Evidence map›Paper›PMID 32130407›Full record

ArticleBlood advances2020

Progression of AITL-like tumors in mice is driven by Tfh signature proteins and T-B cross talk.

Mariko Witalis, Jinsam Chang, Ming-Chao Zhong, Yasser Bouklouch, Vincent Panneton, Joanna Li, Thorsten Buch, Seok Jin Kim, Won Seog Kim, Young Hyeh Ko and 2 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. TCR Pathway Mutations in Mature T Cell Lymphomas.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  8. Article
  9. Targeting TNature immunology · 2022
    Review
  10. Article
  11. Update on recurrent mutations in angioimmunoblastic T-cell lymphoma.International journal of clinical and experimental pathology · 2021
    Review
  12. Review
  13. Review
  14. 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

12 authors at 6 institutions in 3 countries.

Mariko WitalisInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Jinsam ChangInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Ming-Chao ZhongInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Yasser BouklouchInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Vincent PannetonInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Joanna LiInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Thorsten BuchInstitute of Laboratory Animal Science, University of Zürich, Zürich, Switzerland; and.
Seok Jin KimSamsung Medical Center, Sungkyunkwan University, Seoul, Korea.
Won Seog KimSamsung Medical Center, Sungkyunkwan University, Seoul, Korea.
Young Hyeh KoSamsung Medical Center, Sungkyunkwan University, Seoul, Korea.
André VeilletteInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
Woong-Kyung SuhInstitut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, Canada.
McGill University · CAUniversité de Montréal · CAMontreal Clinical Research Institute · CASamsung Medical Center · KRSungkyunkwan University · KRUniversity of Zurich · CH

Funding

CIHR FDN-143338CIHR MOP-82906CIHR MT-14429
6 · The paper itself

Abstract

Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma driven by a pool of neoplastic cells originating from T follicular helper (Tfh) cells and concomitant expansion of B cells. Conventional chemotherapies for AITL have shown limited efficacy, and as such, there is a need for improved therapeutic options. Because AITL originates from Tfh cells, we hypothesized that AITL tumors continue to rely on essential Tfh components and intimate T-cell-B-cell (T-B) interactions. Using a spontaneous AITL mouse model (Roquinsan/+ mice), we found that acute loss of Bcl6 activity in growing tumors drastically reduced tumor size, demonstrating that AITL-like tumors critically depend on the Tfh lineage-defining transcription factor Bcl6. Because Bcl6 can upregulate expression of signaling lymphocytic activation molecule-associated protein (SAP), which is known to promote T-B conjugation, we next targeted the SAP-encoding Sh2d1a gene. We observed that Sh2d1a deletion from CD4+ T cells in fully developed tumors also led to tumor regression. Further, we provide evidence that tumor progression depends on T-B cross talk facilitated by SAP and high-affinity LFA-1. In our study, AITL-like tumors relied heavily on molecular pathways that support Tfh cell identity and T-B collaboration, revealing potential therapeutic targets for AITL.

Indexed as

Immunoblastic LymphadenopathyLymphoma, T-Cell, PeripheralAnimalsMiceT-Lymphocytes, Helper-InducerTranscription FactorsTranscription Factors

Identifiers

PMID32130407
PMCPMC7065475
OpenAlexW3009821158

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.