Evidence map›Paper›PMID 30390416›Full record

ArticleCancer science2019

Mutational activation of the epidermal growth factor receptor down-regulates major histocompatibility complex class I expression via the extracellular signal-regulated kinase in non-small cell lung cancer.

Satomi Watanabe, Hidetoshi Hayashi, Koji Haratani, Shigeki Shimizu, Junko Tanizaki, Kazuko Sakai, Hisato Kawakami, Kimio Yonesaka, Junji Tsurutani, Yosuke Togashi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 54 citations in OpenAlex.

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  10. A CD8International journal of genomics · 2025
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  12. Overcoming EGFR-TKI resistance by targeting the tumor microenvironment.Chinese medical journal pulmonary and critical care medicine · 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

13 authors at 4 institutions in 1 country.

Satomi WatanabeDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Hidetoshi HayashiDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.ORCID http://orcid.org/0000-0001-8787-5587
Koji HarataniDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Shigeki ShimizuDepartment of Pathology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Junko TanizakiDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Kazuko SakaiDepartment of Genome Biology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Hisato KawakamiDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Kimio YonesakaDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Junji TsurutaniDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Yosuke TogashiDivision of Cancer Immunology, Research Institute/EPOC, National Cancer Center, Kashiwa, Chiba, Japan.
Kazuto NishioDepartment of Genome Biology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.ORCID http://orcid.org/0000-0002-8275-0846
Akihiko ItoDepartment of Pathology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Kazuhiko NakagawaDepartment of Medical Oncology, Faculty of Medicine, Kindai University, Osaka-Sayama, Osaka, Japan.
Kindai University Hospital · JPKindai University · JPChiba Cancer Center · JPShowa University · JP

Funding

Japan Society for the Promotion of Science 16K21506
6 · The paper itself

Abstract

The efficacy of programmed cell death-1 (PD-1) blockade in patients with non-small cell lung cancer (NSCLC) positive for epidermal growth factor receptor (EGFR) gene mutations has been found to be limited, but the underlying mechanisms for this poor response have remained obscure. Given that the recognition by T cells of tumor antigens presented by major histocompatibility complex class I (MHC-I) molecules is essential for an antitumor immune response, we examined the effects of EGFR tyrosine kinase inhibitors (TKIs) on MHC-I expression in NSCLC cell lines. Appropriate EGFR-TKIs increased MHC-I expression at the mRNA and cell surface protein levels in NSCLC cells positive for EGFR mutations including those with the T790M secondary mutation. Trametinib, an inhibitor of the extracellular signal-regulated kinase (ERK) kinase MEK, also increased MHC-I expression, whereas the phosphatidylinositol 3-kinase (PI3K) inhibitor buparlisib did not, suggesting that the MEK-ERK pathway mediates the down-regulation of MHC-I expression in response to EGFR activation. Immunohistochemical analysis of EGFR-mutated NSCLC specimens obtained before and after EGFR-TKI treatment also revealed down-regulation of phosphorylated forms of EGFR and ERK in association with up-regulation of MHC-I, an increased number of infiltrating CD8

Indexed as

A549 CellsB7-H1 AntigenCarcinoma, Non-Small-Cell LungCD8-Positive T-LymphocytesCell Line, TumorDown-RegulationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IHumansLung NeoplasmsMAP Kinase Signaling SystemMutationPhosphorylationProtein Kinase InhibitorsB7-H1 AntigenCD274 protein, humanEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHistocompatibility Antigens Class IProtein Kinase Inhibitorsepidermal growth factor receptormajor histocompatibility complex class Inon-small cell lung cancerphosphatidylinositol 3-kinaseT790M mutation

Identifiers

PMID30390416
PMCPMC6317949
OpenAlexW2898682581

What OpenQuestion holds

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LicenceCC BY-NC
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.