Evidence map›Paper›PMID 25627204›Full record

ArticleJournal of medical microbiology2015

Pseudomonas aeruginosa exotoxin T induces potent cytotoxicity against a variety of murine and human cancer cell lines.

Joe Goldufsky, Stephen Wood, Behnam Hajihossainlou, Tooba Rehman, Omar Majdobeh, Howard L Kaufman, Carl E Ruby, Sasha H Shafikhani

Erratum issuedAbstract read
In one paragraph

Article in Journal of medical microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Cells · 2023
    Review
  7. Cells · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Frontiers in oncology · 2022
    Review
  12. Article
  13. Review
  14. Bacteriotherapy in Breast Cancer.International journal of molecular sciences · 2019
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Joe GoldufskyDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA.
Stephen WoodDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA.
Behnam HajihossainlouDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA.
Tooba RehmanDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA.
Omar MajdobehDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA.
Howard L KaufmanRutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Carl E RubyDepartment of Surgery, Rush University Medical Center, Chicago, IL, USA Sarepta Therapeutics, Corvallis, OR, USA.
Sasha H ShafikhaniDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL, USA Rush University Cancer Center, Rush University Medical Center, Chicago, IL, USA sasha_shafikhani@rush.edu.
Rush University Medical Center · USRutgers Cancer Institute of New Jersey

Funding

Molecular dissection of Pseudomonas aeruginosa Exotoxin T virulence functionsR21AI110685 · NIAID · RUSH UNIVERSITY MEDICAL CENTER · PI SHAFIKHANI, SASHA H · 2015 to 2016
$426k
NIAID NIH HHS R21 AI110685
6 · The paper itself

Abstract

In patients with malignancy, the major barrier to achieving complete response is emergence of resistance to current chemotherapeutic agents. One of the major mechanisms by which tumour cells become resistant to therapies is by altering cellular drug targets through mutations and/or deletions. Resistance by this mechanism is achieved more easily if the drug has limited cellular targets and/or processes. We hypothesized that as Pseudomonas aeruginosa exotoxin T (ExoT) targets six proteins that are required for cancer cell survival and proliferation, it is highly unlikely for cancer cells to develop resistance to this toxin. We assessed ExoT's cytotoxicity against multiple invasive and highly resistant tumour cell lines in order to evaluate its potential as a chemotherapeutic agent. Our data demonstrated that ExoT induced potent cytotoxicity in all tumour cell lines that we examined. Collectively, our data highlighted the potential of ExoT as a possible chemotherapeutic candidate for the treatment of cancer.

Indexed as

ADP Ribose TransferasesAnimalsAntineoplastic AgentsCell Line, TumorCell SurvivalFemaleGTPase-Activating ProteinsHumansMiceADP Ribose TransferasesAntineoplastic AgentsExoT protein, Pseudomonas aeruginosaGTPase-Activating Proteins

Identifiers

PMID25627204
PMCPMC4811650
OpenAlexW2055036892

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.