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

PIK3CA mutation as an acquired resistance driver to EGFR-TKIs in non-small cell lung cancer: Clinical challenges and opportunities.

Pharmacological research - 1 Apr 2024

Liu Xiaohong, Mei Wuxuan, Zhang Pengfei, Zeng Changchun

Abstract excerpt

Epithelial growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have significantly enhanced the treatment outcomes in non-small cell lung cancer (NSCLC) patients harboring EGFR mutations. However, the occurrence of acquired resistance to EGFR-TKIs is an unavoidable outcome observed in these patients. Disruption of the PI3K/AKT/mTOR signaling pathway can contribute to the emergence of resistance to EGFR...

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 Class I Phosphatidylinositol 3-Kinases

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to ErbB Receptors

Share to Phosphatidylinositol 3-Kinases

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins c-akt

Share to TOR Serine-Threonine Kinases

Source

Identifiers

PMID: 38432445
DOI: 10.1016/j.phrs.2024.107123

Genes

EGFR
PIK3CA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PIK3CA mutation as an acquired resistance driver to EGFR-TKIs in non-small cell lung cancer: Clinical challenges and opportunities.PMID 38432445Read ↗

New development of inhibitors targeting the PI3K/AKT/mTOR pathway in personalized treatment of non-small-cell lung cancer.Semantic proximity Read ↗

Preclinical rationale for PI3K/Akt/mTOR pathway inhibitors as therapy for epidermal growth factor receptor inhibitor-resistant non-small-cell lung cancer.Semantic proximity Read ↗

Challenge and countermeasures for EGFR targeted therapy in non-small cell lung cancer.Semantic proximity Read ↗

Drug resistance of targeted therapy for advanced non-small cell lung cancer harbored EGFR mutation: from mechanism analysis to clinical strategy.Semantic proximity Read ↗

Convergent Akt activation drives acquired EGFR inhibitor resistance in lung cancer.Semantic proximity Read ↗

Current mechanism of acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors and updated therapy strategies in human nonsmall cell lung cancer.Semantic proximity Read ↗

Molecular target therapeutics of EGF-TKI and downstream signaling pathways in non-small cell lung cancers.Semantic proximity Read ↗

MiR-30a-5p Overexpression May Overcome EGFR-Inhibitor Resistance through Regulating PI3K/AKT Signaling Pathway in Non-small Cell Lung Cancer Cell LinesSemantic proximity Read ↗

Novel PI3K/Akt/mTOR pathway inhibitors plus radiotherapy: Strategy for non-small cell lung cancer with mutant RAS gene.Semantic proximity Read ↗

Unraveling the prevalence of various signalling pathways in non-small-cell lung cancer: a review.Semantic proximity Read ↗

Acquired resistance in oncogene-addicted non-small-cell lung cancer.Semantic proximity Read ↗

Targeting KRASG12D mutation in non-small cell lung cancer: molecular mechanisms and therapeutic potential.Semantic proximity Read ↗

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