Evidence map›Paper›PMID 24062140›Full record

ArticleJournal of neuro-oncology2014

Cytotoxic human peripheral blood-derived γδT cells kill glioblastoma cell lines: implications for cell-based immunotherapy for patients with glioblastoma.

Tsutomu Nakazawa, Mitsutoshi Nakamura, Young Soo Park, Yasushi Motoyama, Yasuo Hironaka, Fumihiko Nishimura, Ichiro Nakagawa, Shuichi Yamada, Ryosuke Matsuda, Kentaro Tamura and 8 more

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

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  16. Zoledronic acid induces apoptosis via stimulating the expressions of ERN1, TLR2, and IRF5 genes in glioma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

18 authors at 2 institutions in 1 country.

Tsutomu NakazawaDepartment of Neurosurgery, Nara Medical University School of Medicine, 840, Shijocho, Kashihara, Nara, 634-8522, Japan, nakazawa@naramed-u.ac.jp.
Mitsutoshi Nakamura
Young Soo Park
Yasushi Motoyama
Yasuo Hironaka
Fumihiko Nishimura
Ichiro Nakagawa
Shuichi Yamada
Ryosuke Matsuda
Kentaro Tamura
Tadashi Sugimoto
Yasuhiro Takeshima
Akiko Marutani
Takahiro Tsujimura
Noriko Ouji
Yukiteru Ouji
Masahide Yoshikawa
Hiroyuki Nakase
Nara Medical University · JPNara City Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is a highly aggressive brain tumor for which novel therapeutic approaches, such as immunotherapy, are urgently needed. Zoledronate (ZOL), an inhibitor of osteoclastic activity, is known to stimulate peripheral blood-derived γδT cells and sensitize tumors to γδT cell-mediated killing. To investigate the feasibility of γδT cell-based immunotherapy for patients with GBM, we focused on the killing of GBM cell lines by γδT cells and the molecular mechanisms involved in these cell-cell interactions. Peripheral blood mononuclear cells were expanded in ZOL and interleukin (IL)-2 for 14 days, and γδT cells were enriched in the expanded cells by the immunomagnetic depletion of αβT cells. Gliomas are resistant to NK cells but susceptible to lymphokine-activated killer cells and some cytotoxic T lymphocytes. When the γδT cell-mediated killing of three GBM cell lines (U87MG, U138MG and A172 cells) and an NK-sensitive leukemia cell line (K562 cells) were tested, 32% U87MG, 15% U138MG, 1% A172, and 50% K562 cells were killed at an effector:target ratio of 5:1. The γδT cell-mediated killing of all three GBM cell lines was significantly enhanced by ZOL and this ZOL-enhanced killing was blocked by an anti-T cell receptor (TcR) antibody. These results indicated that TcR γδ is crucial for the recognition of ZOL-treated GBM cells by γδT cells. Since the low level killing of GBM cells by the γδT cells was enhanced by ZOL, γδT cell-targeting therapy in combination with ZOL treatment could be effective for patients with GBM.

Indexed as

Analysis of VarianceAntigens, CDBone Density Conservation AgentsCell Line, TumorDiphosphonatesFlow CytometryFluoresceinsGlioblastomaHumansImidazolesLeukocytes, MononuclearLymphocyte ActivationReceptors, Antigen, T-Cell, gamma-deltaTime FactorsT-Lymphocyte SubsetsZoledronic AcidAntigens, CDBone Density Conservation Agentscalcein AMDiphosphonatesFluoresceinsImidazolesReceptors, Antigen, T-Cell, gamma-deltaZoledronic Acid

Identifiers

PMID24062140
OpenAlexW2142051677

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.