{'fraction_non_alphanumeric': 0.020342612419700215, 'fraction_numerical': 0.011777301927194861, 'mean_word_length': 5.275167785234899, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Circadian function in cancer: Regulating the DNA damage response

Proper circadian clock function is essential for the coordination of cellular functions within an organism in response to light and dark cycles. Although epidemiological studies have linked altered circadian rhythms to cancer susceptibility (1, 2), the molecular mechanisms tying the circadian clock to cancer are poorly understood. In PNAS, Lee and Sancar (3) demonstrate that loss of the core circadian clock proteins Cry1 and Cry2 can sensitize tumor cells to DNA damage-induced apoptosis. This effect is shown to be particularly relevant in cells that have lost p53 (TP53), a key tumor suppressor and mediator of chemosensitivity, which is mutated or deleted in the majority of human cancers. These findings imply unique roles for circadian rhythm in regulating the DNA damage response and point to a potential avenue for treating refractory p53-deficient cancers.