KEY POINTS
- A549 non-small cell lung cancer cells were irradiated with 8 Gy of X-rays or carbon ions with a linear energy transfer of 73 keV/µm.
- RNA sequencing was performed four hours after irradiation using four independent biological replicates per irradiated condition.
- Both modalities activated shared p53 and apoptosis-associated DNA-damage responses.
- Carbon ions selectively suppressed mitotic regulators including CENPE, KIF2C, PLK1 and BUB1, together with multiple core and linker histone genes.
- High-linear-energy-transfer irradiation also preferentially enriched tumour-necrosis-factor, nuclear-factor-κB, extracellular-matrix, adhesion and KRAS-associated stress pathways.
CLINICAL TAKEAWAY
Carbon ions did more than amplify the early photon response in this model; they produced a qualitatively different transcriptional programme involving mitotic and chromatin regulation. The findings cannot be translated directly to patients because they derive from one cell line, an equal physical rather than biologically equivalent dose, and a single time point.