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Article

BYL719 reverses gefitinib-resistance induced by PI3K/AKT activation in non-small cell lung cancer cells.

BMC cancer - 8 Aug 2023

Yu Yaya, Xiao Zhenzhen, Lei Chenjing, Ma Changju, Ding Lina, Tang Qing, He Yihan, Chen Yadong, Chang Xuesong, Zhu Yanjuan, Zhang Haibo

Abstract excerpt

Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation often obtain de novo resistance or develop secondary resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs), which restricts the clinical benefit for the patients. The activation of phosphatidylinositol 3-kinase (PI3K)/AKT signal pathway is one of the most important mechanisms for the EGFR-TKIs resistance beyond...

Topics

Humans
Carcinoma, Non-Small-Cell Lung
Gefitinib
Proto-Oncogene Proteins c-akt
Phosphatidylinositol 3-Kinases
ErbB Receptors
Lung Neoplasms
Phosphatidylinositol 3-Kinase
Quinazolines
Protein Kinase Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Drug Resistance, Neoplasm

Cell Line, Tumor

Mutation

Source

Open in PubMed Open full text

Identifiers

PMID: 37553597
DOI: 10.1186/s12885-023-11243-0
PMCID: PMC10408073

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-37553597-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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BYL719 reverses gefitinib-resistance induced by PI3K/AKT activation in non-small cell lung cancer cells.PMID 37553597Read ↗

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