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Glioblastoma (GBM) is a high-level glioma, and although more in-depth molecular mechanism studies have been conducted on genomic mutations associated with the disease, the patient's total survival is still only 14.6 months.
Although the strategy of maximal surgical resection, combined with radiotherapy and supplemented by complementary chemotherapy with temozolomide, has made some progress in GBM treatment, the long-term survival rate of patients is still low, with survival rates of 25% and 10% for 2 and 5 years, respectively.
previous studies that have shown that the presence of macrophages and small glial cells, which are necessary for tumor growth and macrophage immersion, can affect the development of glioblastoma and prevent patients from developing long-lasting immune responses.
study found that the dual-functioning cytokine IL-33 can act as a regulatory factor for the micro-environment of glioblastoma and promote the development of tumors.
IL-33 plus gliomas were associated with the recruitment of immune cells, and researchers found that in most human glioma samples and mouse models, il-33 expression levels were associated with an increase in tumor-related macrophages/monocytes/small glial cells.
addition, nuclear-positioned and secretion-type IL-33 regulates a number of degeneration factors that promote the formation of tumor micro-environments by co-recruiting and activating inherent immune cells.
, the absence of nuclear IL-33 weakens the recruitment role and significantly inhibits the growth of gliomas, ultimately improving survival rates in patients.
, the findings reveal an example of immune cells being collected and activated, and provide a potential strategy for treating the disease, focusing not only on individual cancer cells, but also on normal host environments.
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