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Cells run on a 24-hour clock that gates cell division, DNA repair, and drug metabolism. Cancers often break their clocks, and the time of day a drug or immunotherapy is given can change how well it works.
The CLOCK/BMAL1-PER/CRY loop times metabolism, cell-cycle checkpoints, and DNA repair; shift work is a probable carcinogen (IARC 2A) and clock-gene disruption accelerates tumorigenesis in mice. Chronomodulated chemotherapy (Lévi, oxaliplatin/5-FU) improved tolerability in colorectal cancer; retrospective and prospective data (MEMOIR, 2024-25) suggest checkpoint inhibitors given earlier in the day yield longer survival, likely through T-cell trafficking rhythms. Clock-targeting drugs (REV-ERB agonists, CRY stabilisers) are preclinical. Implementation is cheap but trial evidence is still limited.
A city that lowers its bridges only at certain hours. Send the army (drug, T cells) when the bridges are down and it gets in; send it at midnight and it waits outside.
Shares MYC, MYC, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares WEE1, MYC, MYC, p53 / RB / cell-cycle checkpoint and the tag mechanism.
Shares Abramson Cancer Center, University of Pennsylvania, MYC, MYC, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares Abramson Cancer Center, University of Pennsylvania, MYC, MYC and the tag mechanism.
Shares MYC, p53 / RB / cell-cycle checkpoint, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares MYC, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares Abramson Cancer Center, University of Pennsylvania, PD-1 / PD-L1 immune checkpoint & T-cell activation and the tag mechanism.
Shares p53 / RB / cell-cycle checkpoint, Memorial Sloan Kettering Cancer Center and the tag mechanism.