Evidence map›Paper›PMID 28572863›Full record

ReviewClinical epigenetics2017

Epi-drugs in combination with immunotherapy: a new avenue to improve anticancer efficacy.

Roberta Mazzone, Clemens Zwergel, Antonello Mai, Sergio Valente

Open access · goldAbstract readReview
In one paragraph

Review in Clinical epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
8.8field-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

88 citing papers in PubMed, 145 citations in OpenAlex.

  1. Article
  2. Epigenetic regulation in gynecological cancers: a paradigm shift in immunotherapy strategies.Journal of experimental & clinical cancer research : CR · 2025
    Review
  3. Precision epigenetic therapies in oncology.Cancer metastasis reviews · 2025
    Review
  4. Review
  5. CAR-T cell therapy for cancer: current challenges and future directions.Signal transduction and targeted therapy · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Cancer immune escape: the role of antigen presentation machinery.Journal of cancer research and clinical oncology · 2023
    Review
  17. Review
  18. Review
  19. Review
  20. Review

28 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

4 authors at 3 institutions in 1 country.

Roberta MazzoneDipartimento di Chimica e Tecnologie del Farmaco, Sapienza Università di Roma, P.le Aldo Moro 5, 00185 Rome, Italy.
Clemens ZwergelDipartimento di Chimica e Tecnologie del Farmaco, Sapienza Università di Roma, P.le Aldo Moro 5, 00185 Rome, Italy.
Antonello MaiDipartimento di Chimica e Tecnologie del Farmaco, Sapienza Università di Roma, P.le Aldo Moro 5, 00185 Rome, Italy.ORCID 0000-0001-9176-2382
Sergio ValenteDipartimento di Chimica e Tecnologie del Farmaco, Sapienza Università di Roma, P.le Aldo Moro 5, 00185 Rome, Italy.
Sapienza University of Rome · ITIstituto Pasteur · ITItalian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint factors, such as programmed cell death protein-1/2 (PD-1, PD-2) or cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) receptors, are targets for monoclonal antibodies (MAbs) developed for cancer immunotherapy. Indeed, modulating immune inhibitory pathways has been considered an important breakthrough in cancer treatment. Although immune checkpoint blockade therapy used to treat malignant diseases has provided promising results, both solid and haematological malignancies develop mechanisms that enable themselves to evade the host immune system. To overcome some major limitations and ensure safety in patients, recent strategies have shown that combining epigenetic modulators, such as inhibitors of histone deacetylases (HDACi) or DNA methyltransferases (DNMTi), with immunotherapeutics can be useful. Preclinical data generated using mouse models strongly support the feasibility and effectiveness of the proposed approaches. Indeed, co-treatment with pan- or class I-selective HDACi or DNMTi improved beneficial outcomes in both in vitro and in vivo studies. Based on the evidence of a pivotal role for HDACi and DNMTi in modulating various components belonging to the immune system, recent clinical trials have shown that both HDACi and DNMTi strongly augmented response to anti-PD-1 immunotherapy in different tumour types. This review describes the current strategies to increase immunotherapy responses, the effects of HDACi and DNMTi on immune modulation, and the advantages of combinatorial therapy over single-drug treatment.

Indexed as

AnimalsAntibodies, MonoclonalAntineoplastic Combined Chemotherapy ProtocolsClinical Trials as TopicDNA MethylationDNA Modification MethylasesEnzyme InhibitorsEpigenesis, GeneticHistone Deacetylase InhibitorsHumansImmunotherapyNeoplasmsAntibodies, MonoclonalDNA Modification MethylasesEnzyme InhibitorsHistone Deacetylase InhibitorsCancerDNA methylationEpigeneticsHDAC inhibitorsImmune checkpoint inhibitorsImmunotherapy

Identifiers

PMID28572863
PMCPMC5450222
OpenAlexW2620472170

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.