Evidence map›Paper›PMID 28433633›Full record

ArticleBiochemical and biophysical research communications2017

Angiotensin-converting enzyme 2 is a potential therapeutic target for EGFR-mutant lung adenocarcinoma.

Miki Yamaguchi, Sachie Hirai, Toshiyuki Sumi, Yusuke Tanaka, Makoto Tada, Yukari Nishii, Tadashi Hasegawa, Hiroaki Uchida, Gen Yamada, Atsushi Watanabe and 2 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  13. From ACE2 to COVID-19: A multiorgan endothelial disease.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 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

12 authors at 2 institutions in 1 country.

Miki YamaguchiDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sachie HiraiDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Toshiyuki SumiDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yusuke TanakaDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Makoto TadaDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yukari NishiiDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tadashi HasegawaDepartment of Surgical Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroaki UchidaDivision of Bioengineering, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Gen YamadaDepartment of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Atsushi WatanabeDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroki TakahashiDepartment of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yuji SakumaDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan. Electronic address: sakuma@sapmed.ac.jp.
Sapporo Medical University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EGFR-mutant lung adenocarcinomas contain a subpopulation of cells that have undergone epithelial-to-mesenchymal transition and can grow independently of EGFR. To kill these cancer cells, we need a novel therapeutic approach other than EGFR inhibitors. If a molecule is specifically expressed on the cell surface of such EGFR-independent EGFR-mutant cancer cells, it can be a therapeutic target. We found that a mesenchymal EGFR-independent subline derived from HCC827 cells, an EGFR-mutant lung adenocarcinoma cell line, expressed angiotensin-converting enzyme 2 (ACE2) to a greater extent than its parental cells. ACE2 was also expressed at least partially in most of the primary EGFR-mutant lung adenocarcinomas examined, and the ACE2 expression level in the cancer cells was much higher than that in normal lung epithelial cells. In addition, we developed an anti-ACE2 mouse monoclonal antibody (mAb), termed H8R64, that was internalized by ACE2-expressing cells. If an antibody-drug conjugate consisting of a humanized mAb based on H8R64 and a potent anticancer drug were produced, it could be effective for the treatment of EGFR-mutant lung adenocarcinomas.

Indexed as

Molecular Targeted TherapyAdenocarcinomaAdenocarcinoma of LungAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAnimalsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorErbB ReceptorsHumansLung NeoplasmsACE2 protein, humanAce2 protein, mouseAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsErbB ReceptorsPeptidyl-Dipeptidase AAngiotensin-converting enzyme 2 (ACE2)Antibody-drug conjugate (ADC)EGFR-mutant lung adenocarcinomaEpithelial-to-mesenchymal transition (EMT)Monoclonal antibody (mAb)Tyrosine kinase inhibitors (TKIs)

Identifiers

PMID28433633
PMCPMC7092918
OpenAlexW2607216367

What OpenQuestion holds

Textmetadata
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.