Evidence map›Paper›PMID 28218497›Full record

ArticleMolecular oncology2017

Chemotherapy induces tumor immune evasion by upregulation of programmed cell death ligand 1 expression in bone marrow stromal cells.

Mengqi Yang, Panpan Liu, Kefeng Wang, Christophe Glorieux, Yumin Hu, Shijun Wen, Wenqi Jiang, Peng Huang

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

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  17. Modeling chemical effects on breast cancer: the importance of the microenvironment in vitro.Integrative biology : quantitative biosciences from nano to macro · 2020
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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

8 authors at 3 institutions in 2 countries.

Mengqi YangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Panpan LiuSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Kefeng WangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Christophe GlorieuxSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yumin HuSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Shijun WenSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Wenqi JiangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Peng HuangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Sun Yat-sen University · CNState Key Laboratory of Oncology in South ChinaSun Yat-sen University Cancer Center · CN

Funding

Novel Strategies to Target Leukemia-Stromal InteractionsR01CA172724 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PELICANO, HELENE · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA172724
6 · The paper itself

Abstract

Programmed cell death ligand 1 (PD-L1) is a negative regulator of the immune response that enables tumor cells to escape T-cell immunity. Although PD-L1 expression in cancer cells has been extensively studied, the expression of PD-L1 in stromal cells and its clinical significance remain largely unknown. Here, we show that bone marrow stromal cells express a low level of PD-L1 and that this molecule is significantly upregulated by key drugs used in the treatment of lymphoma at clinically relevant concentrations. Mechanistically, chemotherapeutic drugs induce PD-L1 expression in stromal cells through upregulation of granulocyte macrophage colony-stimulating factor and activation of the extracellular signal-regulated kinase (ERK) 1/2 signaling pathway. Suppression of ERK by a chemical inhibitor or genetic silencing of ERK2 expression prevents drug-induced PD-L1 expression. PD-L1 expression is upregulated in the bone marrow stromal cells of mice treated with doxorubicin and in drug-treated bone marrow specimens from lymphoma patients. Drug-induced PD-L1 expression in stromal cells can cause significant impairment of T-cell functions. Overall, our study reveals a previously unrecognized mechanism by which chemotherapy induces tumor immune evasion by upregulation of PD-L1 in bone marrow stromal cells, and provides new evidence for the combination of chemotherapy and anti-PD-L1/PD-1 as an effective strategy for treatment of lymphoma and other cancers.

Indexed as

AnimalsAntineoplastic AgentsB7-H1 AntigenCells, CulturedCell SurvivalGranulocyte-Macrophage Colony-Stimulating FactorHumansLymphomaMAP Kinase Signaling SystemMesenchymal Stem CellsMice, Inbred C57BLT-LymphocytesTumor EscapeUp-RegulationAntineoplastic AgentsB7-H1 AntigenGranulocyte-Macrophage Colony-Stimulating Factorbone marrow stromal cellschemotherapeutic agentsERK signaling pathwayimmune suppressionprogrammed death ligand 1

Identifiers

PMID28218497
PMCPMC5527486
OpenAlexW2562584621

What OpenQuestion holds

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LicenceCC BY
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.