Evidence map›Paper›PMID 14737102›Full record

ArticleOncogene2004

Myeloid leukemia with promyelocytic features in transgenic mice expressing hCG-NuMA-RARalpha.

Mahadeo A Sukhai, Xuemei Wu, Yali Xuan, Tong Zhang, Patricia P Reis, Karina Dubé, Eduardo M Rego, Mantu Bhaumik, Denis J Bailey, Richard A Wells and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Association of the NuMA region on chromosome 11q13 with breast cancer susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  13. The C terminus of the nuclear protein NuMA: phylogenetic distribution and structure.Protein science : a publication of the Protein Society · 2004
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Mahadeo A SukhaiDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Xuemei Wu
Yali Xuan
Tong Zhang
Patricia P Reis
Karina Dubé
Eduardo M Rego
Mantu Bhaumik
Denis J Bailey
Richard A Wells
Suzanne Kamel-Reid
Pier Paolo Pandolfi
Memorial Sloan Kettering Cancer Center · USOntario Institute for Cancer Research · CAUniversity Health Network · CAUniversity of Toronto · CA

Funding

THE APL PARADIGM FOR ABERRANT TRANSCRIPTION, CANCER ANDU01CA084292 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1999 to 2008
$5.0M
FUSION PROTEINS IN THE MOLECULAR PATHOGENESIS OF APLR01CA074031 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1997 to 2009
$3.8M
PML, PLZF, NPM AND NUMA IN THE PATHOGENESIS OF APLR01CA071692 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1996 to 2005
$1.8M
NCI NIH HHS R01 CA71692NCI NIH HHS R01 CA74031NCI NIH HHS U01 CA84292
6 · The paper itself

Abstract

Acute promyelocytic leukemia (APL) is characterized by the accumulation of abnormal promyelocytes in the bone marrow (BM), and by the presence of a reciprocal chromosomal translocation involving retinoic acid receptor alpha (RARalpha). To date, five RARalpha partner genes have been identified in APL. NuMA-RARalpha was identified in a pediatric case of APL carrying a translocation t(11;17)(q13;q21). Using a construct containing the NuMA-RARalpha fusion gene driven by the human cathepsin G promoter (hCG-NuMA-RARalpha), two transgenic mouse lines were generated. Transgenic mice were observed to have a genetic myeloproliferation (increased granulopoiesis in BM) at an early age, and rapidly developed a myeloproliferative disease-like myeloid leukemia. This leukemia was morphologically and immunophenotypically indistinguishable from human APL, with a penetrance of 100%. The phenotype of transgenic mice was consistent with a blockade of neutrophil differentiation. NuMA-RARalpha is therefore sufficient for disease development in this APL model.

Indexed as

AnimalsAntigens, NuclearBase SequenceCathepsin GCathepsinsCell Cycle ProteinsDNA PrimersGenotypeHematopoietic Stem CellsHumansImmunophenotypingLeukemia, MyeloidMiceMice, TransgenicNuclear Matrix-Associated ProteinsNuclear ProteinsAntigens, NuclearCathepsin GCathepsinsCell Cycle ProteinsCTSG protein, humanCtsg protein, mouseDNA PrimersNuclear Matrix-Associated ProteinsNuclear ProteinsNUMA1 protein, humanNuma1 protein, mouseRARA protein, humanRara protein, mouseReceptors, Retinoic AcidRetinoic Acid Receptor alphaSerine Endopeptidases

Identifiers

PMID14737102
OpenAlexW2114645996

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.