Evidence map›Paper›PMID 19139084›Full record

ArticleBlood2009

Constitutive JAK3 activation induces lymphoproliferative syndromes in murine bone marrow transplantation models.

Melanie G Cornejo, Michael G Kharas, Miriam B Werneck, Séverine Le Bras, Sandra A Moore, Brian Ball, Marie Beylot-Barry, Scott J Rodig, Jon C Aster, Benjamin H Lee and 4 more

Abstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. "Next top" mouse models advancing CTCL research.Frontiers in cell and developmental biology · 2024
    Review
  8. NewCells · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. In vivo impact of JAK3 A573V mutation revealed using zebrafish.Cellular and molecular life sciences : CMLS · 2022
    Article
  13. Article
  14. The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021
    Review
  15. Article
  16. Identification of U937Frontiers in oncology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Genetic alterations of 9p24 in lymphomas and their impact for cancer (immuno-)therapy.Virchows Archiv : an international journal of pathology · 2019
    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

14 authors at 5 institutions in 2 countries.

Melanie G CornejoDivision of Hematology, Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Michael G Kharas
Miriam B Werneck
Séverine Le Bras
Sandra A Moore
Brian Ball
Marie Beylot-Barry
Scott J Rodig
Jon C Aster
Benjamin H Lee
Harvey Cantor
Jean-Philippe Merlio
D Gary Gilliland
Thomas Mercher
Brigham and Women's Hospital · USCentre Hospitalier Universitaire de Bordeaux · FRDana-Farber Cancer Institute · USBoston Children's Museum · USHarvard University · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
SIGNAL TRANSDUCTION PATHWAYS IN STABLE PHASE CHRONIC MYELOID LEUKEMIA CELLSP01DK050654 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN DAVID · 1996 to 2006
$10.3M
Howard Hughes Medical InstituteNCI NIH HHS CA66996NCI NIH HHS P01 CA066996NIDDK NIH HHS DK50654NIDDK NIH HHS P01 DK050654
6 · The paper itself

Abstract

The tyrosine kinase JAK3 plays a well-established role during normal lymphocyte development and is constitutively phosphorylated in several lymphoid malignancies. However, its contribution to lymphomagenesis remains elusive. In this study, we used the newly identified activating JAK3A572V mutation to elucidate the effect of constitutive JAK3 signaling on murine lymphopoiesis. In a bone marrow transplantation model, JAK3A572V induces an aggressive, fatal, and transplantable lymphoproliferative disorder characterized by the expansion of CD8(+)TCRalphabeta(+)CD44(+)CD122(+)Ly-6C(+) T cells that closely resemble an effector/memory T-cell subtype. Compared with wild-type counterparts, these cells show increased proliferative capacities in response to polyclonal stimulation, enhanced survival rates with elevated expression of Bcl-2, and increased production of interferon-gamma (IFNgamma) and tumor necrosis factor-alpha (TNFalpha), correlating with enhanced cytotoxic abilities against allogeneic target cells. Of interest, the JAK3A572V disease is epidermotropic and produces intraepidermal microabscesses. Taken together, these clinical features are reminiscent of those observed in an uncommon but aggressive subset of CD8(+) human cutaneous T-cell lymphomas (CTCLs). However, we also observed a CD4(+) CTCL-like phenotype when cells are transplanted in an MHC-I-deficient background. These data demonstrate that constitutive JAK3 activation disrupts T-cell homeostasis and induces lymphoproliferative diseases in mice.

Indexed as

Point MutationAnimalsAntigens, LyBone Marrow TransplantationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesEnzyme InductionHumansHyaluronan ReceptorsInterleukin-2 Receptor beta SubunitJanus Kinase 3Lymphoma, T-Cell, CutaneousLymphopoiesisLymphoproliferative DisordersMiceMice, Inbred C57BLAntigens, LyCd44 protein, mouseHyaluronan ReceptorsIl2rb protein, mouseInterleukin-2 Receptor beta SubunitJAK3 protein, humanJanus Kinase 3Ly-6C antigen, mouseReceptors, Antigen, T-Cell, alpha-betaRecombinant Fusion Proteins

Identifiers

PMID19139084
PMCPMC2661862
OpenAlexW2038312559

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.