Evidence map›Paper›PMID 36811663›Full record

ArticleCancer immunology, immunotherapy : CII2023

Expression of soluble CD27 in extranodal natural killer/T-cell lymphoma, nasal type: potential as a biomarker for diagnosis and CD27/CD70-targeted therapy.

Toshihiro Nagato, Hiroki Komatsuda, Ryusuke Hayashi, Miki Takahara, Kan Kishibe, Shunsuke Yasuda, Yuki Yajima, Akemi Kosaka, Takayuki Ohkuri, Kensuke Oikawa and 11 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. 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

21 authors at 2 institutions in 1 country.

Toshihiro NagatoDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan. rijun@asahikawa-med.ac.jp.
Hiroki KomatsudaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Ryusuke HayashiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Miki TakaharaDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Kan KishibeDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Shunsuke YasudaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Yuki YajimaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Akemi KosakaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Takayuki OhkuriDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Kensuke OikawaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan.
Shohei HarabuchiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Michihisa KonoDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Hidekiyo YamakiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Risa WakisakaDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Yui Hirata-NozakiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Kenzo OharaDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Takumi KumaiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Akihiro KatadaDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Tatsuya HayashiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Yasuaki HarabuchiDepartment of Otolaryngology-Head and Neck Surgery, Asahikawa Medical University, Asahikawa, Japan.
Hiroya KobayashiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, 078-8510, Japan. hiroya@asahikawa-med.ac.jp.
Asahikawa Medical University · JPHokuto Hospital · JP

Funding

Japan Society for the Promotion of Science 18K09310Japan Society for the Promotion of Science 21H03082Japan Society for the Promotion of Science 22H02838
6 · The paper itself

Abstract

The engagement of CD27 on lymphocytes with its ligand, CD70, on tumors is believed to mediate tumor immune evasion and the elevation of serum soluble CD27 (sCD27) levels in patients with CD70-positive malignancies. We previously showed that CD70 is expressed in extranodal natural killer/T-cell lymphoma, nasal type (ENKL), an Epstein-Barr virus (EBV)-related malignancy. However, little is known about serum sCD27 expression and its association with the clinical characteristics of, and the CD27/CD70 interaction in, ENKL. In the present study, we show that serum sCD27 is significantly elevated in the sera of patients with ENKL. The levels of serum sCD27 provided excellent diagnostic accuracy for discriminating patients with ENKL from healthy subjects, correlated positively with the levels of other diagnostic markers (lactate dehydrogenase, soluble interleukin-2 receptor, and EBV-DNA), and decreased significantly following treatment. Elevated serum sCD27 levels also correlated significantly with advanced clinical stage and tended to correspond with shorter survival, in patients with ENKL. Immunohistochemistry indicated that CD27-positive tumor-infiltrating immune cells exist adjacent to CD70-positive lymphoma cells. In addition, serum sCD27 levels in patients with CD70-positive ENKL were significantly higher than those in patients with CD70-negative ENKL, suggesting that the intra-tumoral CD27/CD70 interaction boosts the release of sCD27 in serum. Furthermore, the EBV-encoded oncoprotein latent membrane protein 1 upregulated CD70 expression in ENKL cells. Our results suggest that sCD27 may serve as a novel diagnostic biomarker and also may serve as a tool for evaluating the applicability of CD27/CD70-targeted therapies by predicting intra-tumoral CD70 expression and CD27/CD70 interaction in ENKL.

Indexed as

Epstein-Barr Virus InfectionsLymphoma, T-CellBiomarkersCD27 LigandHerpesvirus 4, HumanHumansKiller Cells, NaturalTumor Necrosis Factor Receptor Superfamily, Member 7BiomarkersCD27 LigandCD70 protein, humanTumor Necrosis Factor Receptor Superfamily, Member 7CD27CD70Extranodal NK/T-cell lymphomaImmunotherapySoluble form

Identifiers

PMID36811663
PMCPMC10992534
OpenAlexW4321487797

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.