Evidence map›Paper›PMID 23625115›Full record

ArticleLeukemia2013

Targeting oncogene expression to endothelial cells induces proliferation of the myelo-erythroid lineage by repressing the Notch pathway.

E Alghisi, M Distel, M Malagola, V Anelli, C Santoriello, L Herwig, A Krudewig, C V Henkel, D Russo, M C Mione

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019
    Review
  11. Genetic Models of Leukemia in Zebrafish.Frontiers in cell and developmental biology · 2018
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Current pathobiology reports · 2014
    Article
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

10 authors at 7 institutions in 5 countries.

E Alghisi1] Chair of Hematology and Unit of Blood Disease and Stem Cell Transplantation Department of Clinical and Experimental Sciences, University of Brescia Medical School, Brescia, Italy [2] Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, Karlsruhe, Germany.
M Distel
M Malagola
V Anelli
C Santoriello
L Herwig
A Krudewig
C V Henkel
D Russo
M C Mione
University of Brescia · ITUniversity of Basel · CHHarvard University · USKarlsruhe Institute of Technology · DENew York Hospital Queens · USUniversity of California, San Diego · USZF Screens (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human oncogenes involved in the development of hematological malignancies have been widely used to model experimental leukemia. However, models of myeloid leukemia rarely reproduce the human disease in full, due to genetic complexity or to difficulties in targeting leukemia initiating cells. Here, we used a zebrafish genetic model to induce the expression of oncogenic RAS in endothelial cells, including the hemogenic endothelium of the dorsal aorta that generates hematopoietic cells, and observed the development of a myelo-erythroid proliferative disorder. In larvae, the phenotype is characterized by disruption of the vascular system and prominent expansion of the caudal hematopoietic tissue. In few surviving juveniles, increased number of immature hematopoietic cells and arrest of myeloid maturation was found in kidney marrow. Peripheral blood showed increased erythroblasts and myeloid progenitors. We found that the abnormal phenotype is associated with a downregulation of the Notch pathway, whereas overexpressing an activated form of Notch together with the oncogene prevents the expansion of the myelo-erythroid compartment. This study identifies the downregulation of the Notch pathway following an oncogenic event in the hemogenic endothelium as an important step in the pathogenesis of myelo-erythroid disorders and describes a number of potential effectors of this transformation.

Indexed as

Cell LineageCell ProliferationAnimalsApoptosisBlotting, WesternCell DifferentiationCell Transformation, NeoplasticEndothelium, VascularErythroid Precursor CellsFluorescent Antibody TechniqueHematopoiesisHumansMyeloid CellsProto-Oncogene Protein c-fli-1Proto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)FLI1 protein, humanKRAS protein, humanProto-Oncogene Protein c-fli-1Proto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsReceptor, Notch1RNA, Messenger

Identifiers

PMID23625115
OpenAlexW2028107524

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.