ArticleNeoplasia (New York, N.Y.)2024
Spatial whole exome sequencing reveals the genetic features of highly-aggressive components in lung adenocarcinoma.
Article in Neoplasia (New York, N.Y.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A radiomics-based machine learning model for the preoperative differentiation of lung adenocarcinoma subtypes.Quantitative imaging in medicine and surgery · 2026Article
- Comprehensive analysis of a machine learning prognostic model for the interaction between mitochondrial function and lactylation in lung adenocarcinoma.Discover oncology · 2025Article
- A core driver gene set identified based on geMER reveals its potential driver mechanism in pan-cancer.NPJ precision oncology · 2025Article
- Multi‑omics analysis identifies different molecular subtypes with unique outcomes in early-stage poorly differentiated lung adenocarcinoma.Molecular cancer · 2025Article
- Predicting pathological grade of stage I pulmonary adenocarcinoma: a CT radiomics approach.Frontiers in oncology · 2024Article
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28 authors.
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Abstract
In invasive lung adenocarcinoma (LUAD), patients with micropapillary (MIP) or solid (SOL) components had a significantly poorer prognosis than those with only lepidic (LEP), acinar (ACI) or papillary (PAP) components. It is interesting to explore the genetic features of different histologic subtypes, especially the highly aggressive components. Based on a cohort of 5,933 patients, this study observed that in different tumor size groups, LUAD with MIP/SOL components showed a different prevalence, and patients with ALK alteration or TP53 mutations had a higher probability of developing MIP/SOL components. To control individual differences, this research used spatial whole-exome sequencing (WES) via laser-capture microdissection of five patients harboring these five coexistent components and identified genetic features among different histologic components of the same tumor. In tracing the evolution of components, we found that titin (TTN) mutation might serve as a crucial intratumor potential driver for MIP/SOL components, which was validated by a cohort of 146 LUAD patients undergoing bulk WES. Functional analysis revealed that TTN mutations enriched the complement and coagulation cascades, which correlated with the pathway of cell adhesion, migration, and proliferation. Collectively, the histologic subtypes of invasive LUAD were genetically different, and certain trunk genotypes might synergize with branching TTN mutation to develop highly aggressive components.
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