Evidence map›Paper›PMID 38814541›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2024

Almonertinib and alflutinib show novel inhibition on rare EGFR S768I mutant cells.

Xiangkai Wei, Guoliang Zhang, Qian Liu, Zhiyuan Niu, Chunhong Chu, Chenxue Liu, Ke Wang, Lanxin Li, Rui Wang, Wenrui Cui and 4 more

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Xiangkai Wei *Department of Anesthesiology, The First Affiliated Hospital of Henan University, Henan University, No. 357, Ximen Avenue, Kaifeng, 475000, Henan, China.
Guoliang Zhang *Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Qian LiuDepartment of Anesthesiology, The First Affiliated Hospital of Henan University, Henan University, No. 357, Ximen Avenue, Kaifeng, 475000, Henan, China.
Zhiyuan NiuDepartment of Anesthesiology, The First Affiliated Hospital of Henan University, Henan University, No. 357, Ximen Avenue, Kaifeng, 475000, Henan, China.
Chunhong ChuTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Chenxue LiuTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Ke WangTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Lanxin LiTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Rui WangTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Wenrui CuiTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Huixia XuTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Chenyang LiuTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China.
Ying WangDepartment of Anesthesiology, The First Affiliated Hospital of Henan University, Henan University, No. 357, Ximen Avenue, Kaifeng, 475000, Henan, China. Wangy1528@126.com.
Lei AnTranslational Medicine Center, Huaihe Hospital of Henan University, Henan University, No. 115, Ximen Avenue, Kaifeng, 475000, China. anlei@henu.edu.cn.ORCID http://orcid.org/0000-0002-9778-2787

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeEGFR classical mutations respond well to EGFR tyrosine kinase inhibitors. However, it is uncertain whether currently available EGFR-TKIs are effective against rare EGFR mutations and compound mutations. Herein, the effectiveness of almonertinib and alflutinib, the third-generation tyrosine kinase inhibitors developed in China, on rare EGFR S768I mutations and compound mutations is identified.

methodsIn this study, using CRISPR method, four EGFR S768I mutation cell lines were constructed, and the sensitivity of EGFR to almonertinib and alflutinib was tested, with positive controls being the 1st (gefitinib), 2nd (afatinib), and 3rd (osimertinib) generation drugs.

resultsThe present results indicate that almonertinib and alflutinib can effectively inhibit cell viability and proliferation in rare EGFR S768I mutations through the ERK or AKT pathways in a time-dependent manner, by blocking the cell cycle and inhibiting apoptosis.

conclusionsThese findings suggest that almonertinib and alflutinib may be potential therapeutic options for non-small cell lung cancer patients with the EGFR S768I mutation.

Indexed as

ApoptosisCell ProliferationErbB ReceptorsMutationProtein Kinase InhibitorsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell SurvivalHumansIndazolesLung NeoplasmsMorpholinesPyrazines6-(1H-indazol-6-yl)-N-(4-morpholinophenyl)imidazo(1,2-a)pyrazin-8-amineAntineoplastic AgentsEGFR protein, humanErbB ReceptorsIndazolesMorpholinesProtein Kinase InhibitorsPyrazinesAlflutinibAlmonertinibCytotoxicologyEGFRMutantTyrosine kinase inhibitor

Identifiers

PMID38814541

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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.