Evidence map›Paper›PMID 15647352›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Targeting gene expression selectively in cancer cells by using the progression-elevated gene-3 promoter.

Zhao-Zhong Su, Devanand Sarkar, Luni Emdad, Gregory J Duigou, Charles S H Young, Joy Ware, Aaron Randolph, Kristoffer Valerie, Paul B Fisher

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 77 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Zhao-Zhong SuDepartment of Pathology, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY 10032, USA.
Devanand Sarkar
Luni Emdad
Gregory J Duigou
Charles S H Young
Joy Ware
Aaron Randolph
Kristoffer Valerie
Paul B Fisher
Columbia University Irving Medical Center · USVirginia Commonwealth University Medical Center · US

Funding

MDA-7: Novel Cancer Therapeutic GeneR01CA097318 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2002 to 2012
$2.8M
PROGRESSION OF THE TRANSFORMED PHENOTYPER01CA035675 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 1985 to 2007
$1.9M
Novel Approaches for Pancreatic Cancer TherapyR01CA098712 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2003 to 2007
$1.8M
NCI NIH HHS R01 CA035675NCI NIH HHS R01 CA097318NCI NIH HHS R01 CA098712
6 · The paper itself

Abstract

One impediment to effective cancer-specific gene therapy is the rarity of regulatory sequences targeting gene expression selectively in tumor cells. Although many tissue-specific promoters are recognized, few cancer-selective gene promoters are available. Progression-elevated gene-3 (PEG-3) is a rodent gene identified by subtraction hybridization that displays elevated expression as a function of transformation by diversely acting oncogenes, DNA damage, and cancer cell progression. The promoter of PEG-3, PEG-Prom, displays robust expression in a broad spectrum of human cancer cell lines with marginal expression in normal cellular counterparts. Whereas GFP expression, when under the control of a CMV promoter, is detected in both normal and cancer cells, when GFP is expressed under the control of the PEG-Prom, cancer-selective expression is evident. Mutational analysis identifies the AP-1 and PEA-3 transcription factors as primary mediators of selective, cancer-specific expression of the PEG-Prom. Synthesis of apoptosis-inducing genes, under the control of the CMV promoter, inhibits the growth of both normal and cancer cells, whereas PEG-Prom-mediated expression of these genes kills only cancer cells and spares normal cells. The efficacy of the PEG-Prom as part of a cancer gene therapeutic regimen is further documented by in vivo experiments in which PEG-Prom-controlled expression of an apoptosis-inducing gene completely inhibited prostate cancer xenograft growth in nude mice. These compelling observations indicate that the PEG-Prom, with its cancer-specific expression, provides a means of selectively delivering genes to cancer cells, thereby providing a crucial component in developing effective cancer gene therapies.

Indexed as

Genetic TherapyAnimalsAntigens, DifferentiationCell Cycle ProteinsGenes, Tumor SuppressorHumansInterleukin-24InterleukinsMaleMiceNeoplasm ProteinsNeoplasmsPromoter Regions, GeneticProtein Phosphatase 1ProteinsProto-Oncogene ProteinsAntigens, DifferentiationCell Cycle ProteinsInterleukin-24InterleukinsNeoplasm ProteinsPPP1R15A protein, humanPpp1r15a protein, mousePpp1r15a protein, ratProtein Phosphatase 1ProteinsProto-Oncogene ProteinsTranscription Factor AP-1transcription factor PEA3Transcription Factors

Identifiers

PMID15647352
PMCPMC545837
OpenAlexW2110166030

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.