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Acquired Resistance Mechanisms to Osimertinib in EGFR Mutant Lung Cancer

ABSTRACT: Acquired Resistance Mechanisms to Osimertinib in EGFR Mutant Lung Cancer

PROVIDER: PRJNA616047 | ENA |

REPOSITORIES: ENA

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Acquired Resistance Mechanisms to Osimertinib in EGFR Mutant Lung Cancer

Project description:Acquired Resistance Mechanisms to Osimertinib in EGFR Mutant Lung Cancer

| PRJNA616048 | ENA

The landscape of therapeutic vulnerabilities in EGFR inhibitor osimertinib drug tolerant persister cells [RNA-seq]

Project description:Third-generation EGFR tyrosine kinase inhibitors (EGFR-TKIs), including osimertinib, an irreversible EGFR-TKI, are important treatments for non-small cell lung cancer with EGFR-TKI sensitizing or EGFR T790M resistance mutations. Whilst patients treated with osimertinib show clinical benefit, disease progression and drug resistance are common. Emergence of de novo acquired resistance from a drug tolerant persister (DTP) cell population is one mechanism proposed to explain progression on osimertinib and other targeted cancer therapies. Here we profiled osimertinib DTPs using RNA-seq, ChIP-seq, and ATAC-seq to characterize the features of these cells and performed drug screens to identify therapeutic opportunities.

2022-04-06 | GSE193258 | GEO

The landscape of therapeutic vulnerabilities in EGFR inhibitor osimertinib drug tolerant persister cells [ChIP-seq]

2022-04-06 | GSE193257 | GEO

The landscape of therapeutic vulnerabilities in EGFR inhibitor osimertinib drug tolerant persister cells [ATAC-seq]

2022-04-06 | GSE193256 | GEO

3' UTR RNA-sequencing of human EGFR-mutant lung cancer cell lines under osimertinib treatment

Project description:Human EGFR-mutant lung cancer cells lines were investigated for their dynamic transcriptional response upon treatment with EGFR-inhibitor osimertinib in a time-series experiment

2021-07-19 | E-MTAB-9884 | biostudies-arrayexpress

The expression profiles of exosomal miRNAs associated with resistance to osimertinib (AZD9291) in EGFR-mutant NSCLC cells

Project description:Exosomal miRNAs involved in resistance to osimertinib in EGFR-mutant NSCLC cells were successfully identified through the microoarray analysis.

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IFITM3-MET interaction drives osimertinib resistance through AKT pathway activation in EGFR-mutant non–small cell lung cancer

Project description:Despite an initial favorable response of EGFR mutant non–small cell lung cancer (NSCLC) to osimertinib, an EGFR tyrosine kinase inhibitor (TKI), resistance inevitably develops. We here performed transcriptomics analysis of pretreatment specimens and identified IFITM3 as a gene specifically upregulated in tumors that develop early resistance to osimertinib. Immunohistochemistry confirmed patients with IFITM3-positive tumors experienced a shorter progression-free survival. Spatial transcriptomics and other analyses further revealed that IFITM3 expression was increased in response to cytokines derived from the tumor microenvironment (TME) during osimertinib treatment. IFITM3 was found to promote the development of osimertinib resistance through interaction with MET and activation of the AKT pathway. Furthermore, combined treatment with a MET inhibitor suppressed the development of osimertinib resistance in a mouse model. Our findings thus reveal that upregulation of IFITM3 represents a previously unrecognized mechanism of osimertinib resistance, and they suggest that targeting the IFITM3-MET axis may improve treatment outcomes.

2025-12-03 | GSE289383 | GEO

HDAC5, an early osimertinib-responsive gene, is a novel therapeutic target for the drug resistance in EGFR-mutant lung adenocarcinoma cells.

Project description:Aberrant epigenetic regulation is closely associated with drug tolerance, an early step in the acquisition of drug resistance. We previously reported that a pioneer transcriptional factor (also called an epigenetic initiator) rapidly induced by osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, plays a pivotal role in promoting the formation of osimertinib-tolerant cells. In this study, to identify novel epigenetic factors associated with osimertinib-tolerance, we performed a comprehensive screening of epigenetic factors whose expression is rapidly induced by osimertinib. Our results revealed that HDAC5, a class IIa histone deacetylase (HDAC), is the most prominently induced epigenetic factor in EGFR-mutant non-small cell lung cancer (NSCLC) cell lines during the early response to osimertinib. Knockdown of HDAC5 significantly reduced the emergence of osimertinib-resistant cells. Furthermore, treatment with LMK235, a selective HDAC5 inhibitor, significantly increased global histone acetylation and enhanced osimertinib-induced apoptosis. These findings underscore the potential of HDAC5 as a novel therapeutic target to overcome osimertinib-resistance and propose LMK235 as a promising compound to provide significant therapeutic benefits for EGFR-mutant NSCLC patients undergoing osimertinib treatment.

2025-04-30 | GSE283536 | GEO

IFITM3-MET interaction drives osimertinib resistance through AKT pathway activation in EGFR-mutant non–small cell lung cancer II

2025-12-03 | GSE289619 | GEO

Relation between TP53 GOF mutation and Osimertinib treatment in EGFR mutant lung cancer: ChIP-seq

Project description:Background: Although TP53 gain-of-function (GOF) mutations promote cancer survival, its effect on EGFR-TKI efficacy remains unclear. We established EGFR-mutant lung cancer cell lines expressing various TP53 genotypes using CRISPR-Cas9 technology and found that TP53-GOF mutant cells develop an early resistance to EGFR-TKI osimertinib.The goal of this study is to elucidate the mechanisms underlying resistance to osimertinib treatment in TP53 GOF mutations through comprehensive gene analysis using ChIP-seq.

2024-01-22 | GSE253478 | GEO

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