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

Genetic instability and recurrent MYC amplification in ALK-translocated NSCLC: a central role of TP53 mutations.

The Journal of pathology - 1 Sept 2018

Alidousty Christina, Baar Till, Martelotto Luciano G, Heydt Carina, Wagener Svenja, Fassunke Jana, Duerbaum Nicolai, Scheel Andreas H, Frank Sandra, Holz Barbara, Binot Elke, Kron Anna, Merkelbach-Bruse Sabine, Ihle Michaela A, Wolf Jürgen, Buettner Reinhard, Schultheis Anne Maria

Abstract excerpt

The anaplastic lymphoma kinase (ALK) rearrangement defines a distinct molecular subtype of non-small cell lung cancer (NSCLC). Despite the excellent initial efficacy of ALK inhibitors in patients with ALK+ lung cancer, resistance occurs almost inevitably. To date, there is no reliable biomarker allowing the identification of patients at higher risk of relapse. Here, we analysed a subset of 53 ALK+ tumours with...

Read the complete abstract on PubMed

Topics

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

Share to Anaplastic Lymphoma Kinase
Share to Gene Amplification

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genomic Instability

Share to Microtubule-Associated Proteins

Share to Oncogene Proteins, Fusion

Share to Proto-Oncogene Proteins c-myc

Share to Serine Endopeptidases

Share to Translocation, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 29885057
DOI: 10.1002/path.5110
PMCID: PMC6120547

Genes

ALK
MYC
EML4
CCND1
TERT
YAP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic instability and recurrent MYC amplification in ALK-translocated NSCLC: a central role of TP53 mutations.PMID 29885057Read ↗

Analysis of the Genomic Landscape in ALK+ NSCLC Patients Identifies Novel Aberrations Associated with Clinical Outcomes.Semantic proximity Read ↗

Anaplastic lymphoma kinase rearrangements in non-small-cell lung cancer: novel applications in diagnostics and treatment.Semantic proximity Read ↗

TP53 or CDKN2A/B covariation in ALK/RET/ROS1-rearranged NSCLC is associated with a high TMB, tumor immunosuppressive microenvironment and poor prognosisSemantic proximity Read ↗

Impact of TP53 mutation status on systemic treatment outcome in ALK-rearranged non-small-cell lung cancer.Semantic proximity Read ↗

ALK gene alterations in cancer: biological aspects and therapeutic implications.Semantic proximity Read ↗

TP53 or CDKN2A/B covariation in ALK/RET/ROS1-rearranged NSCLC is associated with a high TMB, tumor immunosuppressive microenvironment and poor prognosis.Semantic proximity Read ↗

The Genomic Characteristics of ALK Fusion Positive Tumors in Chinese NSCLC PatientsSemantic proximity Read ↗

ALK rearrangements: Biology, detection and opportunities of therapy in non-small cell lung cancerSemantic proximity Read ↗

A Pan-Cancer Review of ALK Mutations: Implications for Carcinogenesis and Therapy.Semantic proximity Read ↗

Molecular heterogeneity and co-altered genes in MET-amplified ALK-positive lung cancer: Implications for MET targeted therapy.Semantic proximity Read ↗

Rare Complex Mutational Profile in an ALK Inhibitor-resistant Non-small Cell Lung Cancer.Semantic proximity Read ↗

Clinical significance of TP53 alterations in advanced NSCLC patients treated with EGFR, ALK and ROS1 tyrosine kinase inhibitors: An update.Semantic proximity Read ↗

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