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- W2998747451 abstract "Chemotherapy is important for cancer treatment, however, toxicities limit its use. While great strides have been made to ameliorate the acute toxicities induced by chemotherapy, long-term comorbidities including bone loss remain a significant problem. Chemotherapy-driven estrogen loss is postulated to drive bone loss, but significant data suggests the existence of an estrogen-independent mechanism of bone loss. Using clinically relevant mouse models, we showed that senescence and its senescence-associated secretory phenotype (SASP) contribute to chemotherapy-induced bone loss that can be rescued by depleting senescent cells. Chemotherapy-induced SASP could be limited by targeting the p38MAPK-MK2 pathway, which resulted in preservation of bone integrity in chemotherapy-treated mice. These results transform our understanding of chemotherapy-induced bone loss by identifying senescent cells as major drivers of bone loss and the p38MAPK-MK2 axis as a putative therapeutic target that can preserve bone and improve a cancer survivor's quality of life. SIGNIFICANCE: Senescence drives chemotherapy-induced bone loss that is rescued by p38MAPK or MK2 inhibitors. These findings may lead to treatments for therapy-induced bone loss, significantly increasing quality of life for cancer survivors." @default.
- W2998747451 created "2020-01-23" @default.
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- W2998747451 date "2020-03-01" @default.
- W2998747451 modified "2023-10-17" @default.
- W2998747451 title "Therapy-Induced Senescence Drives Bone Loss" @default.
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- W2998747451 doi "https://doi.org/10.1158/0008-5472.can-19-2348" @default.
- W2998747451 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7056549" @default.
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