Evidence map›Paper›PMID 21778999›Full record

ArticleLeukemia2011

Hypoxia-microRNA-16 downregulation induces VEGF expression in anaplastic lymphoma kinase (ALK)-positive anaplastic large-cell lymphomas.

E Dejean, M H Renalier, M Foisseau, X Agirre, N Joseph, G R de Paiva, T Al Saati, J Soulier, C Desjobert, L Lamant and 7 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 108 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Evaluating the prognostic role of glucose-to-lymphocyte ratio in patients with metastatic renal cell carcinoma treated with tyrosine kinase inhibitors in first line: a study by the Turkish Oncology Group Kidney Cancer Consortium (TKCC).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Genome-Wide miRNA Expression Profiling of Molecular Subgroups of Peripheral T-cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  9. Low miR-16 expression induces regulatory CD4American journal of cancer research · 2021
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019
    Review
  20. 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

17 authors at 8 institutions in 4 countries.

E DejeanCentre de Recherches en Cancérologie de Toulouse, INSERM-UMR 1037-Université Toulouse III Paul Sabatier, Toulouse, France.
M H Renalier
M Foisseau
X Agirre
N Joseph
G R de Paiva
T Al Saati
J Soulier
C Desjobert
L Lamant
F Prósper
D W Felsher
J Cavaillé
H Prats
G Delsol
S Giuriato
F Meggetto
Université Toulouse III - Paul Sabatier · FRInserm · FRCentre National de la Recherche Scientifique · FRUniversidad de Navarra · ESCentre de Recherche en Cancérologie de Toulouse · FRInstitut Universitaire de France · FRLaboratoire de Biologie Moléculaire des Eucaryotes · FRStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anaplastic lymphoma kinase (ALK), tyrosine kinase oncogene is implicated in a wide variety of cancers. In this study we used conditional onco-ALK (NPM-ALK and TPM3-ALK) mouse MEF cell lines (ALK+ fibroblasts) and transgenic models (ALK+ B-lymphoma) to investigate the involvement and regulation of angiogenesis in ALK tumor development. First, we observed that ALK expression leads to downregulation of miR-16 and increased Vascular Endothelial Growth Factor (VEGF) levels. Second, we found that modification of miR-16 levels in TPM3-ALK MEF cells greatly affected VEGF levels. Third, we demonstrated that miR-16 directly interacts with VEGF mRNA at the 3'-untranslated region and that the regulation of VEGF by miR-16 occurs at the translational level. Fourth, we showed that expression of both the ALK oncogene and hypoxia-induced factor 1α (HIF1α) is a prerequisite for miR-16 downregulation. Fifth, in vivo, miR-16 gain resulted in reduced angiogenesis and tumor growth. Finally, we highlighted an inverse correlation between the levels of miR-16 and VEGF in human NPM-ALK+ Anaplastic Large Cell Lymphomas (ALCL). Altogether, our results demonstrate, for the first time, the involvement of angiogenesis in ALK+ ALCL and strongly suggest an important role for hypoxia-miR-16 in regulating VEGF translation.

Indexed as

Gene Expression Regulation, NeoplasticAnaplastic Lymphoma KinaseAnimalsBlotting, NorthernBlotting, WesternCase-Control StudiesCell AdhesionCell MovementCells, CulturedDNA MethylationDown-RegulationEmbryo, MammalianEnzyme-Linked Immunosorbent AssayFemaleFibroblastsHumansALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN16 microRNA, humanMirn16 microRNA, mouseReceptor Protein-Tyrosine KinasesRNA, MessengerVascular Endothelial Growth Factor A

Identifiers

PMID21778999
OpenAlexW2147563499

What OpenQuestion holds

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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.