CCNB2: A Promising Target for Cancer Immunotherapy and Drug Sensitivity

In addition to the PI3K-Akt-mTOR inhibitors mentioned above, high expression of CCNB2 is also sensitive to CDK4/6 inhibitors, which are endocrine drugs used in breast cancer treatment. Unfortunately, high expression of CCNB2 confers resistance to drugs that cause DNA damage, inhibit DNA repair, or induce tumor apoptosis. One possible mechanism is that overexpression of CCNB2 can regulate cell cycle arrest and inhibit apoptosis of tumor cells. This suggests that a promising strategy may involve targeting CCNB2 therapy in combination with cell cycle inhibitors or immunotherapy. \n\nOur study has several limitations. Firstly, since multiple information from diverse databases was retrieved for the analysis, systematic bias exists. Secondly, the information from TCGA may be biased, despite our validation in cell lines and clinical specimens. Thirdly, since our results are based on a public database and computational algorithm, further studies are needed to investigate the function and mechanism of biomarkers in BRCA using in vivo and in vitro approaches. Further efforts are needed to explore the role of CCNB2 in cancer and its value as a potential immune target in anticancer therapy. \n\nIn conclusion, our analysis demonstrates, for the first time, a clinically significant correlation of CCNB2 with prognosis, immune cell infiltration, immunity markers such as TMB and MSI, immune checkpoint molecules, and drug sensitivity. This provides valuable insights into the role of CCNB2 in tumorigenesis and immunotherapy.