Evidence map›Paper›PMID 26343199›Full record

ReviewPharmacology & therapeutics2015

Therapeutic applications of TRAIL receptor agonists in cancer and beyond.

Gustavo P Amarante-Mendes, Thomas S Griffith

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors.

Gustavo P Amarante-MendesDepartamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, SP, Brazil; Instituto de Investigação em Imunologia, Instituto Nacional de Ciência e Tecnologia, Brazil. Electronic address: gpam@usp.br.
Thomas S GriffithDepartment of Urology, Masonic Cancer Center, Center for Immunology, University of Minnesota, Minneapolis, MN, USA; Minneapolis VA Health Care System, Minneapolis, MN 55417, USA. Electronic address: tgriffit@umn.edu.

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
TRAIL-expressing Recombinant Adenovirus Based Immunotherapy for RCCR01CA109446 · NCI · UNIVERSITY OF MINNESOTA · PI GRIFFITH, THOMAS S · 2004 to 2013
$2.6M
Using microbially-experienced mice to study the innate immune response in sepsisI01BX001324 · VA · MINNEAPOLIS VA MEDICAL CENTER · PI GRIFFITH, THOMAS S · 2013 to 2025
–
BLRD VA I01 BX001324NCI NIH HHS CA109446NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA109446
6 · The paper itself

Abstract

TRAIL/Apo-2L is a member of the TNF superfamily first described as an apoptosis-inducing cytokine in 1995. Similar to TNF and Fas ligand, TRAIL induces apoptosis in caspase-dependent manner following TRAIL death receptor trimerization. Because tumor cells were shown to be particularly sensitive to this cytokine while normal cells/tissues proved to be resistant along with being able to synthesize and release TRAIL, it was rapidly appreciated that TRAIL likely served as one of our major physiologic weapons against cancer. In line with this, a number of research laboratories and pharmaceutical companies have attempted to exploit the ability of TRAIL to kill cancer cells by developing recombinant forms of TRAIL or TRAIL receptor agonists (e.g., receptor-specific mAb) for therapeutic purposes. In this review article we will describe the biochemical pathways used by TRAIL to induce different cell death programs. We will also summarize the clinical trials related to this pathway and discuss possible novel uses of TRAIL-related therapies. In recent years, the physiological importance of TRAIL has expanded beyond being a tumoricidal molecule to one critical for a number of clinical settings - ranging from infectious disease and autoimmunity to cardiovascular anomalies. We will also highlight some of these conditions where modulation of the TRAIL/TRAIL receptor system may be targeted in the future.

Indexed as

AnimalsAntineoplastic AgentsCell DeathHumansImmunotherapyNeoplasmsReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandAntineoplastic AgentsReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandApoptosisCancerCell deathImmune therapyTRAIL

Identifiers

PMID26343199
PMCPMC4955572

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.