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Preclinical investigation reveals chemotherapy-induced stromal damage promotes metastatic outgrowth in breast cancer models, indicating that senolytic BCL-xL inhibition is insufficient.
, chemotherapy treatment induces SASP expression in normal tissues; however, the accumulation of senescent cells is limited, and BCL-xL inhibitors are unable to reduce chemotherapy-enhanced metastasis. This likely reflects that chemotherapy-exposed stromal cells do not enter a BCL-xL-dependent phenotype or switch their dependency to other anti-apoptotic BCL-2 family members. This study highlights the role of the metastatic microenvironment in controlling outgrowth of disseminated tumor cells and the need to identify additional approaches to limit the pro-tumorigenic effects of therapy-induced normal tissue damage.
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Perkins et al. (2023) studied this question.
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