Evidence map›Paper›PMID 19597463›Full record

ArticleOncogene2009

Cancer targeted gene therapy of BikDD inhibits orthotopic lung cancer growth and improves long-term survival.

Y-P Sher, T-F Tzeng, S-F Kan, J Hsu, X Xie, Z Han, W-C Lin, L-Y Li, M-C Hung

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Lipid-based nucleic acid therapeutics with in vivo efficacy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2023
    Review
  2. Article
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  8. Review
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  11. Proteasome inhibition enhances the killing effect of BikDD gene therapy.American journal of translational research · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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 3 institutions in 2 countries.

Y-P SherCenter for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University & Hospital, Taichung, Taiwan.
T-F Tzeng
S-F Kan
J Hsu
X Xie
Z Han
W-C Lin
L-Y Li
M-C Hung
China Medical University Hospital · TWThe University of Texas MD Anderson Cancer Center · USChina Medical University · TW

Funding

UTMDACC SPORE in Breast CancerP50CA116199 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ANDREEFF, MICHAEL · 2005 to 2009
$11.9M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
Tumor Progression of Nuclear EGFR in Breast CancerR01CA109311 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2004 to 2014
$3.0M
NCI NIH HHS 1P50 CA116199NCI NIH HHS P01 CA099031NCI NIH HHS P20 CA101936NCI NIH HHS P50 CA116199NCI NIH HHS R01 CA109311
6 · The paper itself

Abstract

Lung cancer is a leading cause of cancer death due to the high incidence of metastasis; therefore, novel and effective treatments are urgently needed. A current strategy is cancer-specific targeted gene therapy. Although many identified that cancer-specific promoters are highly specific, they tend to have low activity compared with the ubiquitous cytomegalovirus (CMV) promoter, limiting their application. We developed a targeted gene therapy expression system for lung cancer that is highly specific with strong activity. Our expression vector uses the survivin promoter, highly expressed in many cancers but not normal adult tissues. We enhanced the survivin promoter activity comparable to the CMV promoter in lung cancer cell lines using an established platform technology, whereas the survivin promoter remained weak in normal cells. In mouse models, the transgene was specifically expressed in the lung tumor tissue, compared with the CMV promoter that was expressed in both normal and tumor tissues. In addition, the therapeutic gene BikDD, a mutant form of pro-apoptotic Bcl2 interacting killer, induced cell killing in vitro, and inhibited cell growth and prolonged mouse survival in vivo. Importantly, there was virtually no toxicity when BikDD was expressed with our expression system. Thus, the current report provides a therapeutic efficacy and safe strategy worthy of development in clinical trials treating lung cancer.

Indexed as

AnimalsApoptosis Regulatory ProteinsCell Line, TumorCell ProliferationClinical Trials as TopicCytomegalovirusGenetic TherapyHumansInhibitor of Apoptosis ProteinsLung NeoplasmsMaleMembrane ProteinsMiceMicrotubule-Associated ProteinsMitochondrial ProteinsMutant ProteinsApoptosis Regulatory ProteinsBIK protein, humanBIRC5 protein, humanInhibitor of Apoptosis ProteinsMembrane ProteinsMicrotubule-Associated ProteinsMitochondrial ProteinsMutant ProteinsSurvivin

Identifiers

PMID19597463
PMCPMC2763377
OpenAlexW1981827594

What OpenQuestion holds

Textmetadata
LicenceTDM
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.