Immune Boost from Senolytics in Breast and Pancreatic Cancer

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Researchers at Washington University School of Medicine in St. Louis are exploring a new angle in cancer therapy: targeting specific senescent cells that stop dividing. This approach aims to curb the inflammation linked to unchecked growth in breast and pancreatic tumors. The findings are reported in Cancer Discovery.

Senescent cells, which have lost the ability to multiply, show diminished nutrient uptake and reduced capacity to repair chromosomal damage. When these cells accumulate, they can fuel a chronic inflammatory state throughout the body, which is associated with cancer development. The medical term for removing these cells with medication is senolytic therapy.

In mouse models of several breast cancer subtypes, removing particular senescent cells within the tumor microenvironment prompted an immune response. Natural killer cells and other immune components were activated, contributing to slowed tumor progression. Similar strategies using drugs that selectively eliminate nondividing cells sparked activity from T lymphocytes in pancreatic cancer models, also resulting in slower tumor growth.

The researchers believe senolytic drugs could become a valuable addition to existing cancer treatments such as immunotherapy and chemotherapy. They also note that senescent cells influence the immune system differently depending on the cancer type, including breast versus pancreatic cancer. More work is needed to fine tune senolytic therapy to the specific cancer being targeted.

Earlier work in the field showed that cancer cells can adapt to resist certain therapies, underlining the need for complementary strategies like senolytics to enhance treatment effectiveness and resilience across tumor types.

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