Evidence map›Paper›PMID 20093773›Full record

ArticleThe Journal of clinical investigation2010

c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis.

Shenghao Jin, Huiwu Zhao, Yan Yi, Yuji Nakata, Anna Kalota, Alan M Gewirtz

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
  2. Article
  3. Menin in Cancer.Genes · 2024
    Review
  4. Article
  5. MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Transcription regulation ofAnnals of translational medicine · 2018
    Review
  19. Review
  20. Structural basis for cooperative regulation of KIX-mediated transcription pathways by the HTLV-1 HBZ activation domain.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article

17 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

6 authors at 1 institution in 1 country.

Shenghao JinDivision of Hematology/Oncology, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Huiwu Zhao
Yan Yi
Yuji Nakata
Anna Kalota
Alan M Gewirtz
University of Pennsylvania · US

Funding

VAV ANTISENSE ODN--A NOVEL THERAPEUTIC FOR HUMAN LEUKEMIASP01CA072765 · NCI · UNIVERSITY OF PENNSYLVANIA · PI GEWIRTZ, ALAN M · 1997 to 2007
$8.5M
NCI NIH HHS 2P01CA072765-11NCI NIH HHS P01 CA072765
6 · The paper itself

Abstract

Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia. These chromosomal translocations commonly result in MLL fusion proteins that dysregulate transcription. Recent data suggest that the MYB proto-oncogene, which is an important regulator of hematopoietic cell development, has a role in leukemogenesis driven by the MLL-ENL fusion protein, but exactly how is unclear. Here we have demonstrated that c-Myb is recruited to the MLL histone methyl transferase complex by menin, a protein important for MLL-associated leukemic transformation, and that it contributes substantially to MLL-mediated methylation of histone H3 at lysine 4 (H3K4). Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus. This decreased occupancy was associated with a diminished ability of an MLL-ENL fusion protein to transform normal mouse hematopoietic cells. Previous studies have shown that MYB expression is regulated by Hoxa9 and Meis1, indicating the existence of an autoregulatory feedback loop. The finding that c-Myb has the ability to direct epigenetic marks, along with its participation in an autoregulatory feedback loop with genes known to transform hematopoietic cells, lends mechanistic and translationally relevant insight into its role in MLL-associated leukemogenesis.

Indexed as

AnimalsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHistonesHomeodomain ProteinsHumansLeukemiaMiceMyeloid-Lymphoid Leukemia ProteinProtein BindingProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-mybRecombinant Fusion ProteinsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHistoneshomeobox protein HOXA9Homeodomain ProteinsKMT2A protein, humanMAS1 protein, humanMEN1 protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-mybRecombinant Fusion Proteins

Identifiers

PMID20093773
PMCPMC2810070
OpenAlexW2024532072

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.