Evidence map›Paper›PMID 22643706›Full record

ArticleLeukemia2012

T-cell receptor diversity prevents T-cell lymphoma development.

S Newrzela, N Al-Ghaili, T Heinrich, M Petkova, S Hartmann, B Rengstl, A Kumar, H-M Jäck, S Gerdes, I Roeder and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Modifying enzyme replacement therapy - A perspective.Journal of cellular and molecular medicine · 2023
    Review
  7. Precision medicine: In vivo CAR therapy as a showcase for receptor-targeted vector platforms.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  8. Article
  9. Review
  10. Two cases of T cell lymphoma following Piggybac-mediated CAR T cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. T cell engineering as therapy for cancer and HIV: our synthetic future.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  20. Engineering T Cells to Functionally Cure HIV-1 Infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    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

12 authors at 6 institutions in 2 countries.

S NewrzelaSenckenberg Institute of Pathology, Goethe-University Hospital, Frankfurt am Main, Germany.
N Al-Ghaili
T Heinrich
M Petkova
S Hartmann
B Rengstl
A Kumar
H-M Jäck
S Gerdes
I Roeder
M-L Hansmann
D von Laer
Goethe University Frankfurt · DEUniversity Hospital Frankfurt · DEGeorg Speyer Haus · DEUniversity Hospital Carl Gustav Carus · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEInnsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mature T-cell lymphomas (MTCLs) have an extremely poor prognosis and are much less frequent than immature T-cell leukemias. This suggests that malignant outgrowth of mature T lymphocytes is well controlled. Indeed, in a previous study we found that mature T cells are resistant to transformation with known T-cell oncogenes. Here, however, we observed that T-cell receptor (TCR) mono-/oligoclonal mature T cells from TCR transgenic (tg) mice (OT-I, P14) expressing the oncogenes NPM/ALK or ΔTrkA readily developed MTCLs in T-cell-deficient recipients. Analysis of cell surface markers largely ruled out that TCR tg lymphomas were derived from T-cell precursors. Furthermore, cotransplanted non-modified TCR polyclonal T cells suppressed malignant outgrowth of oncogene expressing TCR tg T lymphocytes. A dominant role of an anti-leukemic immune response or Tregs in the control of MTCLs seems unlikely as naïve T cells derived from oncogene expressing stem cells, which should be tolerant to leukemic antigens, as well as purified CD4 and CD8 were resistant to transformation. However, our results are in line with a model in which homeostatic mechanisms that stabilize the diversity of the normal T-cell repertoire, for example, clonal competition, also control the outgrowth of potentially malignant T-cell clones. This study introduces a new innate mechanism of lymphoma control.

Indexed as

AnimalsBlotting, WesternCell DifferentiationCell Transformation, NeoplasticFemaleFlow CytometryHematopoietic Stem CellsHumansLymphoma, T-CellMaleMiceMice, Inbred C57BLMice, SCIDMice, TransgenicPhosphoproteinsPrecursor Cells, T-LymphoidPhosphoproteinsReceptors, Antigen, T-Cell

Identifiers

PMID22643706
OpenAlexW2075993231

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.