Evidence map›Paper›PMID 20944599›Full record

ReviewNature biotechnology2010

Epigenetic modifications as therapeutic targets.

Theresa K Kelly, Daniel D De Carvalho, Peter A Jones

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03467178 (Randomized Phase II Study on Decitabine Plus Carboplatin Versus Physician's Choice Chemotherapy in Recurrent, Platinum-resistant Ovarian Cancer.), which is not on this map. Cited by 388 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
388citing papers in PubMed, 2 pooled it
–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.

NCT03467178 phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

Randomized Phase II Study on Decitabine Plus Carboplatin Versus Physician's Choice Chemotherapy in Recurrent, Platinum-resistant Ovarian Cancer.

TypeinterventionalSponsorFondazione IRCCS Istituto Nazionale dei Tumori, MilanoRan2018 to 2021Enrolled119ConditionsRecurrent, Platinum-resistant Ovarian CancerArmsDecitabine, Carboplatin, Pegylated Liposomal Doxorubicin, Gemcitabine, Paclitaxel
3 · Its place in the literature

Who cites it

388 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Biodistribution, Tumor Detection, and Radiation Dosimetry ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2019
    Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. New Personalized Medicine Model for Medication Management.Journal of personalized medicine · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

328 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.

Theresa K KellyDepartments of Urology and Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Daniel D De Carvalho
Peter A Jones

Funding

DE NOVO DNA METHYLATION IN BLADDER CANCERR01CA083867 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A, LIANG, GANGNING · 2000 to 2014
$4.7M
Mechanisms of De Novo Methylation in CancerR37CA082422 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 2009 to 2013
$2.2M
DNA METHYLATION IN DEVELOPMENT AND CANCERR35CA049758 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 1989 to 2000
$121k
NCI NIH HHS R01CA083867NCI NIH HHS R35 CA049758NCI NIH HHS R37 CA082422NCI NIH HHS R37CA082422
6 · The paper itself

Abstract

Epigenetic modifications work in concert with genetic mechanisms to regulate transcriptional activity in normal tissues and are often dysregulated in disease. Although they are somatically heritable, modifications of DNA and histones are also reversible, making them good targets for therapeutic intervention. Epigenetic changes often precede disease pathology, making them valuable diagnostic indicators for disease risk or prognostic indicators for disease progression. Several inhibitors of histone deacetylation or DNA methylation are approved for hematological malignancies by the US Food and Drug Administration and have been in clinical use for several years. More recently, histone methylation and microRNA expression have gained attention as potential therapeutic targets. The presence of multiple epigenetic aberrations within malignant tissue and the abilities of cells to develop resistance suggest that epigenetic therapies are most beneficial when combined with other anticancer strategies, such as signal transduction inhibitors or cytotoxic treatments. A key challenge for future epigenetic therapies will be to develop inhibitors with specificity to particular regions of chromosomes, thereby potentially reducing side effects.

Indexed as

Antineoplastic AgentsDNA MethylationEpigenesis, GeneticHistone Deacetylase InhibitorsHistonesHumansNeoplasmsNucleosidesAntineoplastic AgentsHistone Deacetylase InhibitorsHistonesNucleosides

Identifiers

PMID20944599
PMCPMC3022972

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.