Evidence map›Paper›PMID 20357260›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

TAp63 regulates VLA-4 expression and chronic lymphocytic leukemia cell migration to the bone marrow in a CD74-dependent manner.

Inbal Binsky, Frida Lantner, Valentin Grabovsky, Nurit Harpaz, Lev Shvidel, Alain Berrebi, David M Goldenberg, Lin Leng, Richard Bucala, Ronen Alon and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Cells · 2020
    Article
  8. MIF-Dependent Control of Tumor Immunity.Frontiers in immunology · 2020
    Review
  9. Knockdown of CD-74 in the Proliferative and Apoptotic Activity of Breast Cancer Cells.Open access Macedonian journal of medical sciences · 2019
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. CD74 is a novel transcription regulator.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

12 authors at 4 institutions in 2 countries.

Inbal BinskyDepartment of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Frida Lantner
Valentin Grabovsky
Nurit Harpaz
Lev Shvidel
Alain Berrebi
David M Goldenberg
Lin Leng
Richard Bucala
Ronen Alon
Michal Haran
Idit Shachar
Weizmann Institute of Science · ILKaplan Medical Center · ILYale University · USCenter for Molecular Medicine and Immunology · US

Funding

Targeted Therapy of B-cell MalignanciesP01CA103985 · NCI · CTR FOR MOLECULAR MEDICINE/IMMUNOLOGY · PI GOLDENBERG, DAVID M · 2005 to 2009
$7.0M
INNATE AND ADAPTIVE MECHANISMS IN ARTHRITISR01AR050498 · NIAMS · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2004 to 2013
$3.6M
NCI NIH HHS P01 CA103985NCI NIH HHS P01-CA103985NIAMS NIH HHS R01 AR050498
6 · The paper itself

Abstract

The hallmark of chronic lymphocytic leukemia (CLL) is the relentless accumulation of mature lymphocytes, mostly due to their decreased apoptosis. CD74 was recently shown to serve as a survival receptor on CLL cells. In this study, we show that stimulation of CD74 with its natural ligand, migration inhibitory factor, initiates a signaling cascade that results in upregulation of TAp63, which directly regulates CLL survival. In addition, TAp63 expression elevates the expression of the integrin VLA-4, particularly during the advanced stage of the disease. Blocking of CD74, TAp63, or VLA-4 inhibits the in vivo homing of CLL cells to the bone marrow (BM). Thus, CD74 and its target genes TAp63 and VLA-4 facilitate migration of CLL cells back to the BM, where they interact with the supportive BM environment that rescues them from apoptosis. These results could form the basis of novel therapeutic strategies aimed at blocking homing of CLL cells in their return to the BM and attenuating their survival.

Indexed as

AdultAgedAged, 80 and overAnimalsAntibodies, BlockingAntigens, Differentiation, B-LymphocyteAntigens, NeoplasmApoptosis Regulatory ProteinsBone Marrow CellsCell Migration InhibitionCell MovementCell SurvivalFemaleGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IIHumansAntibodies, BlockingAntigens, Differentiation, B-LymphocyteAntigens, NeoplasmApoptosis Regulatory ProteinsHistocompatibility Antigens Class IIIntegrin alpha4beta1Intramolecular Oxidoreductasesinvariant chainMacrophage Migration-Inhibitory FactorsMIF protein, humanTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID20357260
PMCPMC3129539
OpenAlexW2169087490

What OpenQuestion holds

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LicenceTDM
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.