Evidence map›Paper›PMID 23878725›Full record

ArticleeLife2013

MYBL2 is a sub-haploinsufficient tumor suppressor gene in myeloid malignancy.

Stefan Heinrichs, Lillian F Conover, Carlos E Bueso-Ramos, Outi Kilpivaara, Kristen Stevenson, Donna Neuberg, Mignon L Loh, Wen-Shu Wu, Scott J Rodig, Guillermo Garcia-Manero and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  19. Oncotarget · 2018
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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

12 authors at 7 institutions in 3 countries.

Stefan HeinrichsInstitute of Transfusion Medicine , University Hospital Essen , Essen , Germany ; Department of Pediatric Oncology , Dana-Farber Cancer Institute , Boston , United States.
Lillian F Conover
Carlos E Bueso-Ramos
Outi Kilpivaara
Kristen Stevenson
Donna Neuberg
Mignon L Loh
Wen-Shu Wu
Scott J Rodig
Guillermo Garcia-Manero
Hagop M Kantarjian
A Thomas Look
Dana-Farber Cancer Institute · USThe University of Texas MD Anderson Cancer Center · USBoston University · USEssen University Hospital · DEHarvard University Press · USUniversity of California, San Francisco · USUniversity of Helsinki · FI

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tyrosine Kinases, Serine-Threonine Kinases,&Phosophatases in PathogenesisP01CA108631 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ESTEY, ELIHU · 2005 to 2009
$9.7M
NCI NIH HHS P01 CA108631NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

A common deleted region (CDR) in both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN) affects the long arm of chromosome 20 and has been predicted to harbor a tumor suppressor gene. Here we show that MYBL2, a gene within the 20q CDR, is expressed at sharply reduced levels in CD34+ cells from most MDS cases (65%; n = 26), whether or not they harbor 20q abnormalities. In a murine competitive reconstitution model, Mybl2 knockdown by RNAi to 20-30% of normal levels in multipotent hematopoietic progenitors resulted in clonal dominance of these 'sub-haploinsufficient' cells, which was reflected in all blood cell lineages. By 6 months post-transplantation, the reconstituted mice had developed a clonal myeloproliferative/myelodysplastic disorder originating from the cells with aberrantly reduced Mybl2 expression. We conclude that downregulation of MYBL2 activity below levels predicted by classical haploinsufficiency underlies the clonal expansion of hematopoietic progenitors in a large fraction of human myeloid malignancies. DOI:http://dx.doi.org/10.7554/eLife.00825.001.

Indexed as

Genes, Tumor SuppressorCell Cycle ProteinsDosage Compensation, GeneticHaploinsufficiencyHumansKaryotypingMyelodysplastic SyndromesMyeloproliferative DisordersTrans-ActivatorsCell Cycle ProteinsMYBL2 protein, humanTrans-Activators20q CDRHumanMouseMYBL2Myelodysplastic Syndromes

Identifiers

PMID23878725
PMCPMC3713455
OpenAlexW1966772408

What OpenQuestion holds

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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.