Evidence map›Paper›PMID 31142289›Full record

ArticleBMC cancer2019

A survivin-responsive, conditionally replicating adenovirus induces potent cytocidal effects in adult T-cell leukemia/lymphoma.

Shinsuke Suzuki, Hiroki Kofune, Kimiharu Uozumi, Makoto Yoshimitsu, Naomichi Arima, Kenji Ishitsuka, Shin-Ichi Ueno, Ken-Ichiro Kosai

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Shinsuke SuzukiDepartment of Clinical Oncology, Course of Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima, 890-8520, Japan. suzuki2@m.kufm.kagoshima-u.ac.jp.ORCID http://orcid.org/0000-0001-5284-7885
Hiroki KofuneDepartment of Hematology and Rheumatology, Kagoshima University Hospital, Kagoshima, Japan.
Kimiharu UozumiDepartment of Medical Oncology, National Hospital Organization Kagoshima Medical Center, Kagoshima, Japan.
Makoto YoshimitsuDepartment of Hematology and Rheumatology, Kagoshima University Hospital, Kagoshima, Japan.
Naomichi ArimaDepartment of Hematology and Rheumatology, Kagoshima University Hospital, Kagoshima, Japan.
Kenji IshitsukaDepartment of Hematology and Rheumatology, Kagoshima University Hospital, Kagoshima, Japan.
Shin-Ichi UenoDepartment of Clinical Oncology, Course of Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima, 890-8520, Japan.
Ken-Ichiro KosaiDepartment of Gene Therapy and Regenerative Medicine, Course of Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kagoshima University Hospital · JPKagoshima University · JPNational Hospital Organization · JP

Funding

Japan Society for the Promotion of Science 15K06911Japan Society for the Promotion of Science 15K10031Japan Society for the Promotion of Science 23591398
6 · The paper itself

Abstract

backgroundAdult T-cell leukemia/lymphoma (ATL) is a peripheral T-cell malignancy caused by long-term human T-cell leukemia virus type I (HTLV-1) infection. Survivin-responsive, conditionally replicating adenoviruses regulated by multiple tumor-specific factors (Surv.m-CRAs), in which the expression of the adenoviral early region 1A gene is regulated by the survivin (BIRC5) promoter, can be used to treat several cancers. As survivin is overexpressed in ATL, we examined the effects of Surv.m-CRAs on ATL-selective replication and survival.

methodsWe tested two ATL cell lines and four HTLV-1-infected T-cell lines. The cells were subjected to infection with either E1-deleted, replication-defective adenoviruses or Surv.m-CRAs at various multiplicities of infection.

resultsStrong activation of survivin promoter was observed in all six cell lines. Moreover, the expression of the coxsackie and adenovirus receptor (CAR), which is important for adenoviral infection, was high in the cell lines. In contrast, we observed the absence of survivin promoter activity and a low expression of CAR in activated peripheral blood lymphocytes (PBLs) from healthy subjects. Surv.m-CRAs actively replicated and induced cytocidal effects in five out of six cell lines; conversely, we observed minimal viral replication and no marked cytotoxicity in normal activated PBLs.

conclusionsThis is the first report demonstrating that Surv.m-CRAs constitute attractive potential anti-ATL agents.

Indexed as

AdenoviridaeAdenovirus E1A ProteinsCell Line, TumorHumansLeukemia-Lymphoma, Adult T-CellPromoter Regions, GeneticSurvivinVirus ReplicationAdenovirus E1A ProteinsBIRC5 protein, humanSurvivinATLConditionally replicating adenovirusesSurvivin

Identifiers

PMID31142289
PMCPMC6542078
OpenAlexW2947722251

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.