ArticleCancer medicine2023
Genomic landscape of non-small-cell lung cancer with methylthioadenosine phosphorylase (MTAP) deficiency.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Global research trends in immunotherapy for non-small cell lung cancer patients with KRAS mutations: a bibliometric analysis.Frontiers in oncology · 2024Pooled it
- Integrated transcriptomic and in silico structural analysis identifies NFS1 and HSPA9 as potential regulators associated with mitochondrial ferroptosis and cell death resistance in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Transcriptomic profiling and structural characterization reveal UQCRC1 and COX4I1 as key mitochondrial regulators associated with oxidative stress in multiple sclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Presenting features and outcomes to standard systemic therapies in patients with MTAP-deleted advanced non-small cell lung cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Prevalence and clinico-morphological correlates of STK11 mutations in a large cohort of NSCLC lung adenocarcinomas.Virchows Archiv : an international journal of pathology · 2026Article
- Machine learning-based multi-omic analysis identifies CEP55, DLGAP5, and EZH2 as regulated cell death biomarkers linked to immunotherapy resistance in hepatocellular carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- MTAP Deletion in Oncogenesis: A Synthetic Lethality Scenario.Cancer research · 2026Review
- Review
- SMARCA4-deficient non-small cell lung cancer and immunotherapy resistance: mechanisms and novel strategies-a mini-review.Discover oncology · 2026Review
- Prevalence and Actionability of MTAP Loss in Oncogene-Driven Lung Cancer.bioRxiv : the preprint server for biology · 2026Article
- MTAP-Null Tumors: A Comprehensive Review on Synthetic Vulnerabilities and Therapeutic Strategies.Cells · 2025Review
- Tumor Genomic and Transcriptomic Analysis Integrated With Liquid Biopsy ctDNA Monitoring: Analytical Validation and Clinical Insights.Cancer medicine · 2025Article
- Immune checkpoint inhibitors have limited efficacy inTranslational lung cancer research · 2025Article
- PRMT5 highly expressed on CD16 + CD56- natural killer cells is correlated with NK cells exhaustion in colorectal cancer mesenchyme.Cancer immunology, immunotherapy : CII · 2025Article
- Clinicopathological characterisation ofJournal of clinical pathology · 2025Article
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- AMG 193, a Clinical Stage MTA-Cooperative PRMT5 Inhibitor, Drives Antitumor Activity Preclinically and in Patients with MTAP-Deleted Cancers.Cancer discovery · 2025Article
- Article
- Fuel for thought: targeting metabolism in lung cancer.Translational lung cancer research · 2024Review
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNew treatment strategies for advanced non-small-cell lung carcinoma (NSCLC) include synthetic lethality targets focused on protein arginine methyl transferases such as PRMT5 that exploit the impact of genomic loss of methylthioadenosine phosphorylase (MTAP).
methodsTwenty nine thousand three hundred seventy nine advanced NSCLC cases underwent hybrid-capture based comprehensive genomic profiling between June 1, 2018 and May 31, 2020. PD-L1 expression was determined by immunohistochemistry (Dako 22C3 PharmDx assay).
results13.4% (3928/29,379) NSCLC cases exhibited MTAP loss distributed in adenocarcinoma (59%), squamous cell carcinoma (22%), NSCLC not otherwise specified (16%), and 1% each for large-cell neuroendocrine, sarcomatoid, and adenosquamous carcinoma. Statistically significant differences in mitogenic driver alterations included more KRAS G12C mutations in MTAP-intact versus MTAP-lost (12% vs. 10%, p = 0.0003) and fewer EGFR short variant mutations in MTAP-intact versus MTAP-lost NSCLC (10% vs. 13%, p < 0.0001). Statistically significant differences in currently untargetable genomic alterations included higher frequencies of TP53 (70% vs. 63%, p < 0.0001) and RB1 inactivation (10% vs. 2%, p < 0.0001) in MTAP-intact compared to MTAP-lost NSCLC. SMARCA4 inactivation (7% vs. 10%, p < 0.0001) was less frequent in MTAP-intact versus MTAP-lost NSCLC. Alterations in ERBB2, MET, ALK, ROS1, and NTRK1 did not significantly differ between the two groups. Predictors of immunotherapy efficacy were higher in MTAP-intact versus MTAP-lost NSCLC including tumor mutational burden (9.4 vs. 8.6 mut/Mb, p = 0.001) and low (30% vs. 28%, p = 0.01) and high PD-L1 (32% vs. 30%, p = 0.01) expression. Alterations in biomarkers potentially predictive of immune checkpoint inhibitor resistance (STK11, KEAP1, and MDM2) were similar in the two groups.
conclusionsMTAP loss occurs in 13% of NSCLC, supporting the development of targeted therapies to exploit PRMT5 hyper-dependence. MTAP loss is accompanied by small differences in targeted and immunotherapy options which may impact future combination strategies.
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