Evidence map›Paper›PMID 31513320›Full record

ReviewCancer science2019

Regulation of programmed death-ligand 1 expression in response to DNA damage in cancer cells: Implications for precision medicine.

Hiro Sato, Penny A Jeggo, Atsushi Shibata

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Immune Cell Contribution to Mammary Gland Development.Journal of mammary gland biology and neoplasia · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Crosstalk between immune checkpoint and DNA damage response inhibitors for radiosensitization of tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Genotoxicity of Novel Pyrazolo[4,3-International journal of molecular sciences · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Hiro SatoDepartment of Radiation Oncology, Graduate School of Medicine, Gunma University, Maebashi, Japan.
Penny A JeggoGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, UK.ORCID https://orcid.org/0000-0002-8481-1462
Atsushi ShibataSignal Transduction Program, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Maebashi, Japan.ORCID https://orcid.org/0000-0001-8912-6977
Gunma University · JPUniversity of Sussex · GB

Funding

Cell Science Research FoundationDaiichi Sankyo Foundation of Life ScienceJapan Society for the Promotion of Science JP17H04713Japan Society for the Promotion of Science JP17K16420Program of the Network-type Joint Usage/Research Center for Radiation Disaster Medical Science of Hiroshima University, Nagasaki University, and Fukushima Medical UniversityTakeda Science FoundationYasuda Memorial Medical Foundation
6 · The paper itself

Abstract

Anti-programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) therapy, which is one of the most promising cancer therapies, is licensed for treating various tumors. Programmed death-ligand 1, which is expressed on the surface of cancer cells, leads to the inhibition of T lymphocyte activation and immune evasion if it binds to the receptor PD-1 on CTLs. Anti-PD-1/PD-L1 Abs inhibit interactions between PD-1 and PD-L1 to restore antitumor immunity. Although certain patients achieve effective responses to anti-PD-1/PD-L1 therapy, the efficacy of treatment is highly variable. Clinical trials of anti-PD-1/PD-L1 therapy combined with radiotherapy/chemotherapy are underway with suggestive evidence of favorable outcome; however, the molecular mechanism is largely unknown. Among several molecular targets that can influence the efficacy of anti-PD-1/PD-L1 therapy, PD-L1 expression in tumors is considered to be a critical biomarker because there is a positive correlation between the efficacy of combined treatment protocols and PD-L1 expression levels. Therefore, understanding the mechanisms underlying the regulation of PD-L1 expression in cancer cells, particularly the mechanism of PD-L1 expression following DNA damage, is important. In this review, we consider recent findings on the regulation of PD-L1 expression in response to DNA damage signaling in cancer cells.

Indexed as

DNA Breaks, Double-StrandedDNA RepairPrecision MedicineB7-H1 AntigenCell CommunicationCell Cycle CheckpointsCell DeathCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA DamageDNA FragmentationDNA, NeoplasmHumansLymphocyte ActivationMembrane ProteinsMicrosatellite InstabilityMutationB7-H1 AntigenCD274 protein, humancGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, NeoplasmMembrane ProteinsNucleotidyltransferasesProgrammed Cell Death 1 ReceptorRNA, MessengerSTING1 protein, humanSTING Proteinclinical protocolcombined modality therapycytotoxic T lymphocyteDNA damagesignal transduction

Identifiers

PMID31513320
PMCPMC6824998
OpenAlexW2973095158

What OpenQuestion holds

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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.