Evidence map›Paper›PMID 31570827›Full record

ReviewNature reviews. Clinical oncology2020

Combining epigenetic drugs with other therapies for solid tumours - past lessons and future promise.

Daphné Morel, Daniel Jeffery, Sandrine Aspeslagh, Geneviève Almouzni, Sophie Postel-Vinay

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed
–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

226 citing papers in PubMed.

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  2. A Phase I/II Open-Label Study of Molibresib for the Treatment of Relapsed/Refractory Hematologic Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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166 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

5 authors.

Daphné Morel *ATIP-Avenir Group, UMR981, INSERM (French National Institute of Health and Medical Research), Gustave Roussy Cancer Campus, Villejuif, France.ORCID http://orcid.org/0000-0002-9121-4973
Daniel Jeffery *Nuclear Dynamics Unit - UMR3664, National Centre for Scientific Research, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0003-2289-8379
Sandrine AspeslaghUniversity Hospital Brussels, Brussels, Belgium.
Geneviève Almouzni *Nuclear Dynamics Unit - UMR3664, National Centre for Scientific Research, Institut Curie, Paris, France. genevieve.almouzni@curie.fr.ORCID http://orcid.org/0000-0001-5570-0723
Sophie Postel-Vinay *ATIP-Avenir Group, UMR981, INSERM (French National Institute of Health and Medical Research), Gustave Roussy Cancer Campus, Villejuif, France. sophie.postel-vinay@gustaveroussy.fr.ORCID http://orcid.org/0000-0001-5562-1857

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic dysregulation has long been recognized as a key factor contributing to tumorigenesis and tumour maintenance that can influence all of the recognized hallmarks of cancer. Despite regulatory approvals for the treatment of certain haematological malignancies, the efficacy of the first generation of epigenetic drugs (epi-drugs) in patients with solid tumours has been disappointing; however, successes have now been achieved in selected solid tumour subtypes, thanks to the development of novel compounds and a better understanding of cancer biology that have enabled precision medicine approaches. Several lines of evidence support that, beyond their potential as monotherapies, epigenetic drugs could have important roles in synergy with other anticancer therapies or in reversing acquired therapy resistance. Herein, we review the mechanisms by which epi-drugs can modulate the sensitivity of cancer cells to other forms of anticancer therapy, including chemotherapy, radiation therapy, hormone therapy, molecularly targeted therapy and immunotherapy. We provide a critical appraisal of the preclinical rationale, completed clinical studies and ongoing clinical trials relating to combination therapies incorporating epi-drugs. Finally, we propose and discuss rational clinical trial designs and drug development strategies, considering key factors including patient selection, tumour biomarker evaluation, drug scheduling and response assessment and study end points, with the aim of optimizing the development of such combinations.

Indexed as

Antineoplastic AgentsClinical Trials as TopicCombined Modality TherapyDNA, NeoplasmEpigenesis, GeneticEpigenomicsGenetic TherapyHumansMolecular Targeted TherapyNeoplasmsAntineoplastic AgentsDNA, Neoplasm

Identifiers

What Socratic 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 Socratic graph.