Evidence map›Paper›PMID 27307795›Full record

SynthesisClinical epigenetics2016

Targeting epigenetic pathways in acute myeloid leukemia and myelodysplastic syndrome: a systematic review of hypomethylating agents trials.

Seongseok Yun, Nicole D Vincelette, Ivo Abraham, Keith D Robertson, Martin E Fernandez-Zapico, Mrinal M Patnaik

Open access · goldAbstract readComparative StudySystematic Review
In one paragraph

Synthesis in Clinical epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Seongseok YunDepartment of Medicine, University of Arizona, 1501 N. Campbell Ave., Tucson, AZ 85721 USA ; Hematology and Oncology, H. Lee Moffitt Cancer Center, Tampa, FL 12902 USA.
Nicole D VinceletteMolecular Pharmacology and Experimental Therapeutics, Department of Medicine, Mayo Clinic, Rochester, MN 55905 USA.
Ivo AbrahamCenter for Health Outcomes and PharmacoEconomic Research, University of Arizona, Tucson, AZ 85721 USA ; Arizona Cancer Center, University of Arizona, Tucson, AZ 85721 USA.
Keith D RobertsonPharmacology, Department of Medicine, Mayo Clinic, Rochester, MN 55905 USA.
Martin E Fernandez-ZapicoSchulze Center for Novel Therapeutics, Department of Medicine, Mayo Clinic, Rochester, MN 55905 USA.
Mrinal M PatnaikDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN 55905 USA.
Mayo Clinic in Arizona · USUniversity of Arizona · USNovel (United States) · USWinnMed · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant DNA methylation has been identified as a key molecular event regulating the pathogenesis of myelodysplastic syndromes (MDS); myeloid neoplasms with an inherent risk of transformation to acute myeloid leukemia (AML). Based on the above findings, DNA hypomethylating agents (HMA) have been widely used to treat AML and MDS, especially in elderly patients and in those who are not eligible for allogeneic stem cell transplantation (SCT). Our goal was to determine if there is any therapeutic advantage of HMA vs. conventional care regimens (CCR) and indirectly compare the efficacy of azacitidine and decitabine in this patient population.

methodsEligible studies were limited to randomized controlled trials comparing HMA to CCR in adult patients with AML or MDS.

resultsOverall survival (OS) rate was 33.2 vs. 21.4 % (RR 0.83, 95 % CI 0.71-0.98) and overall response rate (ORR) 23.7 vs. 13.4 % (RR 0.87, 95 % CI 0.81-0.93) for HMA and CCR, respectively. In subgroup analyses, only azacitidine treatment showed OS improvement (RR 0.75, 95 % CI 0.64-0.98) and not decitabine. Cytogenetic risk or bone marrow blast count did not have independent prognostic impact.

conclusionCollectively, these results demonstrate that HMA have superior outcomes compared to CCR and suggest that azacitidine in comparison to decitabine, may be more effective.

Indexed as

AgedAntimetabolites, AntineoplasticAzacitidineDecitabineDNA MethylationEpigenesis, GeneticFemaleHumansLeukemia, Myeloid, AcuteMaleMyelodysplastic SyndromesPrognosisRandomized Controlled Trials as TopicSurvival RateTreatment OutcomeAntimetabolites, AntineoplasticAzacitidineDecitabineAMLDNA hypomethylating agentsEpigeneticsMDS

Identifiers

PMID27307795
PMCPMC4908810
OpenAlexW2436188093

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.