Evidence map›Paper›PMID 39121370›Full record

ArticleBlood advances2024

Altered enhancer-promoter interaction leads to MNX1 expression in pediatric acute myeloid leukemia with t(7;12)(q36;p13).

Dieter Weichenhan, Anna Riedel, Etienne Sollier, Umut H Toprak, Joschka Hey, Kersten Breuer, Justyna A Wierzbinska, Aurore Touzart, Pavlo Lutsik, Marion Bähr and 17 more

Abstract read
In one paragraph

Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 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.

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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Mechanisms of enhancer-driven oncogene activation.International journal of cancer · 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

27 authors.

Dieter WeichenhanDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-7915-412X
Anna RiedelDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-0626-3894
Etienne SollierDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-3612-8562
Umut H ToprakDivision of Neuroblastoma Genomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0009-0009-6923-6816
Joschka HeyDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0003-2842-764X
Kersten BreuerDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0003-3716-7739
Justyna A WierzbinskaDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.
Aurore TouzartDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.
Pavlo LutsikDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0001-9383-8555
Marion BährDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.
Anders ÖstlundDepartment of Laboratory Medicine, University of Gothenburg, Gothenburg, Sweden.
Tina NilssonDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Susanna JacobssonDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Marcel EdlerDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Ahmed WarakyDepartment of Laboratory Medicine, University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0003-4635-021X
Yvonne Lisa BehrensDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.
Gudrun GöhringDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.
Brigitte SchlegelbergerDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-5256-1270
Clemens SteinekFaculty of Biology, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.ORCID 0000-0003-3590-2103
Hartmann HarzFaculty of Biology, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.ORCID 0000-0003-1218-2107
Heinrich LeonhardtFaculty of Biology, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.ORCID 0000-0002-5086-6449
Anna DolnikDepartment of Hematology, Oncology, and Tumor Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-University Berlin, Berlin, Germany.
Dirk ReinhardtDepartment of Pediatric Oncology, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0002-7027-4483
Lars BullingerDepartment of Hematology, Oncology, and Tumor Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-University Berlin, Berlin, Germany.
Lars PalmqvistDepartment of Laboratory Medicine, University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0001-9274-360X
Daniel B LipkaSection of Translational Cancer Epigenomics, Division of Translational Medical Oncology, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0001-5081-7869
Christoph PlassDivision of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0003-2554-3952

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractAcute myeloid leukemia (AML) with the t(7;12)(q36;p13) translocation occurs only in very young children and has a poor clinical outcome. The expected oncofusion between break point partners (motor neuron and pancreas homeobox 1 [MNX1] and ETS variant transcription factor 6 [ETV6]) has only been reported in a subset of cases. However, a universal feature is the strong transcript and protein expression of MNX1, a homeobox transcription factor that is normally not expressed in hematopoietic cells. Here, we map the translocation break points on chromosomes 7 and 12 in affected patients to a region proximal to MNX1 and either introns 1 or 2 of ETV6. The frequency of MNX1 overexpression in pediatric AML is 2.4% and occurs predominantly in t(7;12)(q36;p13) AML. Chromatin interaction assays in a t(7;12)(q36;p13) induced pluripotent stem cell line model unravel an enhancer-hijacking event that explains MNX1 overexpression in hematopoietic cells. Our data suggest that enhancer hijacking may be a more widespread consequence of translocations in which no oncofusion product was identified, including t(1;3) or t(4;12) AML.

Indexed as

Chromosomes, Human, Pair 7Enhancer Elements, GeneticHomeodomain ProteinsLeukemia, Myeloid, AcutePromoter Regions, GeneticTranscription FactorsTranslocation, GeneticAdolescentChildChild, PreschoolETS Translocation Variant 6 ProteinFemaleGene Expression Regulation, LeukemicHumansInfantMaleETS Translocation Variant 6 ProteinHomeodomain ProteinsMNX1 protein, humanProto-Oncogene Proteins c-etsRepressor ProteinsTranscription Factors

Identifiers

PMID39121370
PMCPMC11460460

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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.