Evidence map›Paper›PMID 17043144›Full record

ArticleThe Journal of experimental medicine2006

Triggering CD40 on endothelial cells contributes to tumor growth.

Claudia Chiodoni, Manuela Iezzi, Cristiana Guiducci, Sabina Sangaletti, Isabella Alessandrini, Chiara Ratti, Francesca Tiboni, Piero Musiani, D Neil Granger, Mario P Colombo

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Effective anti-neu-initiated antitumor responses require the complex role of CD4+ T cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  20. Agonistic CD40 antibodies and cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Claudia ChiodoniImmunotherapy and Gene Therapy Unit, Department of Experimental Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, 20133 Milan, Italy.
Manuela Iezzi
Cristiana Guiducci
Sabina Sangaletti
Isabella Alessandrini
Chiara Ratti
Francesca Tiboni
Piero Musiani
D Neil Granger
Mario P Colombo
Fondazione IRCCS Istituto Nazionale dei Tumori · ITUniversity of Chieti-Pescara · ITLouisiana State University Health Sciences Center Shreveport · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory cells can either promote or inhibit tumor growth. Here we studied whether CD40, a key molecule for adaptive immune response, has any role in mammary carcinogenesis of BALB/NeuT transgenic tumor-prone mice. We transferred the HER2/neu oncogene into CD40-null background to obtain the CD40-KO/NeuT strain. CD40-KO/NeuT mice showed delayed tumor onset and reduced tumor multiplicity. BM (BM) transplantation experiments excluded a role of BM-derived cells in the reduced tumorigenicity associated with CD40 deficiency. Rather, CD40 expressed by endothelial cells (ECs) takes part to the angiogenic process. Accordingly, large vessels, well organized around the tumor lobular structures, characterize BALB/NeuT tumors, whereas tiny numerous vessels with scarce extracellular matrix are dispersed in the parenchyma of poorly organized CD40-KO/NeuT tumors. Activated platelets, which may interact with and activate ECs, are a possible source of CD40L. Their localization within tumor vessels prompted the idea of treating BALB/NeuT and CD40-KO/NeuT mice chronically with the anti-platelet drug clopidogrel, known to inhibit platelet CD40L expression. Treatment of BALB/NeuT mice reduced tumor growth to a level similar to CD40-deficient mice, whereas CD40-KO/NeuT mice treated or not showed the same attenuated tumor outgrowth, indicating that activated platelets are the likely source of CD40L in this model. Collectively, these data point to a participation of CD40/CD40L in the angiogenic processes associated with mammary carcinogenesis of BALB/NeuT mice.

Indexed as

Cell ProliferationAnimalsCD40 AntigensEndothelium, VascularFemaleMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicRatsCD40 Antigens

Identifiers

PMID17043144
PMCPMC2118135
OpenAlexW2170640588

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.