Evidence map›Paper›PMID 26059686›Full record

ArticleBMC cancer2015

Cytotoxic effects of replication-competent adenoviruses on human esophageal carcinoma are enhanced by forced p53 expression.

Shan Yang, Kiyoko Kawamura, Shinya Okamoto, Suguru Yamauchi, Masato Shingyoji, Ikuo Sekine, Hiroshi Kobayashi, Yuji Tada, Koichiro Tatsumi, Kenzo Hiroshima and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 4 institutions in 1 country.

Shan YangDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, 260-8717, Chiba, Japan. yswish2009@163.com.
Kiyoko KawamuraDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, 260-8717, Chiba, Japan. kkawamur@chiba-cc.jp.
Shinya OkamotoDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, 260-8717, Chiba, Japan. sokamoto@chiba-cc.jp.
Suguru YamauchiDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, 260-8717, Chiba, Japan. mr_children4hero@yahoo.co.jp.
Masato ShingyojiDivision of Respirology, Chiba Cancer Center, Chiba, Japan. mshingyoji@chiba-cc.jp.
Ikuo SekineDivision of Respirology, Chiba Cancer Center, Chiba, Japan. isekine@chiba-u.jp.
Hiroshi KobayashiDepartment of Biochemistry, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan. hiroshi.k@mx6.ttcn.ne.jp.
Yuji TadaDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan. ytada25@yahoo.co.jp.
Koichiro TatsumiDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan. tatsumi@faculty.chiba-u.jp.
Kenzo HiroshimaDepartment of Pathology, Tokyo Women's Medical University Yachiyo Medical Center, Chiba, Japan. kenzo@tymc.twmu.ac.jp.
Hideaki ShimadaDepartment of Surgery, School of Medicine, Toho University, Tokyo, Japan. hideaki.shimada@med.toho-u.ac.jp.
Masatoshi TagawaDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, 260-8717, Chiba, Japan. mtagawa@chiba-cc.jp.
Chiba Cancer Center · JPChiba University · JPToho University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImprovement of transduction and augmentation of cytotoxicity are crucial for adenoviruses (Ad)-mediated gene therapy for cancer. Down-regulated expression of type 5 Ad (Ad5) receptors on human tumors hampered Ad-mediated transduction. Furthermore, a role of the p53 pathways in cytotoxicity mediated by replication-competent Ad remained uncharacterized.

methodsWe constructed replication-competent Ad5 of which the E1 region genes were activated by a transcriptional regulatory region of the midkine or the survivin gene, which is expressed preferentially in human tumors. We also prepared replication-competent Ad5 which were regulated by the same region but had a fiber-knob region derived from serotype 35 (AdF35). We examined the cytotoxicity of these Ad and a possible combinatory use of the replication-competent AdF35 and Ad5 expressing the wild-type p53 gene (Ad5/p53) in esophageal carcinoma cells. Expression levels of molecules involved in cell death, anti-tumor effects in vivo and production of viral progenies were also investigated.

resultsReplication-competent AdF35 in general achieved greater cytotoxic effects to esophageal carcinoma cells than the corresponding replication-competent Ad5. Infection with the AdF35 induced cleavages of caspases and increased sub-G1 fractions, but did not activate the autophagy pathway. Transduction with Ad5/p53 in combination with the replication-competent AdF35 further enhanced the cytotoxicity in a synergistic manner. We also demonstrated the combinatory effects in an animal model. Transduction with Ad5/p53 however suppressed production of replication-competent AdF35 progenies, but the combination augmented Ad5/p53-mediated p53 expression levels and the downstream pathways.

conclusionsCombination of replication-competent AdF35 and Ad5/p53 achieved synergistic cytotoxicity due to enhanced p53-mediated apoptotic pathways.

Indexed as

Genetic TherapyAdenoviridaeApoptosisCarcinomaCell Line, TumorCell ProliferationEsophageal NeoplasmsGene Expression Regulation, NeoplasticGenetic VectorsHumansRNA, MessengerTransduction, GeneticTumor Suppressor Protein p53RNA, MessengerTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26059686
PMCPMC4460641
OpenAlexW1594036852

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.