Evidence map›Paper›PMID 16052226›Full record

ArticleCancer gene therapy2006

Targeting and killing of prostate cancer cells using lentiviral constructs containing a sequence recognized by translation factor eIF4E and a prostate-specific promoter.

D Yu, C Scott, W W Jia, A De Benedetti, B J Williams, L Fazli, Y Wen, M Gleave, C Nelson, P S Rennie

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Strategies to Improve the Safety of iPSC-Derived β Cells for β Cell Replacement in Diabetes.Transplant international : official journal of the European Society for Organ Transplantation · 2022
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Transcriptional and translational dual-regulated oncolytic herpes simplex virus type 1 for targeting prostate tumors.Molecular therapy : the journal of the American Society of Gene Therapy · 2010
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. 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

10 authors at 4 institutions in 2 countries.

D YuThe Prostate Center at Vancouver General Hospital, University of British Columbia, Canada.
C Scott
W W Jia
A De Benedetti
B J Williams
L Fazli
Y Wen
M Gleave
C Nelson
P S Rennie
Vancouver General Hospital · CAUniversity of British Columbia · CALouisiana State University Health Sciences Center Shreveport · USUniversity Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To develop a gene therapy that would selectively kill prostate cancer cells while sparing normal cells, we have constructed lentiviral vectors that contain a therapeutic gene with a short DNA sequence in the 5'-untranslated region (UTR) that is recognized by the translation initiation factor, eIF4E, which is often overexpressed in malignant cells. Infection of cancer (LNCaP, PC-3M, DU145, and MCF-7 cells) and noncancer cell lines (BPH-1, 267-B1, Plat-E, and Huvec-c cells) with lentivirus having a CMV-promoter and EGFP reporter resulted in high levels of EGFP expression in all cells, whereas, inclusion of the eIF4E UTR recognition sequence restricted high expression to cancer cells and Plat-E cells, which also express substantial levels of eIF4E. Infection of the cells with lentiviral vectors having this UTR in front of the HSV thymidine kinase suicide gene resulted in differential sensitivity to the killing effects of ganciclovir, with at least 100-fold more drug required to kill noncancer cells than cancer cells. Furthermore, in experiments where the CMV promoter was replaced by the prostate-specific ARR(2)PB promoter, the killing effects of ganciclovir were restricted to prostate cancer cells and not seen in nonprostate cancer cells. Our results indicate that combined translational regulation, by incorporation of an eIF4E-UTR recognition sequence into a therapeutic gene, together with transcriptional regulation with a prostate-specific promoter, may provide a means to selectively destroy prostate cancer cells while sparing normal prostate cells.

Indexed as

Gene Expression Regulation, NeoplasticCell DeathDose-Response Relationship, DrugEukaryotic Initiation Factor-4EGenetic VectorsHumansImmunohistochemistryLentivirusMaleModels, GeneticPromoter Regions, GeneticProstatic NeoplasmsThymidine KinaseTransfectionTumor Cells, CulturedEukaryotic Initiation Factor-4EThymidine Kinase

Identifiers

PMID16052226
OpenAlexW1997740604

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.