Evidence map›Paper›PMID 15789059›Full record

ArticleGene therapy2005

Selective induction of tumor-associated antigens in murine pulmonary vasculature using double-targeted adenoviral vectors.

M Everts, S-A Kim-Park, M A Preuss, M J Passineau, J N Glasgow, A V Pereboev, P J Mahasreshti, W E Grizzle, P N Reynolds, D T Curiel

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 31 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

10 authors at 2 institutions in 2 countries.

M EvertsDivision of Human Gene Therapy, Department of Medicine, and the Gene Therapy Center, University of Alabama at Birmingham, Birmingham, AL 35294-2172, USA.
S-A Kim-Park
M A Preuss
M J Passineau
J N Glasgow
A V Pereboev
P J Mahasreshti
W E Grizzle
P N Reynolds
D T Curiel
University of Alabama at Birmingham · USRoyal Adelaide Hospital · AU

Funding

UAB Rexinoids for Breast Cancer PreventionP50CA089019 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GRIZZLE, WILLIAM E. · 2000 to 2011
$26.0M
VASCULAR TOPOGRAPHY OF CD39/NTPDASESP01HL076540 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AIRD, WILLIAM C · 2004 to 2014
$20.3M
BASIC MECHANISMS OF LUNG DISEASEST32HL007553 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOTHER, JANET L · 1985 to 2007
$2.2M
Endothelial Gene Delivery for Pulmonary HypertensionR01HL067962 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CURIEL, DAVID TERRY · 2001 to 2004
$1.5M
In situ therapeutic anti-AB delivery/adenoviral vectorsR01AG021875 · NIA · MAYO CLINIC JACKSONVILLE · PI GOLDE, TODD E. · 2002 to 2004
$707k
NCI NIH HHS CA-835911-05NCI NIH HHS CA 89019-04NHLBI NIH HHS 1 P01 HL076540NHLBI NIH HHS P01 HL075640-01NHLBI NIH HHS R01 HL67962NHLBI NIH HHS T32 HL07553NIA NIH HHS R01 AG021875
6 · The paper itself

Abstract

Targeted therapies directed to tumor-associated antigens are being investigated for the treatment of cancer. However, there are few suitable animal models for testing the ability to target these tumor markers. Therefore, we have exploited mice transgenic for the human coxsackie and adenovirus receptor (hCAR) to establish a new model for transient expression of human tumor-associated antigens in the pulmonary vasculature. Systemic administration of Ad in hCAR mice resulted in an increase in transgene expression in the lungs compared to wild-type mice, as determined using a luciferase reporter gene. To reduce transgene expression in the liver, the predominant organ of ectopic Ad localization and transgene expression following systemic administration, we utilized the endothelial-specific flt-1 promoter, which resulted in a further increased lung-to-liver ratio of luciferase expression. Administration of an adenoviral vector encoding the tumor-associated antigen carcinoembryonic antigen (CEA) under transcriptional control of the flt-1 promoter resulted in selective expression of this antigen in the pulmonary vasculature of hCAR mice. Feasibility of targeting to expressed CEA was subsequently demonstrated using adenoviral vectors preincubated with a bifunctional adapter molecule recognizing this tumor-associated antigen, thus demonstrating utility of this transient transgenic animal model.

Indexed as

AdenoviridaeAnimalsCarcinoembryonic AntigenExtracellular Matrix ProteinsGene ExpressionGene TargetingGenetic TherapyGenetic VectorsImmunohistochemistryLiverLuciferasesMiceMice, TransgenicMyosin Heavy ChainsNonmuscle Myosin Type IIBPromoter Regions, Geneticadenovirus receptorCarcinoembryonic AntigenExtracellular Matrix ProteinsFLT1 protein, humanFlt1 protein, mouseLuciferasesMyosin Heavy ChainsNonmuscle Myosin Type IIBnonmuscle myosin type IIB heavy chainProteinsReceptors, VirusVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID15789059
OpenAlexW1980270107

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.