Evidence map›Paper›PMID 28255357›Full record

ArticleTheranostics2017

STAT3/NF-κB-Regulated Lentiviral TK/GCV Suicide Gene Therapy for Cisplatin-Resistant Triple-Negative Breast Cancer.

Wei-Ying Kuo, Luen Hwu, Chun-Yi Wu, Jhih-Shian Lee, Chi-Wei Chang, Ren-Shyan Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Theranostics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.Journal of experimental & clinical cancer research : CR · 2019
    Pooled it
  2. Logic-Gated HSV-TK/GCV Suicide Gene Circuit for Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  20. Prodrugs and prodrug-activated systems in gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Review
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

6 authors at 2 institutions in 1 country.

Wei-Ying KuoDepartment of Biomedical Imaging and Radiological Sciences, School of Biomedical and Engineering, National Yang-Ming University, Taipei, Taiwan.
Luen HwuMolecular and Genetic Imaging Core/Taiwan Mouse Clinic, NRPB, Department of Nuclear Medicine and National PET/Cyclotron Center, Taipei Veterans General Hospital, Taipei, Taiwan.
Chun-Yi WuDepartment of Biomedical Imaging and Radiological Science, China Medical University, Taichung, Taiwan.
Jhih-Shian LeeDepartment of Biomedical Imaging and Radiological Sciences, School of Biomedical and Engineering, National Yang-Ming University, Taipei, Taiwan.
Chi-Wei ChangDepartment of Nuclear Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Ren-Shyan LiuDepartment of Nuclear Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.; Biomedical Imaging Research Center, Department of Biomedical Imaging and Radiological Sciences, School of Biomedical and Engineering, Institute of Clinical Medicine, School of Medicine, National Yang-Ming University.
China Medical University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) represents approximately 20% of all breast cancers and appears resistance to conventional cytotoxic chemotherapy, demonstrating a particularly poor prognosis and a significantly worse clinical outcome than other types of cancer. Suicide gene therapy has been used for the in vivo treatment of various solid tumors in recent clinical trials. In tumor microenvironment, STAT3/NF-κB pathways are constitutively activated in stromal cells as well as in cancer stem cells (CSCs). In this study, we have cloned a novel STAT3/NF-κB-based reporter system to drive the expression of herpes simplex virus thymidine kinase (HSV-TK) against breast cancer. Lentiviral vector expressing HSV-TK under the regulation of STAT3/NF-κB fused response element was developed. In this setting, we exploited the constitutive STAT3/NF-κB activation in tumors to achieve higher transgene expression than that driven by a constitutively active CMV promotor

Indexed as

AnimalsAntineoplastic AgentsCisplatinDisease Models, AnimalDrug ResistanceGanciclovirGenetic TherapyGenetic VectorsLentivirusMiceNF-kappa B p50 SubunitSTAT3 Transcription FactorThymidine KinaseTransduction, GeneticTreatment OutcomeTriple Negative Breast NeoplasmsAntineoplastic AgentsCisplatinGanciclovirNF-kappa B p50 SubunitNfkb1 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorThymidine KinaseCisplatin resistance.TK/GCV suicide gene therapyTriple-negative breast cancer

Identifiers

PMID28255357
PMCPMC5327640
OpenAlexW2575404391

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.