Evidence map›Paper›PMID 18538728›Full record

ArticleCancer cell2008

MLL-AF9 leukemia stem cells: hardwired or taking cues from the microenvironment?

Andrew G Muntean, Jay L Hess

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Cancer cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Andrew G MunteanDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Jay L Hess
University of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MLL rearrangements in humans lead to both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL). While AML has been successfully produced in mice, modeling ALL has been more difficult. In this issue of Cancer Cell, Wei et al. (2008) describe generation of AML, ALL, and biphenotypic leukemia by manipulating the cytokine milieu of human progenitor cells expressing MLL-AF9. They demonstrate that both multipotent and lineage-restricted progenitors are targeted by MLL-AF9 fusion proteins and that Rac signaling is crucial for survival. This study demonstrates the heterogeneity of MLL-AF9 leukemic stem cells and the importance of the microenvironment in determining lineage outcome.

Indexed as

Cell LineageAnimalsApoptosisBone MarrowCell Culture TechniquesCell Line, TransformedCell ProliferationCell Transformation, NeoplasticEnvironmentFetal Stem CellsGene Expression Regulation, LeukemicGenotypeHumansIntercellular Signaling Peptides and ProteinsLeukemia, Myeloid, AcuteMultipotent Stem CellsIntercellular Signaling Peptides and ProteinsMLL-AF9 fusion protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, Fusionrac GTP-Binding Proteins

Identifiers

PMID18538728
OpenAlexW2021771060

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.