Evidence map›Paper›PMID 15141159›Full record

ArticleGene therapy2004

Tumor-specific gene expression using the survivin promoter is further increased by hypoxia.

L Yang, Z Cao, F Li, D E Post, E G Van Meir, H Zhong, W C Wood

Abstract read
In one paragraph

Article in Gene therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Arylsulfonamide 64B Inhibits Hypoxia/HIF-Induced Expression of c-Met and CXCR4 and Reduces Primary Tumor Growth and Metastasis of Uveal Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Arylsulfonamide KCN1 inhibits in vivo glioma growth and interferes with HIF signaling by disrupting HIF-1α interaction with cofactors p300/CBP.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    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

7 authors at 2 institutions in 1 country.

L YangDepartment of Surgery, Emory University School of Medicine, Atlanta, GA 30322, USA.
Z Cao
F Li
D E Post
E G Van Meir
H Zhong
W C Wood
Emory University · USRoswell Park Comprehensive Cancer Center · US

Funding

THERAPEUTIC MODULATION OF ANGIOGENESIS IN HUMAN GLIOMASR01CA086335 · NCI · EMORY UNIVERSITY · PI VAN MEIR, ERWIN G. · 2000 to 2011
$3.9M
A hypoxia-dependent adenovirus for glioma therapyR01CA087830 · NCI · EMORY UNIVERSITY · PI VAN MEIR, ERWIN G · 2002 to 2005
$1.3M
IAPs As Novel Targets for Cancer TherapyR01CA095643 · NCI · EMORY UNIVERSITY · PI YANG, LILY · 2003 to 2007
$1.2M
Hypoxia as a target for the treatment of brain tumorsR21NS041403 · NINDS · EMORY UNIVERSITY · PI VAN MEIR, ERWIN G · 2001 to 2003
$571k
DEATH SIGNALING IN HSV-TK GENE MODIFIED TUMOR CELLSR29CA080017 · NCI · EMORY UNIVERSITY · PI YANG, LILY · 1999 to 2003
$425k
NCI NIH HHS CA80017NCI NIH HHS CA86335NCI NIH HHS CA87830NCI NIH HHS CA95643NCI NIH HHS R01 CA086335NCI NIH HHS R01 CA095643NCI NIH HHS R29 CA080017NINDS NIH HHS NS41403
6 · The paper itself

Abstract

Increasing evidence indicates that survivin, an inhibitor of apoptosis protein (IAP), is expressed in human cancer cells but is absent from most normal adult tissues. Here, we examined the feasibility of using a survivin promoter (Sur-P) to direct therapeutic expression of a proapoptotic gene specifically in human tumor cells. First, we demonstrated that this promoter was highly active in human tumor cells but not in normal cells. Second, we found that Sur-P activity was upregulated by hypoxia in tumor cells. Third, to further enhance this promoter's activity under hypoxia, we added a hypoxia-responsive element (HRE) from the vascular endothelial growth factor gene promoter in its 5' region, and showed that this combination resulted in a further increase in the level of gene expression in hypoxic tumor cells. Finally, we demonstrated that expression of an autocatalytic reverse caspase-3 gene by this promoter specifically induced apoptotic cell death in human tumor cells but not in normal cells. These findings support the use of promoters Sur-P or chimeric HRE-Sur-P for generating novel vectors for cancer gene therapy.

Indexed as

Promoter Regions, GeneticApoptosisBlotting, WesternBreast NeoplasmsCaspase 3Caspase InhibitorsCell LineCell Line, TumorFemaleGene ExpressionGenetic TherapyHumansHypoxiaInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsBIRC5 protein, humanCASP3 protein, humanCaspase 3Caspase InhibitorsInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsRecombinant Fusion ProteinsSurvivinVascular Endothelial Growth Factor A

Identifiers

PMID15141159
PMCPMC3163156
OpenAlexW2092386950

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.