Evidence map›Paper›PMID 35482455›Full record

ArticleBlood advances2022

Platelets upregulate tumor cell programmed death ligand 1 in an epidermal growth factor receptor-dependent manner in vitro.

Qiuchen Guo, Michael W Malloy, Harvey G Roweth, Sandra S McAllister, Joseph E Italiano, Elisabeth M Battinelli

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Oncogenic KRASInternational journal of molecular sciences · 2025
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  18. Platelets in Alcohol-Associated Liver Disease: Interaction With Neutrophils.Cellular and molecular gastroenterology and hepatology · 2024
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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

6 authors at 3 institutions in 1 country.

Qiuchen GuoDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.ORCID 0000-0001-5332-4752
Michael W MalloyDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Harvey G RowethDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Sandra S McAllisterDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Joseph E ItalianoDepartment of Medicine, Harvard Medical School, Boston, MA.
Elisabeth M BattinelliDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Brigham and Women's Hospital · USBoston Children's Hospital · USBroad Institute · US

Funding

How does malignancy subvert platelet and megakaryocytic biology?R01CA200748 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BATTINELLI, ELISABETH M, ITALIANO, JOSEPH E · 2017 to 2021
$2.7M
NCI NIH HHS R01 CA200748
6 · The paper itself

Abstract

Programmed death ligand 1 (PD-L1) is an immune checkpoint protein that suppresses cytotoxic T lymphocytes and is often overexpressed in cancers. Due to favorable clinical trial results, immune checkpoint inhibition (ICI) is part of Food and Drug Administration approved immuno-oncology therapies; however, not all patients benefit from ICI therapy. High blood platelet-to-lymphocyte ratio has been associated with failure of ICI treatment, but whether platelets have a role in hindering ICI response is unclear. Here, we report that coculturing platelets with cancer cell lines increased protein and gene expression of tumor cell PD-L1, which was reduced by antiplatelet agents, such as aspirin and ticagrelor. Platelet cytokine arrays revealed that the well-established cytokines, including interferon-γ, were not the main regulators of platelet-mediated PD-L1 upregulation. Instead, the high molecular weight epidermal growth factor (EGF) is abundant in platelets, which caused an upregulation of tumor cell PD-L1. Both an EGF-neutralizing antibody and cetuximab (EGF receptor [EGFR] monoclonal antibody) inhibited platelet-induced increases in tumor cell PD-L1, suggesting that platelets induce tumor cell PD-L1 in an EGFR-dependent manner. Our data reveal a novel mechanism for platelets in tumor immune escape and warrant further investigation to determine if targeting platelets improves ICI therapeutic responses.

Indexed as

B7-H1 AntigenNeoplasmsAntibodies, NeutralizingAspirinBlood PlateletsCetuximabEpidermal Growth FactorErbB ReceptorsHumansImmune Checkpoint InhibitorsImmune Checkpoint ProteinsInterferon-gammaPlatelet Aggregation InhibitorsTicagrelorUnited StatesAntibodies, NeutralizingAspirinB7-H1 AntigenCetuximabEpidermal Growth FactorErbB ReceptorsImmune Checkpoint InhibitorsImmune Checkpoint ProteinsInterferon-gammaPlatelet Aggregation InhibitorsTicagrelor

Identifiers

PMID35482455
PMCPMC9582587
OpenAlexW4225099655

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.