Evidence map›Paper›PMID 28401019›Full record

ArticleAmerican journal of cancer research2017

A tumor vessel-targeting fusion protein elicits a chemotherapeutic bystander effect in pancreatic ductal adenocarcinoma.

Chun-Te Chen, Yi-Chun Chen, Yi Du, Zhenbo Han, Haoqiang Ying, Richard R Bouchard, Jennifer L Hsu, Jung-Mao Hsu, Trevor M Mitcham, Mei-Kuang Chen and 6 more

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

Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

16 authors at 3 institutions in 1 country.

Chun-Te ChenDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Yi-Chun ChenDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Yi DuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Zhenbo HanDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Haoqiang YingDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Department of Cancer Biology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA.
Richard R BouchardDepartment of Imaging Physics, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA.
Jennifer L HsuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical UniversityTaichung 404, Taiwan; Department of Biotechnology, Asia UniversityTaichung 413, Taiwan.
Jung-Mao HsuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Trevor M MitchamDepartment of Imaging Physics, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Mei-Kuang ChenDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA.
Hui-Lung SunDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Shih-Shin ChangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA.
Donghui LiDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Ping ChangDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center Houston, Texas 77030, USA.
Ronald A DePinhoDepartment of Cancer Biology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA.
Mien-Chie HungDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterHouston, Texas 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Houston Health Science CenterHouston, Texas 77030, USA; Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical UniversityTaichung 404, Taiwan; Department of Biotechnology, Asia UniversityTaichung 413, Taiwan.
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at Houston · USThe University of Texas at Austin · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease characterized by a prominent desmoplastic stroma that may constrain tumor progression but also limit the access of therapeutic drugs. In this study, we explored a tumor-targeting strategy that enlists an engineered anti-angiogenic protein consisting of endostatin and cytosine deaminase linked to uracil phosphoribosyltransferase (EndoCD). This protein selectively binds to tumor vessels to compromise tumor angiogenesis and converts the non-toxic 5-fluorocytosine (5-FC) to the cytotoxic 5-fluorouracil to produce a chemotherapeutic bystander effect at the pancreatic tumor site. We found that resveratrol increased the protein stability of EndoCD through suppression of chymotrypsin-like proteinase activity and synergistically enhances EndoCD-mediated 5-FC-induced cell killing. In various PDAC mouse models, the EndoCD/5-FC/resveratrol regimen decreased intratumoral vascular density and stroma formation and enhances apoptosis in tumors cells as well as in surrounding endothelial, pancreatic stellate, and immune cells, leading to reduced tumor growth and extended survival. Thus, the EndoCD/5-FC/resveratrol combination may be an effective treatment option for PDAC.

Indexed as

EndoCDMRIPDACresveratroltwo photonultrasound

Identifiers

PMID28401019
PMCPMC5385650
OpenAlexW2611312151

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.