Evidence map›Paper›PMID 23744294›Full record

ArticleCell death and differentiation2014

Contribution of humoral immune responses to the antitumor effects mediated by anthracyclines.

D Hannani, C Locher, T Yamazaki, V Colin-Minard, M Vetizou, L Aymeric, S Viaud, D Sanchez, M J Smyth, P Bruhns and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. EZH2 elicits CD8Communications biology · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Targeting disease by immunomodulation.Cell death and differentiation · 2015
    Article
  16. Multiplexed quantitative analysis of CD3, CD8, and CD20 predicts response to neoadjuvant chemotherapy in breast cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  17. Review
  18. 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.

D Hannani1] INSERM U1015, Equipe labellisée Ligue contre le Cancer, Villejuif, France [2] Institut de Cancérologie Gustave Roussy, Villejuif, France [3] University of Paris Sud XI, Villejuif, France.
C Locher
T Yamazaki
V Colin-Minard
M Vetizou
L Aymeric
S Viaud
D Sanchez
M J Smyth
P Bruhns
G Kroemer
L Zitvogel
Université Paris-Sud · FRInserm · FRCzech Academy of Sciences, Institute of Microbiology · CZDélégation Paris 5 · FRInstitut Gustave Roussy · FRThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunogenic cell death induced by cytotoxic compounds contributes to the success of selected chemotherapies by eliciting a protective anticancer immune response, which is mediated by CD4(+) and CD8(+) T cells producing interferon-γ. In many instances, cancer progression is associated with high titers of tumor-specific antibodies, which become detectable in the serum, but whose functional relevance is elusive. Here, we explored the role of humoral immune responses in the anticancer efficacy of anthracyclines. Chemotherapy reduced the number of tumor-infiltrating B cells, and failed to promote humoral responses against immunodominant tumor antigens. Although anthracycline-based anticancer chemotherapies failed in T cell-deficient mice, they successfully reduced the growth of cancers developing in mice lacking B lymphocytes (due to the injection of a B-cell-depleting anti-CD20 antibody), immunoglobulins (Igs) or Ig receptors (Fc receptor) due to genetic manipulations. These results suggest that the humoral arm of antitumor immunity is dispensable for the immune-dependent therapeutic effect of anthracyclines against mouse sarcoma. In addition, we show here that the titers of IgA and IgG antibodies directed against an autoantigen appearing at the cell surface of tumor cells post chemotherapy (calreticulin, CRT) did not significantly increase in patients treated with anthracyclines, and that anti-CRT antibodies had no prognostic or predictive significance. Collectively, our data indicate that humoral anticancer immune responses differ from cellular responses in, thus far, that they do not contribute to the success of anthracycline-mediated anticancer therapies in human breast cancers and mouse sarcomas.

Indexed as

Immunity, HumoralAnimalsAnthracyclinesAntibodiesAntineoplastic AgentsApoptosisB-LymphocytesBreast NeoplasmsCalreticulinCell Line, TumorFemaleHumansMiceMice, Inbred C57BLMiddle AgedReceptors, FcAnthracyclinesAntibodiesAntineoplastic AgentsCalreticulinReceptors, Fc

Identifiers

PMID23744294
PMCPMC3857618
OpenAlexW2001076778

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.