Evidence map›Paper›PMID 16331271›Full record

ArticleOncogene2006

Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR alpha, PLZF/RAR alpha or NPM/RAR alpha.

E M Rego, D Ruggero, C Tribioli, G Cattoretti, S Kogan, R L Redner, P P Pandolfi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Function of PML-RARA in Acute Promyelocytic Leukemia.Advances in experimental medicine and biology · 2024
    Review
  2. Article
  3. Review
  4. Article
  5. Eya2, a Target Activated by Plzf, Is Critical forMolecular and cellular biology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

7 authors at 4 institutions in 1 country.

E M RegoCancer Biology and Genetics Program, Department of Pathology, Memorial Sloan-Kettering Cancer Center, Sloan Kettering Institute, New York, NY 10021, USA.
D Ruggero
C Tribioli
G Cattoretti
S Kogan
R L Redner
P P Pandolfi
Memorial Sloan Kettering Cancer Center · USColumbia University · USUniversity of California, San Francisco · USUniversity of Pittsburgh Medical Center · US

Funding

FUSION PROTEINS IN THE MOLECULAR PATHOGENESIS OF APLR01CA074031 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1997 to 2009
$3.8M
NCI NIH HHS CA-74031
6 · The paper itself

Abstract

Recurrent chromosomal translocations involving the RAR alpha locus on chromosome 17 are the hallmark of acute promyelocytic leukemia (APL). The RAR alpha gene fuses to variable partners (PML, PLZF, NPM, NuMA and STAT5B: X genes) leading to the expression of APL-specific fusion proteins with identical RAR alpha moieties. To analyse whether the variable X moiety could affect the activity of the fusion protein in vivo, we generated and characterized, on a comparative basis, NPM/RAR alpha transgenic mice (TM) in which the fusion gene is expressed under the control of a human Cathepsin G (hCG) minigene. We compared the features of the leukemia observed in these TM with those in hCG-PML/RAR alpha and hCG-PLZF/RAR alpha TM. In all three transgenic models, leukemia developed after a variably long latency, with variable penetrance. However, the three leukemias displayed distinct cytomorphological features. hCG-NPM/RAR alpha leukemic cells resembled monoblasts. This phenotype contrasts with what was observed in the hCG-PML/RAR alpha TM model in which the leukemic phase was characterized by the proliferation of promyelocytic blasts. Similarly, hCG-PLZF/RAR alpha TM displayed a different phenotype where terminally differentiated myeloid cells predominated. Importantly, the NPM/RAR alpha oncoprotein was found to localize in the nucleolus, unlike PML/RAR alpha and PLZF/RAR alpha, thus possibly interfering with the normal function of NPM. Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Taken together, our results underscore the critical relevance of the X moiety in dictating the biology of the disease and the activity of the APL fusion oncoprotein.

Indexed as

Gene FusionAnimalsAntineoplastic AgentsCathepsin GCathepsinsCell ProliferationCell Transformation, NeoplasticDNA-Binding ProteinsHumansKruppel-Like Transcription FactorsLeukemia, Promyelocytic, AcuteMiceMice, TransgenicNeoplasm ProteinsNuclear ProteinsPhenotypeAntineoplastic AgentsCathepsin GCathepsinsCTSG protein, humanCtsg protein, mouseDNA-Binding ProteinsKruppel-Like Transcription FactorsNeoplasm ProteinsNuclear ProteinsPML protein, humanPml protein, mousePromyelocytic Leukemia ProteinPromyelocytic Leukemia Zinc Finger ProteinRARA protein, humanRara protein, mouseReceptors, Retinoic AcidRetinoic Acid Receptor alphaSerine EndopeptidasesTranscription FactorsTretinoinTumor Suppressor ProteinsZBTB16 protein, humanZbtb16 protein, mouse

Identifiers

PMID16331271
OpenAlexW1542112366

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.