Evidence map›Paper›PMID 21289859›Full record

ArticleOncoTargets and therapy2010

Survivin-T34A: molecular mechanism and therapeutic potential.

Jonathan R Aspe, Nathan R Wall

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Exosomes and cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2021
    Review
  9. Review
  10. Review
  11. In vivo gene delivery mediated by non-viral vectors for cancer therapy.Journal of controlled release : official journal of the Controlled Release Society · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Targeting PRPK Function Blocks Colon Cancer Metastasis.Molecular cancer therapeutics · 2018
    Article
  16. Survivin-Based Treatment Strategies for Squamous Cell Carcinoma.International journal of molecular sciences · 2018
    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 at 1 institution in 1 country.

Jonathan R AspeCenter for Health Disparities, Research and Molecular Medicine, Division of Biochemistry and Microbiology, Department of Basic Sciences, Loma Linda University, Loma Linda, CA, USA.
Nathan R Wall
Loma Linda University · US

Funding

NIH-LLU Initiative for Maximizing Student DiversityR25GM060507 · NIGMS · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2001 to 2022
$11.3M
The role of imidazoline receptor in type-2 diabetesP20MD001632 · NIMHD · LOMA LINDA UNIVERSITY · PI DELEON, DAISY · 2005 to 2009
$8.0M
Research Training/Education CoreP20MD006988 · NIMHD · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2012 to 2016
$6.2M
NIGMS NIH HHS R25 GM060507NIMHD NIH HHS L60 MD002849NIMHD NIH HHS P20 MD001632NIMHD NIH HHS P20 MD006988
6 · The paper itself

Abstract

The inhibitor of apoptosis protein survivin's threonine 34 to alanine (T34A) mutation abolishes a phosphorylation site for p34(cdc2)-cyclin B1, resulting in initiation of the mitochondrial apoptotic pathway in cancer cells; however, it has little known direct effects on normal cells. The possibility that targeting survivin in this way may provide a novel approach for selective cancer gene therapy has yet to be fully evaluated. Although a flurry of work was undertaken in the late 1990s and early 2000s, only minor advances on this mutant have recently taken place. We recently described that cells generated to express a stable form of the mutant protein released this survivin-T34A to the conditioned medium. When this conditioned medium was collected and deposited on naive tumor cells, conditioned medium T34A was as effective as some chemotherapeutics in the induction of tumor cell apoptosis, and when combined with other forms of genotoxic stressors potentiated their killing effects. We hope with this review to revitalize the T34A field, as there is still much that needs to be investigated. In addition to determining the therapeutic dose and the duration of drug therapy required at the disease site, a better understanding of other key factors is also important. These include knowledge of target cell populations, cell-surface receptors, changes that occur in the target tissue at the molecular and cellular level with progression of the disease, and the mechanism and site of therapeutic action.

Indexed as

apoptosisproliferationsurvivinT34Atherapy

Identifiers

PMID21289859
PMCPMC3024888
OpenAlexW2060693285

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.