Evidence map›Paper›PMID 16507773›Full record

ArticleBlood2006

c-Myb is an essential downstream target for homeobox-mediated transformation of hematopoietic cells.

Jay L Hess, Claudia B Bittner, Deniz T Zeisig, Christian Bach, Uta Fuchs, Arndt Borkhardt, Jon Frampton, Robert K Slany

Open access · greenAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
4.6field-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

103 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
  7. MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

43 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Jay L HessDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
Claudia B Bittner
Deniz T Zeisig
Christian Bach
Uta Fuchs
Arndt Borkhardt
Jon Frampton
Robert K Slany
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Michigan–Ann Arbor · US

Funding

MECHANISMS OF HOX GENE REGULATION BY MLLR01CA078815 · NCI · WASHINGTON UNIVERSITY · PI HESS, JAY L. · 1998 to 2007
$2.3M
NCI NIH HHS CA-78815NCI NIH HHS CA-92251
6 · The paper itself

Abstract

Abdominal-type HoxA genes in combination with Meis1 are well-documented on-cogenes in various leukemias but it is unclear how they exert their transforming function. Here we used a system of conditional transformation by an inducible mixed lineage leukemia-eleven-nineteen leukemia (MLL-ENL) oncoprotein to overexpress Hoxa9 and Meis1 in primary hematopoietic cells. Arrays identified c-Myb and a c-Myb target (Gstm1) among the genes with the strongest response to Hoxa9/Meis1. c-Myb overexpression was verified by Northern blot and quantitative reverse transcription-polymerase chain reaction (RT-PCR). Also MLL-ENL activated c-Myb through up-regulation of Hoxa9 and Meis1. Consequently, short-term suppression of c-Myb by small inhibitory RNA (siRNA) efficiently inhibited transformation by MLL-ENL but did not impair transformation by transcription factor E2A-hepatic leukemia factor (E2A-HLF). The anti c-Myb siRNA effect was abrogated by coexpression of a c-Myb derivative with a mutated siRNA target site. The introduction of a dominant-negative c-Myb mutant had a similar but weaker effect on MLL-ENL-mediated transformation. Hematopoietic precursors from mice homozygous for a hypo-morphic c-Myb allele were more severely affected and could be transformed neither by MLL-ENL nor by E2A-HLF. Ectopic expression of c-Myb induced a differentiation block but c-Myb alone was not transforming in a replating assay similar to Hoxa9/Meis1. These results suggest that c-Myb is essential but not sufficient for Hoxa9/Meis1 mediated transformation.

Indexed as

Hematopoietic Stem Cell TransplantationAnimalsBlotting, NorthernCell Transformation, NeoplasticGene Expression ProfilingGene Expression Regulation, LeukemicGlutathione TransferaseHematopoietic Stem CellsHomeodomain ProteinsLeukemiaMiceMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsProto-Oncogene Proteins c-mybReverse Transcriptase Polymerase Chain ReactionUp-RegulationGlutathione Transferasehomeobox protein HOXA9Homeodomain ProteinsMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsProto-Oncogene Proteins c-myb

Identifiers

PMID16507773
PMCPMC1895838
OpenAlexW2016507620

What OpenQuestion holds

Textmetadata
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.