Evidence map›Paper›PMID 34158547›Full record

ArticleScientific reports2021

PD-L1 upregulation is associated with activation of the DNA double-strand break repair pathway in patients with colitic cancer.

Naoya Ozawa, Takehiko Yokobori, Katsuya Osone, Chika Katayama, Kunihiko Suga, Chika Komine, Yuta Shibasaki, Takuya Shiraishi, Takuhisa Okada, Ryuji Kato and 12 more

Abstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. [Ulcerative colitis-associated carcinogenesis : An update].Pathologie (Heidelberg, Germany) · 2023
    Review
  9. Journal of clinical medicine · 2023
    Article
  10. Inflammation suppresses DLG2 expression decreasing inflammasome formation.Journal of cancer research and clinical oncology · 2022
    Article
  11. Article
  12. Review
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

22 authors.

Naoya OzawaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Takehiko YokoboriDivision of Integrated Oncology Research, Gunma University Initiative for Advanced Research (GIAR), 3-39-22 Showa-machi, Maebashi, Gunma, 371-8511, Japan. bori45@gunma-u.ac.jp.
Katsuya OsoneDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Chika KatayamaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Kunihiko SugaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Chika KomineDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Yuta ShibasakiDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Takuya ShiraishiDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Takuhisa OkadaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Ryuji KatoDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Hiroomi OgawaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Akihiko SanoDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Makoto SakaiDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Makoto SohdaDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Hitoshi OjimaDepartment of Gastroenterological Surgery, Gunma Prefectural Cancer Center, Ohta, Gunma, Japan.
Tatsuya MiyazakiDepartment of Gastroenterological Surgery, Maebashi Red Cross Hospital, Maebashi, Gunma, Japan.
Yoko MotegiDepartment of Gastroenterological Surgery, Maebashi Red Cross Hospital, Maebashi, Gunma, Japan.
Munenori IdeDepartment of Pathology Diagnosis, Maebashi Red Cross Hospital, Maebashi, Gunma, Japan.
Takashi YaoDepartment of Human Pathology, Graduate School of Medicine, Juntendo University, Bunkyo City, Tokyo, Japan.
Hiroyuki KuwanoDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Ken ShirabeDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.
Hiroshi SaekiDepartment of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi, Gunma, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a DNA damage-associated chronic inflammatory disease; the DNA double-strand break (DSB) repair pathway participates in UC-associated dysplasia/colitic cancer carcinogenesis. The DSB/interferon regulatory factor-1 (IRF-1) pathway can induce PD-L1 expression transcriptionally. However, the association of PD-L1/DSB/IRF-1 with sporadic colorectal cancer (SCRC), and UC-associated dysplasia/colitic cancer, remains elusive. Therefore, we investigated the significance of the PD-L1/DSB repair pathway using samples from 17 SCRC and 12 UC patients with rare UC-associated dysplasia/colitic cancer cases by immunohistochemical analysis. We compared PD-L1 expression between patients with SCRC and UC-associated dysplasia/colitic cancer and determined the association between PD-L1 and the CD8+ T-cell/DSB/IRF-1 axis in UC-associated dysplasia/colitic cancer. PD-L1 expression in UC and UC-associated dysplasia/colitic cancer was higher than in normal mucosa or SCRC, and in CD8-positive T lymphocytes in UC-associated dysplasia/colitic cancer than in SCRC. Moreover, PD-L1 upregulation was associated with γH2AX (DSB marker) and IRF-1 upregulation in UC-associated dysplasia/colitic cancer. IRF-1 upregulation was associated with γH2AX upregulation in UC-associated dysplasia/colitic cancer but not in SCRC. Multicolour immunofluorescence staining validated γH2AX/IRF-1/PD-L1 co-expression in colitic cancer tissue sections. Thus, immune cell-induced inflammation might activate the DSB/IRF-1 axis, potentially serving as the primary regulatory mechanism of PD-L1 expression in UC-associated carcinogenesis.

Indexed as

AdultAgedB7-H1 AntigenColitis, UlcerativeColonic NeoplasmsColorectal NeoplasmsDNADNA Breaks, Double-StrandedDNA RepairFemaleGene ExpressionHumansInterferon Regulatory Factor-1Intestinal MucosaMaleMiddle AgedB7-H1 AntigenCD274 protein, humanDNAInterferon Regulatory Factor-1IRF1 protein, human

Identifiers

PMID34158547
PMCPMC8219733

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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.