Evidence map›Paper›PMID 14718672›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Ectopic expression of the homeobox gene Cdx2 is the transforming event in a mouse model of t(12;13)(p13;q12) acute myeloid leukemia.

Vijay P S Rawat, Monica Cusan, Aniruddha Deshpande, Wolfgang Hiddemann, Leticia Quintanilla-Martinez, R Keith Humphries, Stefan K Bohlander, Michaela Feuring-Buske, Christian Buske

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 110 citations in OpenAlex.

  1. Review
  2. Haematologica · 2024
    Article
  3. Article
  4. HOXA9 Regulome and Pharmacological Interventions in Leukemia.Advances in experimental medicine and biology · 2024
    Review
  5. Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Deregulation of the HOXA9/MEIS1 axis in acute leukemia.Current opinion in hematology · 2016
    Review
  18. Review
  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

9 authors at 3 institutions in 2 countries.

Vijay P S RawatGSF-Clinical Cooperative Group Leukemia and Department of Medicine III, Grosshadern, Ludwig Maximilians University, 81377 Munich, Germany.
Monica Cusan
Aniruddha Deshpande
Wolfgang Hiddemann
Leticia Quintanilla-Martinez
R Keith Humphries
Stefan K Bohlander
Michaela Feuring-Buske
Christian Buske
University of British Columbia · CABC Cancer Agency · CALudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Creation of fusion genes by balanced chromosomal translocations is one of the hallmarks of acute myeloid leukemia (AML) and is considered one of the key leukemogenic events in this disease. In t(12;13)(p13;q12) AML, ectopic expression of the homeobox gene CDX2 was detected in addition to expression of the ETV6-CDX2 fusion gene, generated by the chromosomal translocation. Here we show in a murine model of t(12;13)(p13;q12) AML that myeloid leukemogenesis is induced by the ectopic expression of CDX2 and not by the ETV6-CDX2 chimeric gene. Mice transplanted with bone marrow cells retrovirally engineered to express Cdx2 rapidly succumbed to fatal and transplantable AML. The transforming capacity of Cdx2 depended on an intact homeodomain and the N-terminal transactivation domain. Transplantation of bone marrow cells expressing ETV6-CDX2 failed to induce leukemia. Furthermore, coexpression of ETV6-CDX2 and Cdx2 in bone marrow cells did not accelerate the course of disease in transplanted mice compared to Cdx2 alone. These data demonstrate that activation of a protooncogene by a balanced chromosomal translocation can be the pivotal leukemogenic event in AML, characterized by the expression of a leukemia-specific fusion gene. Furthermore, these findings link protooncogene activation to myeloid leukemogenesis, an oncogenic mechanism so far associated mainly with lymphoid leukemias and lymphomas.

Indexed as

Genes, HomeoboxAnimalsBone Marrow TransplantationCDX2 Transcription FactorCell Transformation, NeoplasticChromosomes, Human, Pair 12Chromosomes, Human, Pair 13Disease Models, AnimalETS Translocation Variant 6 ProteinGene ExpressionHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMiceMice, Inbred C3HMice, Inbred C57BLCDX2 Transcription FactorETS Translocation Variant 6 ProteinETV6-CDX2 protein, humanhomeobox protein HOXA9Homeodomain ProteinsMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsOncogene Proteins, FusionTrans-Activators

Identifiers

PMID14718672
PMCPMC321764
OpenAlexW2026414440

What Socratic 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 Socratic graph.