Evidence map›Paper›PMID 31747941›Full record

ArticleMolecular cancer2019

EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression.

Shunli Peng, Rong Wang, Xiaojuan Zhang, Yueyun Ma, Longhui Zhong, Ke Li, Akihiro Nishiyama, Sachiko Arai, Seiji Yano, Wei Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 2 pooled it
13.1field-weighted citation impact, top 1% 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

206 citing papers in PubMed, 2 syntheses or guidelines pooled it, 311 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

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

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

10 authors at 3 institutions in 2 countries.

Shunli PengDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Rong WangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Xiaojuan ZhangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Yueyun MaDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Longhui ZhongDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Ke LiCenter for Clinical Medicine Research, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Akihiro NishiyamaDivisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Sachiko AraiDivisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Seiji YanoDivisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan. syano@staff.kanazawau.ac.jp.
Wei WangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China. wangwei9500@hotmail.com.
Nanfang Hospital · CNKanazawa University · JPSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe ATLANTIC trial reported that higher PD-L1 expression in tumors was involved in a higher objective response in patients with EGFR

methodsThe correlation among PD-L1, c-MET, and HGF was analyzed based on TCGA datasheets and paired NSCLC specimens before and after acquired EGFR-TKI resistance. EGFR-TKI resistant NSCLC cells with three well-known mechanisms, c-MET amplification, hepatocyte growth factor (HGF), and EGFR-T790M, were investigated to determinate PD-L1 expression status and immune escape ability. PD-L1-deleted EGFR-TKIs sensitive and resistant cells were used to evaluate the immune escape ability of tumors in mice xenograft models.

resultsPositive correlations were found among PD-L1, c-MET, and HGF, based on TCGA datasheets and paired NSCLC specimens. Moreover, the above three resistant mechanisms increased PD-L1 expression and attenuated activation and cytotoxicity of lymphocytes in vitro and in vivo, and downregulation of PD-L1 partially restored the cytotoxicity of lymphocytes. Both MAPK and PI3K pathways were involved in the three types of resistance mechanism-induced PD-L1 overexpression, whereas the NF-kappa B pathway was only involved in T790M-induced PD-L1 expression.

conclusionsHGF, MET-amplification, and EGFR-T790M upregulate PD-L1 expression in NSCLC and promote the immune escape of tumor cells through different mechanisms.

Indexed as

AnimalsB7-H1 AntigenCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmErbB ReceptorsGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMolecular Targeted TherapyPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionT-LymphocytesB7-H1 AntigenCD274 protein, humanEGFR protein, humanErbB ReceptorsPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktEGFR-TKIs resistanceImmunotherapyLung cancerPD-L1Signaling pathways

Identifiers

PMID31747941
PMCPMC6864970
OpenAlexW2991567947

What OpenQuestion holds

Textmetadata
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.