Evidence map›Paper›PMID 26768237›Full record

ReviewAnnual review of medicine2016

Epigenetic Therapeutics: A New Weapon in the War Against Cancer.

Nita Ahuja, Anup R Sharma, Stephen B Baylin

Abstract readReview
In one paragraph

Review in Annual review of medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.

0numbers the graph read from it
0cells of the map it votes in
181citing 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

181 citing papers in PubMed.

  1. Trial
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  9. Review
  10. Genetic-epigenetic interactions (meQTLs) in orofacial clefts etiology.medRxiv : the preprint server for health sciences · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Bioavailability, Metabolism, and Excretion of [Clinical pharmacology in drug development · 2025
    Article
  15. Article
  16. Review
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  19. Article
  20. Article

121 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

3 authors.

Nita AhujaCancer Biology Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; email: sbaylin@jhmi.edu.
Anup R SharmaCancer Biology Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; email: sbaylin@jhmi.edu.
Stephen B BaylinCancer Biology Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; email: sbaylin@jhmi.edu.

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
DNA Methyltrasferase Gene Expression in Colon CancerR01ES011858 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI BAYLIN, STEPHEN B., EASWARAN, HARIHARAN · 2002 to 2023
$11.5M
(PQD3)Molecular Profiles associated with Long-Term Survival in pancreas CancerR01CA185357 · NCI · YALE UNIVERSITY · PI AHUJA, NITA, EASWARAN, HARIHARAN · 2014 to 2017
$1.8M
Epigenetic markers involved in colorectal cancer recurrence and metastasesK23CA127141 · NCI · JOHNS HOPKINS UNIVERSITY · PI AHUJA, NITA · 2008 to 2012
$705k
NCI NIH HHS K23 CA127141NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA185357NIEHS NIH HHS ES011858NIEHS NIH HHS R01 ES011858
6 · The paper itself

Abstract

The past 15 years have seen an explosion of discoveries related to the cellular regulation of phenotypes through epigenetic mechanisms. This regulation provides a software that packages DNA, without changing the primary base sequence, to establish heritable patterns of gene expression. In cancer, many aspects of the epigenome, controlled by DNA methylation, chromatin, and nucleosome positioning, are altered as one means by which tumor cells maintain abnormal states of self-renewal at the expense of normal maturation. Epigenetic and genetic abnormalities thus collaborate in cancer initiation and progression, as exemplified by frequent mutations in genes encoding proteins that control the epigenome. There is growing emphasis on using epigenetic therapies to reprogram neoplastic cells toward a normal state. Many agents targeting epigenetic regulation are under development and entering clinical trials. This review highlights the promise that epigenetic therapy, often in combination with other therapies, will become a potent tool for cancer management over the next decade.

Indexed as

Epigenesis, GeneticImmunotherapyAntineoplastic Combined Chemotherapy ProtocolsChromatinClinical Trials as TopicCombined Modality TherapyDNA MethylationHistone Deacetylase InhibitorsHumansMethyltransferasesNeoplasmsRNA, UntranslatedChromatinHistone Deacetylase InhibitorsMethyltransferasesRNA, UntranslatedDNA methyltransferase inhibitorepigeneticshistone deacetylase inhibitor therapy

Identifiers

PMID26768237
PMCPMC4937439

What OpenQuestion holds

Textmetadata
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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.