Evidence map›Paper›PMID 35883645›Full record

ArticleCells2022

Diverse Mechanisms of Resistance against Osimertinib, a Third-Generation EGFR-TKI, in Lung Adenocarcinoma Cells with an

Shigetoshi Nishihara, Toshimitsu Yamaoka, Fumihiro Ishikawa, Tohru Ohmori, Koichi Ando, Sojiro Kusumoto, Yasunari Kishino, Ryo Manabe, Yuki Hasebe, Hironori Sagara and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. MUC1-C Is a Common Driver of Acquired Osimertinib Resistance in NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
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 1 institution in 1 country.

Shigetoshi NishiharaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Toshimitsu YamaokaAdvanced Cancer Translational Research Institute, Showa University, Tokyo 142-8555, Japan.ORCID 0000-0002-6182-6047
Fumihiro IshikawaCenter for Biotechnology, Showa University, Tokyo 142-8555, Japan.
Tohru OhmoriDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Koichi AndoDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0002-6535-8279
Sojiro KusumotoDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Yasunari KishinoDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Ryo ManabeDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Yuki HasebeAdvanced Cancer Translational Research Institute, Showa University, Tokyo 142-8555, Japan.
Hironori SagaraDivision of Respirology and Allergology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0003-2376-1606
Hitoshi YoshidaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Junji TsurutaniAdvanced Cancer Translational Research Institute, Showa University, Tokyo 142-8555, Japan.ORCID 0000-0002-6260-6943
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is used as a first-line treatment for patients with EGFR-mutant non-small cell lung cancer (NSCLC). However, the mechanisms underlying its anticancer activity, particularly the subsequent development of acquired resistance, are unclear. Herein, we investigated the mechanisms underlying the development of osimertinib resistance by treating NSCLC PC-9 cells (harboring an EGFR-activating mutation) with osimertinib, thereby developing five resistant cell lines, i.e., AZDR3, AZDR6, AZDR9, AZDR11, and AZDR14. The amplification of wild-type

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungLung NeoplasmsAcrylamidesAniline CompoundsDrug Resistance, NeoplasmErbB ReceptorsHumansIndolesMutationProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)PyrimidinesAcrylamidesAniline CompoundsEGFR protein, humanErbB ReceptorsIndolesosimertinibProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)Pyrimidinesdrug resistanceEGFRKRASosimertinibthird-generation epidermal growth factor receptor tyrosine kinase inhibitor

Identifiers

PMID35883645
PMCPMC9319811
OpenAlexW4285595138

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.