Evidence map›Paper›PMID 27732937›Full record

ArticleOncotarget2016

Tofacitinib induces G1 cell-cycle arrest and inhibits tumor growth in Epstein-Barr virus-associated T and natural killer cell lymphoma cells.

Shotaro Ando, Jun-Ichi Kawada, Takahiro Watanabe, Michio Suzuki, Yoshitaka Sato, Yuka Torii, Masato Asai, Fumi Goshima, Takayuki Murata, Norio Shimizu and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Refractory Hydroa Vacciniforme-like Lymphoma: Biological Insights from Morphoproteomic Analysis.International journal of hematology-oncology and stem cell research · 2022
    Article
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  15. Review
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  19. Article
  20. The Binary Classification of Protein Kinases.Journal of inflammation research · 2021
    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 2 institutions in 1 country.

Shotaro AndoDepartments of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Jun-Ichi KawadaDepartments of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Takahiro WatanabeDepartments of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Michio SuzukiDepartments of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yoshitaka SatoDepartments of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yuka ToriiDepartments of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Masato AsaiDepartments of Pathology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
Fumi GoshimaDepartments of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Takayuki MurataDepartments of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Norio ShimizuCenter of Stem Cell and Regenerative Medicine, Tokyo Medical and Dental University, Chiyoda-ku, Tokyo 101-0062, Japan.
Yoshinori ItoDepartments of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Hiroshi KimuraDepartments of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) infects not only B cells, but also T cells and natural killer (NK) cells, and is associated with T or NK cell lymphoma. These lymphoid malignancies are refractory to conventional chemotherapy. We examined the activation of the JAK3/STAT5 pathway in EBV-positive and -negative B, T and NK cell lines and in cell samples from patients with EBV-associated T cell lymphoma. We then evaluated the antitumor effects of the selective JAK3 inhibitor, tofacitinib, against these cell lines in vitro and in a murine xenograft model. We found that all EBV-positive T and NK cell lines and patient samples tested displayed activation of the JAK3/STAT5 pathway. Treatment of these cell lines with tofacitinib reduced the levels of phospho-STAT5, suppressed proliferation, induced G1 cell-cycle arrest and decreased EBV LMP1 and EBNA1 expression. An EBV-negative NK cell line was also sensitive to tofacitinib, whereas an EBV-infected NK cell line was more sensitive to tofacitinib than its parental line. Tofacitinib significantly inhibited the growth of established tumors in NOG mice. These findings suggest that tofacitinib may represent a useful therapeutic agent for patients with EBV-associated T and NK cell lymphoma.

Indexed as

Herpesvirus 4, HumanAnimalsApoptosisBiomarkersCell Line, TumorDisease Models, AnimalEpstein-Barr Virus InfectionsG1 Phase Cell Cycle CheckpointsGene Expression Regulation, ViralHumansJanus Kinase 3Killer Cells, NaturalLymphocyte ActivationLymphoma, T-CellMicePiperidinesBiomarkersJanus Kinase 3PiperidinesProtein Kinase InhibitorsPyrimidinesPyrrolesSTAT5 Transcription Factortofacitinibcell-cycle arrestEBVlymphomatofacitinib

Identifiers

PMID27732937
PMCPMC5363550
OpenAlexW2527850649

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.