Evidence map›Paper›PMID 24095735›Full record

ArticleCell reports2013

Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia.

Samantha B Foley, Zacariah L Hildenbrand, Abigail A Soyombo, Jeffery A Magee, Yipin Wu, Katherine I Oravecz-Wilson, Theodora S Ross

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. 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 12% 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, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Engineering chromosome rearrangements in cancer.Disease models & mechanisms · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. miRNome profiling of LSC-enriched CD34Frontiers in pharmacology · 2020
    Article
  12. Review
  13. [Clinical characteristics of chronic myeloid leukemia with T315I mutation and the efficacy of ponatinib].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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 2 institutions in 1 country.

Samantha B FoleyDepartment of Internal Medicine and Cancer Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Zacariah L Hildenbrand
Abigail A Soyombo
Jeffery A Magee
Yipin Wu
Katherine I Oravecz-Wilson
Theodora S Ross
The University of Texas Southwestern Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

Huntington Interacting Protein-1(HIP1) and the Promotion of NeoplasiaR01CA098730 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ROSS, THEODORA S · 2003 to 2012
$2.6M
MECHANISM OF TRANSFORMATION BY HIP1/PDGFBRR01CA082363 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, THEODORA S · 2000 to 2004
$1.3M
NCI NIH HHS R01 CA082363NCI NIH HHS R01 CA098730NCI NIH HHS R01 CA098730-01NCI NIH HHS R01 CA82363-03
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) and some acute lymphoblastic leukemias are characterized by the t(9;22) chromosome, which encodes the BCR/ABL oncogene. Multiple mouse models of CML express BCR/ABL at high levels from non-Bcr promoters, resulting in the development of leukemias. In contrast, a significant fraction of healthy humans have been found to have BCR/ABL-positive hematopoietic cells. To bridge the gap between the information derived from current mouse models and nonleukemic humans with the BCR/ABL oncogene, we generated a knockin model with BCR/ABL p210 expressed from the Bcr locus. Unlike previous models, expression of BCR/ABL from the knockin allele did not induce leukemia. BCR/ABL mutant cells did exhibit favorable bone marrow engraftment compared to control cells. These data suggest that BCR/ABL expression alone is insufficient to induce disease. This model allows for inducible spatial and temporal control of BCR/ABL expression for analysis of early steps in the pathogenesis of BCR/ABL-expressing leukemias.

Indexed as

AllelesAnimalsBone Marrow TransplantationCell Transformation, NeoplasticFusion Proteins, bcr-ablGene Expression RegulationGene Knock-In TechniquesHumansLeukemia, MyeloidMiceMice, TransgenicFusion Proteins, bcr-abl

Identifiers

PMID24095735
PMCPMC3832111
OpenAlexW2022192516

What OpenQuestion holds

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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.