Findings demonstrate distinct epigenetic programs associated with tumor progression in lung adenocarcinoma, suggesting variability across patients.
These findings indicate patient-specific patterns of tumor evolution in LUAD, with one case showing a progressive AT2-to-tumor transition and another driven by ROS1 fusion-mediated oncogenic signaling. Together, they highlight how transcriptional and epigenetic programs diverge across tumor contexts, contributing to inter-patient heterogeneity in LUAD.
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Kim et al. (2026) studied this question.
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