ReviewFrontiers in immunology2016
Is the Antitumor Property of Trypanosoma cruzi Infection Mediated by Its Calreticulin?
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Promising effects of parasite-derived compounds on tumor regression: a systematic review of in vitro and in vivo studies.Environmental science and pollution research international · 2022Pooled it
- An Atomic Force Microscopy analysis of Exosomes derived from Tumor Associated pluripotent Mesenchymal Stem Cells.Fortune journal of health sciences · 2026Article
- Parasite-enhanced immunotherapy: transforming the "cold" tumors to "hot" battlefields.Cell communication and signaling : CCS · 2024Review
- Review
- A novel enemy of cancer: recent investigations into protozoan anti-tumor properties.Frontiers in cellular and infection microbiology · 2023Review
- The many faces of parasite calreticulin.Frontiers in immunology · 2023Review
- Anti-Tumor Effect of Parasitic Protozoans.Bioengineering (Basel, Switzerland) · 2022Review
- Modulation of Inflammation-Induced Tolerance in Cancer.Frontiers in immunology · 2020Review
- Review
- Review
- Does native Trypanosoma cruzi calreticulin mediate growth inhibition of a mammary tumor during infection?BMC cancer · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eight to 10 million people in 21 endemic countries are infected with Trypanosoma cruzi. However, only 30% of those infected develop symptoms of Chagas' disease, a chronic, neglected tropical disease worldwide. Similar to other pathogens, T. cruzi has evolved to resist the host immune response. Studies, performed 80 years ago in the Soviet Union, proposed that T. cruzi infects tumor cells with similar capacity to that displayed for target tissues such as cardiac, aortic, or digestive. An antagonistic relationship between T. cruzi infection and cancer development was also proposed, but the molecular mechanisms involved have remained largely unknown. Probably, a variety of T. cruzi molecules is involved. This review focuses on how T. cruzi calreticulin (TcCRT), exteriorized from the endoplasmic reticulum, targets the first classical complement component C1 and negatively regulates the classical complement activation cascade, promoting parasite infectivity. We propose that this C1-dependent TcCRT-mediated virulence is critical to explain, at least an important part, of the parasite capacity to inhibit tumor development. We will discuss how TcCRT, by directly interacting with venous and arterial endothelial cells, inhibits angiogenesis and tumor growth. Thus, these TcCRT functions not only illustrate T. cruzi interactions with the host immune defensive strategies, but also illustrate a possible co-evolutionary adaptation to privilege a prolonged interaction with its host.
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Registered trials
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.