Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Expression of the non-coding RNA nc886 facilitates the development of tyrosine kinase inhibitor resistance in EGFR-mutated non-small-cell lung cancer cells.

Biochemical and biophysical research communications - 30 Oct 2024

Bui Vivian N V, Daugaard Tina F, Sorensen Boe S, Nielsen Anders L

Abstract excerpt

Treatment of non-small-cell lung cancer (NSCLC) patients possessing EGFR-activating mutations with tyrosine kinase inhibitors (TKIs) can confer an initial promising response. However, TKI resistance inevitably arises. Numerous TKI resistance mechanisms are identified including EGFR secondary mutations, bypass receptor tyrosine kinase (RTK) signaling, and cellular transition e.g. epithelial-mesenchymal transition...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Carcinoma, Non-Small-Cell Lung
Share to DNA Methylation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Epigenesis, Genetic

Share to Epithelial-Mesenchymal Transition

Share to ErbB Receptors

Share to RNA, Untranslated

Share to Tyrosine Kinase Inhibitors

Source

Identifiers

PMID: 39024976
DOI: 10.1016/j.bbrc.2024.150395

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Expression of the non-coding RNA nc886 facilitates the development of tyrosine kinase inhibitor resistance in EGFR-mutated non-small-cell lung cancer cells.PMID 39024976Read ↗

Genome-wide epigenetic and mRNA-expression profiling followed by CRISPR/Cas9-mediated gene-disruptions corroborate the MIR141/MIR200C-ZEB1/ZEB2-FGFR1 axis in acquired EMT-associated EGFR TKI-resistance in NSCLC cellsSemantic proximity Read ↗

Non-coding 886 ( <i>nc886</i> / <i>vtRNA2-1</i> ), the epigenetic odd duck – implications for future studiesSemantic proximity Read ↗

Single-Cell RNA Sequencing in Unraveling Acquired Resistance to EGFR-TKIs in Non-Small Cell Lung Cancer: New PerspectivesSemantic proximity Read ↗

Genomic and Molecular Screenings Identify Different Mechanisms for Acquired Resistance to MET Inhibitors in Lung Cancer Cells.Semantic proximity Read ↗

Liquid biopsy uncovers distinct patterns of DNA methylation and copy number changes in NSCLC patients with different EGFR-TKI resistant mutations.Semantic proximity Read ↗

<i>YES1</i> amplification: a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomicsSemantic proximity Read ↗

NNMT promotes acquired EGFR-TKI resistance by forming EGR1 and lactate-mediated double positive feedback loops in non-small cell lung cancerSemantic proximity Read ↗

YES1 amplification is a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomicsSemantic proximity Read ↗

Integrated Omics Analysis of Non-Small-Cell Lung Cancer Cells Harboring the EGFR C797S Mutation Reveals the Potential of AXL as a Novel Therapeutic Target in TKI-Resistant Lung CancerSemantic proximity Read ↗

Loss of SUV420H2 promotes EGFR inhibitor resistance in NSCLC through upregulation of MET via LINC01510Semantic proximity Read ↗

Loss of KMT5C Promotes EGFR Inhibitor Resistance in NSCLC via LINC01510-Mediated Upregulation of MET.Semantic proximity Read ↗

Next-generation sequencing of paired tyrosine kinase inhibitor-sensitive and -resistant EGFR mutant lung cancer cell lines identifies spectrum of DNA changes associated with drug resistance.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.