Delayed elective nodal irradiation in head-and-neck cancer radiotherapy reduces acute lymphocyte damage, lymphopenia, and modulates immune signatures.
We investigated whether delayed ENI, using an upfront boost to gross disease and involved nodes followed by standard ENI, reduces radiation-induced lymphocyte DNA damage and lymphopenia (RIL) while modulating peripheral immune signaling compared with standard ENI. Exploratory transcriptomic profiling revealed enhanced interferon and metabolic signaling with delayed ENI, whereas standard ENI preferentially activated inflammatory and damage-associated pathways.
We investigated whether delayed ENI, using an upfront boost to gross disease and involved nodes followed by standard ENI, reduces radiation-induced lymphocyte DNA damage and lymphopenia (RIL) while modulating peripheral immune signaling compared with standard ENI. Exploratory transcriptomic profiling revealed enhanced interferon and metabolic signaling with delayed ENI, whereas standard ENI preferentially activated inflammatory and damage-associated pathways.
What the study was
- Study design
- Observational or experimental study
- Population
- Human participants; details are provided in the abstract.
- Category
- Treatment Innovation
- Maturity
- Validated
- Journal
- Clinical and translational radiation oncology
Why it surfaced
Retained as a 8/10 high-priority candidate for Novel therapeutics: immunotherapy, CAR-T, targeted therapy; PubMed metadata and abstract were assessed conservatively.
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