ArticleNPJ precision oncology2023
Clonal dynamics and Stereo-seq resolve origin and phenotypic plasticity of adenosquamous carcinoma.
Article in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- HESTIA: scalable multimodal integration of histology and high-resolution spatial Transcriptomics for robust spatial domain identification.Briefings in bioinformatics · 2026Article
- Accurate, scalable and cross-platform cell identification for high-resolution spatial transcriptomics.Nature genetics · 2026Article
- Translating spatial transcriptomic signatures in adenosquamous carcinoma into bulk prognostic biomarkers in lung adenocarcinoma: a bottom-up approach.NPJ precision oncology · 2026Article
- Squamous transformation of EGFR-mutant lung adenocarcinoma after EGFR-TKI therapy: clonal continuity, tissue-based diagnosis, and therapeutic evidence gaps.Frontiers in oncology · 2026Review
- Molecular features influencing clinical outcome of advanced HER2-positive gastric cancer receiving trastuzumab plus chemotherapy.Annals of medicine · 2025Article
- SC2Spa: a deep learning based approach to map transcriptome to spatial origins at cellular resolution.BMC bioinformatics · 2025Article
- StereoMM: a graph fusion model for integrating spatial transcriptomic data and pathological images.Briefings in bioinformatics · 2025Article
- The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity.International journal of molecular sciences · 2025Review
- Comprehensive analysis of clinicopathological profiles in adenosquamous carcinoma of the lung.American journal of translational research · 2024Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The genomic origin and development of the biphasic lung adenosquamous carcinoma (ASC) remain inconclusive. Here, we derived potential evolutionary trajectory of ASC through whole-exome sequencing, Stereo-seq, and patient-derived xenografts. We showed that EGFR and MET activating mutations were the main drivers in ASCs. Phylogenetically, these drivers and passenger mutations found in both components were trunk clonal events, confirming monoclonal origination. Comparison of multiple lesions also revealed closer genomic distance between lymph node metastases and the ASC component with the same phenotype. However, as mutational signatures of EGFR-positive lung squamous carcinomas (LUSCs) were more comparable to EGFR-positive ASCs than to wild-type LUSCs, we postulated different origination of these LUSCs, with ASC being the potential intermediate state of driver-positive LUSCs. Spatial transcriptomic profiling inferred transformation from adenocarcinoma to squamous cell carcinoma, which was then histologically captured in vivo. Together, our results explained the development of ASC and provided insights into future clinical decisions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.