intrinsic STING function sculpts antigenicity and T cell recognition of melanoma.

Rana Falahat, Anders Berglund, Ryan M Putney, Patricio Perez-Villarroel, Shota Aoyama, Shari Pilon-Thomas, Glen N Barber, James J Mulé

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

118 citing papers in PubMed, 162 citations in OpenAlex.

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  7. Therapeutic targeting of the cGAS-STING pathway in human disease.The Journal of clinical investigation · 2026
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58 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

8 authors at 2 institutions in 1 country.

Rana FalahatDepartment of Immunology, Moffitt Cancer Center, Tampa, FL 33612.ORCID 0000-0001-7489-3807
Anders BerglundDepartment of Biostatistics and Bioinformatics, Moffitt Cancer Center, Tampa, FL 33612.ORCID 0000-0002-0393-3530
Ryan M PutneyDepartment of Biostatistics and Bioinformatics, Moffitt Cancer Center, Tampa, FL 33612.
Patricio Perez-VillarroelDepartment of Immunology, Moffitt Cancer Center, Tampa, FL 33612.
Shota AoyamaDepartment of Immunology, Moffitt Cancer Center, Tampa, FL 33612.
Shari Pilon-ThomasDepartment of Immunology, Moffitt Cancer Center, Tampa, FL 33612.
Glen N BarberDepartment of Cell Biology, University of Miami Miller School of Medicine, Miami, FL 33136.
James J MuléDepartment of Immunology, Moffitt Cancer Center, Tampa, FL 33612; james.mule@moffitt.org.
Moffitt Cancer Center · USUniversity of Miami · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI Christine O'Connell · 1998 to 2026
$93.5M
Tissue, Pathology and BioinformaticsP50CA168536 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MULE, JAMES J. · 2013 to 2017
$8.5M
Biomarkers and Resistance Mechanisms in Melanoma T-cell TherapyR01CA184845 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HWU, PATRICK, MULE, JAMES J. · 2014 to 2018
$1.7M
Designing Lymph Nodes for Cancer ImmunotherapyR01CA148995 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MULE, JAMES J. · 2010 to 2014
$1.7M
NCI NIH HHS P30 CA076292NCI NIH HHS P50 CA168536NCI NIH HHS R01 CA148995NCI NIH HHS R01 CA184845
6 · The paper itself

Abstract

Lack or loss of tumor antigenicity represents one of the key mechanisms of immune escape and resistance to T cell-based immunotherapies. Evidence suggests that activation of stimulator of interferon genes (STING) signaling in tumor cells can augment their antigenicity by triggering a type I IFN-mediated sequence of autocrine and paracrine events. Although suppression of this pathway in melanoma and other tumor types has been consistently reported, the mechanistic basis remains unclear. In this study, we asked whether this suppression is, in part, epigenetically regulated and whether it is indeed a driver of melanoma resistance to T cell-based immunotherapies. Using genome-wide DNA methylation profiling, we show that promoter hypermethylation of

Indexed as

DNA MethylationEpigenesis, GeneticCell Line, TumorCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHistocompatibility Antigens Class IHumansLymphocytes, Tumor-InfiltratingMelanomaMembrane ProteinsNucleotidyltransferasesSTING ProteinT-LymphocytescGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHistocompatibility Antigens Class IMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinantigenicityDNA methylationepigenetic silencingimmune evasionSTING signaling

Identifiers

PMID33827917
PMCPMC8053941
OpenAlexW3152326806

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.