Evidence map›Paper›PMID 23706991›Full record

ReviewSeminars in immunology2013

Complement inhibition in cancer therapy.

Ruben Pio, Daniel Ajona, John D Lambris

Abstract readReview
In one paragraph

Review in Seminars in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Pooled it
  3. Trial
  4. Liposomes in tumor treatment: a double-edged sword.Science China. Life sciences · 2026
    Review
  5. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Plasma proteome fingerprint in kidney diseases.Frontiers in molecular biosciences · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Neutrophils activated by membrane attack complexes increase the permeability of melanoma blood vessels.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 3 countries.

Ruben PioOncology Division, Center for Applied Medical Research-CIMA, Pamplona, Spain. rpio.@unav.es
Daniel Ajona
John D Lambris
Chartered Institute of Management Accountants · GBUniversity of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
NIAID NIH HHS AI068730NIAID NIH HHS P01 AI068730
6 · The paper itself

Abstract

For decades, complement has been recognized as an effector arm of the immune system that contributes to the destruction of tumor cells. In fact, many therapeutic strategies have been proposed that are based on the intensification of complement-mediated responses against tumors. However, recent studies have challenged this paradigm by demonstrating a tumor-promoting role for complement. Cancer cells seem to be able to establish a convenient balance between complement activation and inhibition, taking advantage of complement initiation without suffering its deleterious effects. Complement activation may support chronic inflammation, promote an immunosuppressive microenvironment, induce angiogenesis, and activate cancer-related signaling pathways. In this context, inhibition of complement activation would be a therapeutic option for treating cancer. This concept is relatively new and deserves closer attention. In this article, we summarize the mechanisms of complement activation on cancer cells, the cancer-promoting effect of complement initiation, and the rationale behind the use of complement inhibition as a therapeutic strategy against cancer.

Indexed as

AnimalsCarcinogenesisComplement ActivationComplement System ProteinsHumansImmunotherapyNeoplasmsNeovascularization, PathologicSignal TransductionTumor EscapeComplement System Proteinsage-related macular degenerationAMDAngiogenesisC1-INHC1 inhibitorCancer therapyComplement systemImmunosuppressionInflammationMACMDSCmembrane attack complexmyeloid-derived suppressor cellsregulatory T cellsTGF-βTLRtoll-like receptortransforming growth factor βTregsTumor microenvironment

Identifiers

PMID23706991
PMCPMC3733085
OpenAlexW2029566727

What OpenQuestion holds

Textmetadata
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.