Evidence map›Paper›PMID 26108219›Full record

ReviewOpen biology2015

LMO2 at 25 years: a paradigm of chromosomal translocation proteins.

Jennifer Chambers, Terence H Rabbitts

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.3field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. LMO2 Regulates Epithelial-Mesenchymal Plasticity of Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2026
    Article
  3. Impact of aging on CD146Frontiers in bioengineering and biotechnology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. The LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. LMO2 expression is frequent in T-lymphoblastic leukemia and correlates with survival, regardless of T-cell stage.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  15. Article
  16. Lessons to cancer from studies of leukemia and hematopoiesis.Frontiers in cell and developmental biology · 2022
    Review
  17. A Combined HumanFrontiers in pharmacology · 2022
    Article
  18. Article
  19. Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells.International journal of molecular sciences · 2021
    Review
  20. Fli1Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

2 authors at 2 institutions in 3 countries.

Jennifer ChambersMRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Terence H RabbittsMRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK terence.rabbitts@imm.ox.ac.uk.
Google (United States) · USJohn Radcliffe Hospital · GB

Funding

Medical Research Council G0600914Medical Research Council MC_UU_12009/17Medical Research Council MR/J000612/1Wellcome Trust
6 · The paper itself

Abstract

LMO2 was first discovered through proximity to frequently occurring chromosomal translocations in T cell acute lymphoblastic leukaemia (T-ALL). Subsequent studies on its role in tumours and in normal settings have highlighted LMO2 as an archetypical chromosomal translocation oncogene, activated by association with antigen receptor gene loci and a paradigm for translocation gene activation in T-ALL. The normal function of LMO2 in haematopoietic cell fate and angiogenesis suggests it is a master gene regulator exerting a dysfunctional control on differentiation following chromosomal translocations. Its importance in T cell neoplasia has been further emphasized by the recurrent findings of interstitial deletions of chromosome 11 near LMO2 and of LMO2 as a target of retroviral insertion gene activation during gene therapy trials for X chromosome-linked severe combined immuno-deficiency syndrome, both types of event leading to similar T cell leukaemia. The discovery of LMO2 in some B cell neoplasias and in some epithelial cancers suggests a more ubiquitous function as an oncogenic protein, and that the current development of novel inhibitors will be of great value in future cancer treatment. Further, the role of LMO2 in angiogenesis and in haematopoietic stem cells (HSCs) bodes well for targeting LMO2 in angiogenic disorders and in generating autologous induced HSCs for application in various clinical indications.

Indexed as

Adaptor Proteins, Signal TransducingHumansLeukemia, T-CellLIM Domain ProteinsProto-Oncogene ProteinsTranslocation, GeneticAdaptor Proteins, Signal TransducingLIM Domain ProteinsLMO2 protein, humanProto-Oncogene Proteinsangiogenesischromosomal translocationshaematopoiesisleukaemiaLMO2X chromosome-linked severe combined immuno-deficiency syndrome

Identifiers

PMID26108219
PMCPMC4632508
OpenAlexW2099676339

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.