The paradoxical relationship between chromosomal instability and the tumor microenvironment has been explored in this study, highlighting the therapeutic opportunities arising from this interaction.
The implications of targeting histone deacetylase 4 in MELK-overexpressing cancers and how this approach could lead to new treatment strategies in oncology are discussed.
A CRISPR screen was performed to identify genes that enable cells to withstand high levels of chromosomal instability. This is a common feature in chromosomal instability-positive cancers. With this screening we want to understand better how cancer cells develop resistance to chromosomal instability.
The results of Siqi Zheng's study suggested that high expression of cell division cycle 20 could serve as a predictive biomarker for the effectiveness of spindle assembly checkpoint inhibition therapy. Targeting cell division cycle 20, as discussed in more detail, could exploit this aneuploidy-induced therapeutic vulnerability and provide a novel approach to cancer treatment.
The complex interaction between chromosomal instability and extracellular vesicles in the complex context of triple-negative breast cancer has been investigated. When treating triple-negative breast cancer cells with the MPS1 inhibitor reversine, we observed a significant increase in the production and release of extracellular vesicles. For example, reversine-induced chromosomal instability of extracellular vesicles has been found to promote the migratory and invasive properties of triple-negative breast cancer cell lines. The results reveal a potential therapeutic value of EGF-containing fibulin-like extracellular matrix protein 1 in interventions designed to reduce the metastatic capacity of cancer cells affected by chromosomal instability.
