Evidence map›Paper›PMID 30713805›Full record

ArticleOncoimmunology

Beneficial effects of sunitinib on tumor microenvironment and immunotherapy targeting death receptor5.

Yoko Tsukita, Tatsuma Okazaki, Satoru Ebihara, Riyo Komatsu, Mayumi Nihei, Makoto Kobayashi, Taizou Hirano, Hisatoshi Sugiura, Tsutomu Tamada, Nobuyuki Tanaka and 3 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 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

13 authors at 3 institutions in 1 country.

Yoko TsukitaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tatsuma OkazakiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID 0000-0002-7110-3168
Satoru EbiharaDepartment of Rehabilitation Medicine, Toho University Graduate School of Medicine, Tokyo, Japan.
Riyo KomatsuDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Mayumi NiheiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Makoto KobayashiDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Taizou HiranoDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hisatoshi SugiuraDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tsutomu TamadaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID 0000-0003-0600-0610
Nobuyuki TanakaDivision of Tumor Immunobiology, Department of Cancer Medical Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yasufumi SatoDepartment of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan.
Hideo YagitaDepartment of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Masakazu IchinoseDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tohoku University · JPJuntendo University · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated blood vessels and lymphatics are abnormal and dysfunctional. These are hallmarks of the tumor microenvironment, which has an immunosuppressive nature, such as through hypoxia. Treatment with anti-death receptor5 (DR5) monoclonal antibody MD5-1, which induces tumor cell death, is a potent anti-tumor immunotherapy. Generally, MD5-1 induces cell death mainly via antigen presenting cells (APCs) and generates tumor-specific effector T cells. To date, the effects of a simultaneous functional improvement of abnormal blood vessels and lymphatics on the immune microenvironment are largely unknown. A combination therapy using sunitinib, vascular endothelial growth factor (VEGF) and platelet-derived growth factor receptor inhibitor, and MD5-1 substantially inhibited tumor growth. Sunitinib improved pericyte coverage on endothelial cells and the expression levels of regulator of G-protein signaling 5, suggesting blood vessel normalization. Sunitinib also increased lymph flow from tumors to central lymph nodes, suggesting improved lymphatic function. In concordance with improved vasculature functions, sunitinib alleviated the tumor hypoxia, suggesting an improved tumor microenvironment. Indeed, the combination therapy induced strong activation of CD8

Indexed as

blood vesselsdeath receptor5immunotherapylymphaticstumor microenvironment

Identifiers

PMID30713805
PMCPMC6343781
OpenAlexW2901950073

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.