Evidence map›Paper›PMID 34944745›Full record

ArticleBiomedicines2021

Increased Plasma Soluble PD-1 Concentration Correlates with Disease Progression in Patients with Cancer Treated with Anti-PD-1 Antibodies.

Ryotaro Ohkuma, Katsuaki Ieguchi, Makoto Watanabe, Daisuke Takayanagi, Tsubasa Goshima, Rie Onoue, Kazuyuki Hamada, Yutaro Kubota, Atsushi Horiike, Tomoyuki Ishiguro and 9 more

Abstract read
In one paragraph

Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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  10. Gal-3 blocks the binding between PD-1 and pembrolizumab.Journal for immunotherapy of cancer · 2024
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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

19 authors.

Ryotaro OhkumaDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Katsuaki IeguchiDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Makoto WatanabeDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Daisuke TakayanagiDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Tsubasa GoshimaDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Rie OnoueDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Kazuyuki HamadaDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Yutaro KubotaDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.ORCID 0000-0002-2917-8764
Atsushi HoriikeDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Tomoyuki IshiguroDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Yuya HirasawaDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Hirotsugu AriizumiDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Junji TsurutaniDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Kiyoshi YoshimuraDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Mayumi TsujiDepartment of Pharmacology, Division of Medical Pharmacology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Yuji KiuchiDepartment of Pharmacology, Division of Medical Pharmacology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Shinichi KobayashiClinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.
Takuya TsunodaDepartment of Medicine, Division of Medical Oncology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Satoshi WadaDepartment of Clinical Diagnostic Oncology, Clinical Research Institute for Clinical Pharmacology & Therapeutics, Showa University, 6-11-11, Kitakarasuyama, Setagaya-ku, Tokyo 157-8577, Japan.ORCID 0000-0001-6528-5914

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint inhibitors (ICIs) confer remarkable therapeutic benefits to patients with various cancers. However, many patients are non-responders or develop resistance following an initial response to ICIs. There are no reliable biomarkers to predict the therapeutic effect of ICIs. Therefore, this study investigated the clinical implications of plasma levels of soluble anti-programmed death-1 (sPD-1) in patients with cancer treated with ICIs. In total, 22 patients (13 with non-small-cell lung carcinoma, 8 with gastric cancer, and 1 with bladder cancer) were evaluated for sPD-1 concentration using enzyme-linked immunosorbent assays for diagnostic and anti-PD-1 antibody analyses. sPD-1 levels were low before the administration of anti-PD-1 antibodies. After two and four cycles of anti-PD-1 antibody therapy, sPD-1 levels significantly increased compared with pretreatment levels (

Indexed as

anti-programmed death-1 (PD-1)biomarkersimmune checkpoint inhibitors

Identifiers

PMID34944745
PMCPMC8698555

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Registered trials

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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.