Evidence map›Paper›PMID 25297630›Full record

ArticleCancer research2014

CD47 in the tumor microenvironment limits cooperation between antitumor T-cell immunity and radiotherapy.

David R Soto-Pantoja, Masaki Terabe, Arunima Ghosh, Lisa A Ridnour, William G DeGraff, David A Wink, Jay A Berzofsky, David D Roberts

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

130 citing papers in PubMed, 192 citations in OpenAlex.

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  17. Emerging functions of thrombospondin-1 in immunity.Seminars in cell & developmental biology · 2024
    Review
  18. Targeting HDAC6 improves anti-CD47 immunotherapy.Journal of experimental & clinical cancer research : CR · 2024
    Article
  19. Review
  20. Article

70 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

David R Soto-PantojaLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Masaki TerabeVaccine Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Arunima GhoshLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Lisa A RidnourRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
William G DeGraffRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
David A WinkRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Jay A BerzofskyVaccine Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
David D RobertsLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. dr9y@nih.gov.
National Cancer Institute · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Intramural NIH HHS ZIA SC009172
6 · The paper itself

Abstract

Although significant advances in radiotherapy have increased its effectiveness in many cancer settings, general strategies to widen the therapeutic window between normal tissue toxicity and malignant tumor destruction would still offer great value. CD47 blockade has been found to confer radioprotection to normal tissues while enhancing tumor radiosensitivity. Here, we report that CD47 blockade directly enhances tumor immunosurveillance by CD8(+) T cells. Combining CD47 blockade with irradiation did not affect fibrosarcoma growth in T cell-deficient mice, whereas adoptive transfer of tumor-specific CD8(+) T cells restored combinatorial efficacy. Furthermore, ablation of CD8(+) T cells abolished radiotherapeutic response in immunocompetent syngeneic hosts. CD47 blockade in either target cells or effector cells was sufficient to enhance antigen-dependent CD8(+) CTL-mediated tumor cell killing in vitro. In CD47-deficient syngeneic hosts, engrafted B16 melanomas were 50% more sensitive to irradiation, establishing that CD47 expression in the microenvironment was sufficient to limit tumor radiosensitivity. Mechanistic investigations revealed increased tumor infiltration by cytotoxic CD8(+) T cells in a CD47-deficient microenvironment, with an associated increase in T cell-dependent intratumoral expression of granzyme B. Correspondingly, an inverse correlation between CD8(+) T-cell infiltration and CD47 expression was observed in human melanomas. Our findings establish that blocking CD47 in the context of radiotherapy enhances antitumor immunity by directly stimulating CD8(+) cytotoxic T cells, with the potential to increase curative responses.

Indexed as

Adoptive TransferAnimalsCD47 AntigenCD8-Positive T-LymphocytesCell Line, TumorCytotoxicity, ImmunologicFibrosarcomaGranzymesHumansMelanoma, ExperimentalMiceMice, Inbred C57BLMice, NudeRadiation ToleranceRadiotherapyT-Lymphocytes, CytotoxicCD47 AntigenCd47 protein, mouseGranzymes

Identifiers

PMID25297630
PMCPMC4253868
OpenAlexW2170756973

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.