Evidence map›Paper›PMID 31467431›Full record

ArticleOncogene2020

Microparticles from tumors exposed to radiation promote immune evasion in part by PD-L1.

Michael Timaner, Ruslana Kotsofruk, Ziv Raviv, Ksenia Magidey, Dvir Shechter, Tal Kan, Alexander Nevelsky, Shahar Daniel, Elisabeth G E de Vries, Tongwu Zhang and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  15. Extracellular vesicle-based checkpoint regulation and immune state in cancer.Medical oncology (Northwood, London, England) · 2022
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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 5 institutions in 4 countries.

Michael Timaner *Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Ruslana Kotsofruk *Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Ziv RavivCell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Ksenia MagideyCell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Dvir ShechterCell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Tal KanCell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Alexander NevelskyOncology Institute, Radiation Oncology Unit, Rambam Health Care Campus, Haifa, Israel.
Shahar DanielOncology Institute, Radiation Oncology Unit, Rambam Health Care Campus, Haifa, Israel.
Elisabeth G E de VriesDepartment of Medical Oncology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Tongwu ZhangDivision of Cancer Epidemiology & Genetics, Integrative Tumor Epidemiology Branch, National Cancer Institute, National Institute of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-2124-2706
Orit Kaidar-PersonOncology Institute, Radiation Oncology Unit, Rambam Health Care Campus, Haifa, Israel.
Robert S KerbelSunnybrook Health Sciences Centre, Toronto, ON, Canada.
Yuval ShakedCell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion, Haifa, Israel. yshaked@tx.technion.ac.il.
Rambam Health Care Campus · ILNational Cancer Institute · USSunnybrook Health Science Centre · CATechnion – Israel Institute of Technology · ILUniversity Medical Center Groningen · NL

Funding

European Research Council 260633European Research Council 771112
6 · The paper itself

Abstract

Radiotherapy induces immune-related responses in cancer patients by various mechanisms. Here, we investigate the immunomodulatory role of tumor-derived microparticles (TMPs)-extracellular vesicles shed from tumor cells-following radiotherapy. We demonstrate that breast carcinoma cells exposed to radiation shed TMPs containing elevated levels of immune-modulating proteins, one of which is programmed death-ligand 1 (PD-L1). These TMPs inhibit cytotoxic T lymphocyte (CTL) activity both in vitro and in vivo, and thus promote tumor growth. Evidently, adoptive transfer of CTLs pre-cultured with TMPs from irradiated breast carcinoma cells increases tumor growth rates in mice recipients in comparison with control mice receiving CTLs pre-cultured with TMPs from untreated tumor cells. In addition, blocking the PD-1-PD-L1 axis, either genetically or pharmacologically, partially alleviates TMP-mediated inhibition of CTL activity, suggesting that the immunomodulatory effects of TMPs in response to radiotherapy is mediated, in part, by PD-L1. Overall, our findings provide mechanistic insights into the tumor immune surveillance state in response to radiotherapy and suggest a therapeutic synergy between radiotherapy and immune checkpoint inhibitors.

Indexed as

AnimalsB7-H1 AntigenBreast NeoplasmsCell-Derived MicroparticlesCell Line, TumorFemaleHeterograftsHumansImmune EvasionImmunomodulationMiceProgrammed Cell Death 1 ReceptorSignal TransductionT-Lymphocytes, CytotoxicB7-H1 AntigenCD274 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID31467431
PMCPMC6937213
OpenAlexW2971235103

What OpenQuestion holds

Textmetadata
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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.