Overview
- In tumor-bearing mice, diurnal corticosterone cycles fell by roughly 40–50% within three days, before tumors were palpable.
- Researchers traced the disruption to paraventricular hypothalamic CRH neurons locked in a hyperactive, low-output state through upstream disinhibition.
- Chemogenetic stimulation timed just before the light-to-dark transition reinstated glucocorticoid rhythms.
- Restored cycles coincided with increased intratumoral CD8+ T cells and slower tumor growth, whereas the same stimulation at other times showed no benefit.
- Investigators are probing tumor-to-brain signaling and assessing whether rhythm-enforcing strategies could complement existing therapies, noting the evidence is preclinical.