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Recent work from Taylor Malachowski and others in the lab have shown senescence drives and sustains CIPN, a debilitating side effect of chemotherapy. Her approach can reverse this without compromising the anti-tumor effects of chemotherapy. Will this work in patients??? See:https://www.biorxiv.org/cgi/content/short/2026.08.04.742055v1https://www.biorxiv.org/cgi/content/short/2026.08.04.742055v1
Chemotherapy induces CAR cell senescence that drives bone loss
Macrophage eating breast tumor cell.
Senescent CAFs (senCAFs) are present in human breast cancers
Vignettes
Senescent fibroblasts create immune suppressive environments
Immune cells are found adjacent to senescent cells in human skin (left). A pattern that is similar to what we find in the FASST mouse (right). Further analyses suggest that these cells are immunosuppressive raising the possibility that they contribute to cancer.
Chemotherapy-induced senescence drives bone loss --- stopping therapy-induced co-morbidities to increase patient quality of life.
While estrogen is important for bone homeostasis, woman treated with chemotherapy lose significantly more bone than woman in menopause. We show that chemotherapy-induced senescence drives bone loss. We can rescue chemotherapy-induced bone loss by killing senescent cells or inhibiting the p38MAPK/MK2 pathways.
Targeting the metastatic niche to reduce breast progression --- towards to clinical trial
p38MAPK and MK2 inhibitors limit breast cancer metastasis and preserve bone integrity. When we combine p38i and angonist anti-OX40 we significantly limit metastatic growth in bone and visceral organs.
The microenvironment impacts tumor cell dormancy
Following treatment of primary breast cancer, up to 20% of patients can experience a recurrence 6 months to 25 years later. What maintains tumor cell dormancy and what drives indolent disease to reactivate? It is clear that both cell autonomous and extrinsic factors impact breast cancer tumor cell dormancy. We are studying both aspects of tumor cell dormancy.