Combination treatment with quantum molecular resonance and secretome attenuates the chimeric transcript response to oxidative stress in retinal pigment epithelial cells

Chimeric transcripts, long regarded as hallmarks of oncogenesis, are also generated in non-tumour cells under environmental stress, but remain poorly quantified in perturbation models. We profiled the chimeric transcriptome of retinal pigment epithelial (ARPE-19) cells across a balanced factorial design of 72 biological samples spanning oxidative stress, Quantum Molecular Resonance (QMR) therapy, a therapeutic secretome and their combination. Using a tiered pipeline and depth-normalised count models, oxidative stress increased the chimeric transcript burden by 33% (incidence-rate ratio 1.33, 95% CI 1.21-1.46, permutation p = 0.002). Modelling chimeric junctions jointly, therapy specifically reversed the stress-induced component (stress x therapy interaction IRR 0.52, 95% CI 0.32-0.84, p = 0.007), while constitutive chimeras, a negative control, showed no response (p = 0.49). The derailment was not random with respect to coding potential: oxidative stress preferentially induced chimeras preserving the reading frame, hence translatable (stress x frame ratio 2.59, 95% CI 1.11-6.04, p = 0.028). The effect was strongest for combined QMR+secretome treatment (IRR 0.40, q = 0.007). One junction, CTDNEP1 -ENSG00000262526, survived false-discovery-rate control and was confirmed by orthogonal callers, RT-qPCR and Sanger sequencing. The chimeric burden is thus a measurable, non-random and therapeutically reversible phenotype of oxidative stress; the generative mechanism remains undetermined.