Evidence map›Paper›PMID 25997600›Full record

ArticleNature communications2015

Dissecting the role of aberrant DNA methylation in human leukaemia.

Giovanni Amabile, Annalisa Di Ruscio, Fabian Müller, Robert S Welner, Henry Yang, Alexander K Ebralidze, Hong Zhang, Elena Levantini, Lihua Qi, Giovanni Martinelli and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.2field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
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  5. Article
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  13. Development of theMedical oncology (Northwood, London, England) · 2022
    Article
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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

15 authors at 8 institutions in 6 countries.

Giovanni Amabile1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA.
Annalisa Di Ruscio1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA.
Fabian MüllerMax Plank Institute for Informatics, Saarbrücken 117599, Germany.
Robert S Welner1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA.
Henry YangCancer Science Institute, National University of Singapore, Singapore 66123, Singapore.
Alexander K Ebralidze1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA.
Hong Zhang1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA.
Elena Levantini1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA [3] Institute of Biomedical Technologies, National Research Council (CNR), Pisa 56124, Italy.
Lihua QiCancer Science Institute, National University of Singapore, Singapore 66123, Singapore.
Giovanni MartinelliDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Bologna 40126, Italy.
Thijn BrummelkampNetherlands Cancer Institute, Amsterdam 1066, The Netherlands.
Michelle M Le BeauSection of Hematology/Oncology and the Comprehensive Cancer Center, University of Chicago, Chicago, Illinois 60637, USA.
Maria E FigueroaUniversity of Michigan, Department of Pathology, Ann Arbor, Michigan 48109-2200, USA.
Christoph Bock1] Max Plank Institute for Informatics, Saarbrücken 117599, Germany [2] CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna 1090, Austria [3] Department of Laboratory Medicine, Medical University of Vienna, Vienna 1090, Austria.ORCID 0000000160913088
Daniel G Tenen1] Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138, USA [3] Cancer Science Institute, National University of Singapore, Singapore 66123, Singapore.
Harvard University · USNational University of Singapore · SGAustrian Academy of Sciences · ATDutch Cancer Society · NLMax Planck Institute for Informatics · DEUniversity of Bologna · ITUniversity of Chicago · USUniversity of Michigan · US

Funding

PROGRAM IN BLOOD COAGULATION AND VASCULAR BIOLOGYT32HL007917 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Robert C Flaumenhaft · 1999 to 2026
$11.1M
Distinct acute myeloid leukemia subclasses with CEBPA mutationsR01CA118316 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2007 to 2011
$2.0M
Determining the role of DNMT-interacting RNAs in myeloid disordersR00CA188595 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DI RUSCIO, ANNALISA · 2017 to 2019
$747k
Determining the role of DNMT-interacting RNAs in myeloid disordersK99CA188595 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DI RUSCIO, ANNALISA · 2014 to 2015
$219k
NCI NIH HHS 1K99CA188595-01NCI NIH HHS CA118316NCI NIH HHS K99 CA188595NCI NIH HHS R00 CA188595NCI NIH HHS R01 CA118316NHLBI NIH HHS T32 HL007917NHLBI NIH HHS T32 HL007917-11A1NHLBI NIH HHS T32 HL007917-16A1
6 · The paper itself

Abstract

Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the genetic translocation t(9;22)(q34;q11.2) encoding for the BCR-ABL fusion oncogene. However, many molecular mechanisms of the disease progression still remain poorly understood. A growing body of evidence suggests that the epigenetic abnormalities are involved in tyrosine kinase resistance in CML, leading to leukaemic clone escape and disease propagation. Here we show that, by applying cellular reprogramming to primary CML cells, aberrant DNA methylation contributes to the disease evolution. Importantly, using a BCR-ABL inducible murine model, we demonstrate that a single oncogenic lesion triggers DNA methylation changes, which in turn act as a precipitating event in leukaemia progression.

Indexed as

DNA MethylationGenes, ablAnimalsAzacitidineCell DifferentiationCellular Reprogramming TechniquesHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMice, TransgenicU937 CellsAzacitidine

Identifiers

PMID25997600
PMCPMC4443494
OpenAlexW235002606

What OpenQuestion holds

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Registered trials

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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.