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

Coexistence of p16/CDKN2A homozygous deletions and activating EGFR mutations in lung adenocarcinoma patients signifies a poor response to EGFR-TKIs.

Lung cancer (Amsterdam, Netherlands) - 1 Dec 2016

Jiang Juhong, Gu Yingying, Liu Jing, Wu Ruibin, Fu Lin, Zhao Jin, Guan Yubao

Abstract excerpt

OBJECTIVES: Activating mutations in the epidermal growth factor receptor (EGFR) are strongly predictive of EGFR-tyrosine kinase inhibitor (TKI) activity in non-small cell lung cancer (NSCLC). However, primary resistance to EGFR-TKIs occurs in approximately 20-30% of NSCLC patients with EGFR mutations. The goal of this study was to determine whether p16/CDKN2A homozygous deletion (HD) is associated with primary...

Read the complete abstract on PubMed

Topics

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

Share to Adenocarcinoma
Share to Adenocarcinoma of Lung

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Disease-Free Survival

Share to Drug Resistance, Neoplasm

Share to ErbB Receptors

Share to Neoplasm Staging

Share to Protein Kinase Inhibitors

Source

Identifiers

PMID: 27987577
DOI: 10.1016/j.lungcan.2016.10.015

Genes

EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 8 closest

Coexistence of p16/CDKN2A homozygous deletions and activating EGFR mutations in lung adenocarcinoma patients signifies a poor response to EGFR-TKIs.PMID 27987577Read ↗

Association of p16 homozygous deletions with clinicopathologic characteristics and EGFR/KRAS/p53 mutations in lung adenocarcinoma.Semantic proximity Read ↗

Primary resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in patients with non-small-cell lung cancer harboring TKI-sensitive EGFR mutations: an exploratory study.Semantic proximity Read ↗

Intrinsic Resistance to Osimertinib in EGFR Mutated NSCLC Cell Lines Induced by Alteration in Cell-Cycle Regulators.Semantic proximity Read ↗

Cyclin D1 Amplification and p16(MTS1/CDK4I) Deletion Correlate With Poor Prognosis in Head and Neck TumorsSemantic proximity Read ↗

Putative mechanisms of primary resistance to EGFR-targeted therapies: A retrospective study.Semantic proximity Read ↗

DNA damage response and repair gene mutations are associated with tumor mutational burden and outcomes to platinum-based chemotherapy/immunotherapy in advanced NSCLC patients.Semantic proximity Read ↗

Clinical significance of DNA damage response mutations in stage I and stage IIIa NSCLC.Semantic proximity Read ↗

Dual Biomarker Combining DNA Damage Repair Gene Mutations and PD-L1 Expression for Immune Checkpoint Inhibitors in Non-small Cell Lung Cancer.Semantic proximity Read ↗

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