Evidence map›Paper›PMID 27211271›Full record

ArticleLeukemia2016

Next-generation sequencing identifies major DNA methylation changes during progression of Ph+ chronic myeloid leukemia.

G Heller, T Topakian, C Altenberger, S Cerny-Reiterer, S Herndlhofer, B Ziegler, P Datlinger, K Byrgazov, C Bock, C Mannhalter and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
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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

16 authors at 6 institutions in 2 countries.

G HellerDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
T TopakianDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
C AltenbergerDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
S Cerny-ReitererDivision of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
S HerndlhoferDivision of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
B ZieglerDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
P DatlingerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
K ByrgazovChildren's Cancer Research Institute, Vienna, Austria.
C BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
C MannhalterDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
G HörmannLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.
W R SperrDivision of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
T LionChildren's Cancer Research Institute, Vienna, Austria.
C C ZielinskiDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
P ValentDivision of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.
S Zöchbauer-MüllerDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATComprehensive Cancer Center Vienna · ATLudwig Boltzmann Cluster for Cardiovascular Research · ATAustrian Academy of Sciences · ATCeMM Research Center for Molecular Medicine · ATSt Anna Children's Hospital · AT

Funding

Austrian Science Fund FWF P 24130
6 · The paper itself

Abstract

Little is known about the impact of DNA methylation on the evolution/progression of Ph+ chronic myeloid leukemia (CML). We investigated the methylome of CML patients in chronic phase (CP-CML), accelerated phase (AP-CML) and blast crisis (BC-CML) as well as in controls by reduced representation bisulfite sequencing. Although only ~600 differentially methylated CpG sites were identified in samples obtained from CP-CML patients compared with controls, ~6500 differentially methylated CpG sites were found in samples from BC-CML patients. In the majority of affected CpG sites, methylation was increased. In CP-CML patients who progressed to AP-CML/BC-CML, we identified up to 897 genes that were methylated at the time of progression but not at the time of diagnosis. Using RNA-sequencing, we observed downregulated expression of many of these genes in BC-CML compared with CP-CML samples. Several of them are well-known tumor-suppressor genes or regulators of cell proliferation, and gene re-expression was observed by the use of epigenetic active drugs. Together, our results demonstrate that CpG site methylation clearly increases during CML progression and that it may provide a useful basis for revealing new targets of therapy in advanced CML.

Indexed as

DNA MethylationHigh-Throughput Nucleotide SequencingBlood CellsBone Marrow CellsCase-Control StudiesCpG IslandsDisease ProgressionDown-RegulationHumansLeukemia, Myelogenous, Chronic, BCR-ABL Positive

Identifiers

PMID27211271
PMCPMC5240019
OpenAlexW2394559893

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.