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Pores created in cancer cells by attacking cytotoxic T cells (CTLs) are efficiently repaired by these cancer cells to escape programmed cell death mechanisms. A new study led by scientists at Genentech has found preventing a membrane repair mechanism mediated by the ESCRT pathway may make cancer cells more susceptible to attacks by CTLs and could be therapeutically exploited to increase the efficacy of immunotherapies.
Johns Hopkins Medicine researchers have discovered that blocking a specific group of enzymes called caspases boosts the ability of immune cells, including neutrophils and macrophages, to fight MRSA (methicillin-resistant Staphylococcus aureus) and other dangerous skin infections, such as Streptococcus pyogenes and Pseudomonas aeruginosa, without the use of antibiotics. The serendipitous finding may lead to a solution for the growing threat of antibiotic resistance.
Persistent p53 protein expression is linked to increase in cancer cell death following radiation, even in tissues resistant to radiation, a new study finds. When radiation is followed by administration of an experimental anti-cancer drug that prevents p53 degradation and prolongs p53 signaling, tumors in mouse models are found to shrink significantly compared to either radiation or the drug alone.