Evidence map›Paper›PMID 35304574›Full record

ArticleOncogene2022

Preclinical assessment of combination therapy of EGFR tyrosine kinase inhibitors in a highly heterogeneous tumor model.

Hiroshi Ikeuchi, Takeshi Hirose, Masachika Ikegami, Kazuya Takamochi, Kenji Suzuki, Hiroyuki Mano, Shinji Kohsaka

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  4. Review
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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

7 authors at 3 institutions in 2 countries.

Hiroshi IkeuchiDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.
Takeshi HiroseDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0003-1588-9757
Masachika IkegamiDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.
Kazuya TakamochiDepartment of General Thoracic Surgery, Juntendo University School of Medicine, Tokyo, 113-8431, Japan.
Kenji SuzukiDepartment of General Thoracic Surgery, Juntendo University School of Medicine, Tokyo, 113-8431, Japan.
Hiroyuki ManoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0003-4645-0181
Shinji KohsakaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, 104-0045, Japan. skohsaka@ncc.go.jp.ORCID http://orcid.org/0000-0001-8651-6136
Juntendo University · JPNational Cancer Research Institute · GBTokyo Metropolitan Komagome Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of tyrosine kinase inhibitors (TKIs) has improved the treatment of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations. The current research priority is to provide viable treatments for patients who have drug-resistant EGFR mutations. We evaluated the drug sensitivity of various EGFR mutants to monotherapies and combination therapies of EGFR-TKIs. In vitro, the transforming potential and drug sensitivity of 357 EGFR variants were assessed. In vivo, we tested the sensitivity of EGFR variants to different regimens of EGFR-TKIs by examining changes in the proportion of each variant within the tumor. Out of 357 variants thoroughly examined for transforming activities, 144 (40.3%) and 282 (79.0%) transformed 3T3 and Ba/F3 cells, respectively. Among the latter variants, 50 (17.7%) were found to be resistant or only partly resistant to osimertinib or afatinib. Four of 25 afatinib-resistant variants (16%) were sensitive to osimertinib, whereas 25 of 46 osimertinib-resistant variants (54.3%) were sensitive to afatinib. Despite the lack of a synergistic impact, TKI combination treatment effectively reduced in vivo the heterogeneous tumors composed of 3T3 cells with different EGFR variants. Regimens starting with afatinib and subsequently switched to osimertinib suppressed tumor development more efficiently than the opposite combination. Combination EGFR-TKI treatment may decrease tumor growth and prevent the development of resistant variants. This work created an experimental model of a heterogeneous tumor to find the best combination therapy regimen and proposes a basic notion of EGFR-TKI combination therapy to enhance the prognosis of NSCLC patients.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAfatinibAniline CompoundsAnimalsErbB ReceptorsHumansMiceModels, TheoreticalMutationProtein Kinase InhibitorsAfatinibAniline CompoundsEGFR protein, humanErbB ReceptorsProtein Kinase Inhibitors

Identifiers

PMID35304574
PMCPMC9033582
OpenAlexW4220918018

What Socratic 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 Socratic graph.