Evidence map›Paper›PMID 15755900›Full record

ArticleBlood2005

Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 C-terminus.

Gang G Wang, Martina P Pasillas, Mark P Kamps

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Menin in Cancer.Genes · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. The Historical Relationship Between Meis1 and Leukemia.Advances in experimental medicine and biology · 2022
    Review
  12. Prostaglandin EStem cell reviews and reports · 2021
    Article
  13. Review
  14. Article
  15. MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

13 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

3 authors at 1 institution in 1 country.

Gang G WangDepartment of Pathology and Molecular Pathology Program, School of Medicine, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Martina P Pasillas
Mark P Kamps
University of California San Diego · US

Funding

Hoxa9, Meis1, and Pbx in Self-renewal and LeukemogenesisR01CA056876 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAMPS, MARK P · 1992 to 2012
$4.1M
NCI NIH HHS CA56876
6 · The paper itself

Abstract

Meis1 is a homeodomain transcription factor coexpressed with Hoxa9 in most human acute myeloid leukemias (AMLs). In mouse models of leukemia produced by Hoxa9, Meis1 accelerates leukemogenesis. Because Hoxa9 immortalizes myeloid progenitors in the absence of Meis1 expression, the contribution of Meis1 toward leukemia remains unclear. Here, we describe a cultured progenitor model in which Meis1 programs leukemogenicity. Progenitors immortalized by Hoxa9 in culture are myeloid-lineage restricted and only infrequently caused leukemia after more than 250 days. Coexpressed Meis1 programmed rapid AML-initiating character, maintained multipotent progenitor potential, and induced expression of genes associated with short-term hematopoietic stem cells (HSCs), such as FLT3 and CD34, whose expression also characterizes the leukemia-initiating stem cells of human AML. Meis1 leukemogenesis functions required binding to Pbx, binding to DNA, and a conserved function of its C-terminal tail. We hypothesize that Meis1 is required for the homing and survival of leukemic progenitors within their hematopoietic niches, functions mediated by HSC-specific genes such as CD34 and Fms-like tyrosine kinase 3 (FLT3), respectively. This is the first example of a transcription factor oncoprotein (Meis1) that establishes expression of a tyrosine kinase oncoprotein (FLT3), and explains their coexpression in human leukemia. This cultured progenitor model will be useful to define the genetic basis of leukemogenesis involving Hoxa9 and Meis1.

Indexed as

Acute DiseaseAnimalsCell DifferentiationCell DivisionCell LineageCell Line, TransformedFemalefms-Like Tyrosine Kinase 3Gene Expression Regulation, LeukemicHematopoietic Stem CellsHepatocyte Growth FactorHomeodomain ProteinsLeukemia, MyeloidMiceMice, Inbred BALB CMyeloid Ecotropic Viral Integration Site 1 ProteinFlt3 protein, mousefms-Like Tyrosine Kinase 3Hepatocyte Growth Factorhomeobox protein HOXA9Homeodomain ProteinsMEIS1 protein, humanMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Interleukin-7Transcription Factors

Identifiers

PMID15755900
PMCPMC1895124
OpenAlexW2066472373

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.