Genetic regulation of mitosis and ploidy in cancer

Mitotic abnormality is associated with the onset of aneuploidy, recognized as one of the hallmarks of cancer. The maintenance of a normal ploidy status depends largely on the fidelity of chromosomal division during mitosis. The fidelity of this process is controlled by three main mechanisms: spindle assembly checkpoint (SAC), the amplification cycle of centrosomes, and cytokinesis components and processes. Conversely, deregulation of these mechanisms often leads to abnormal mitotic progression and chromosomal abnormalities, resulting in the onset of aneuploidy. Importantly, several regulatory mechanisms, such as post-translational modification, proteasomal degradation, miRNA-mediated decay, and transcriptional regulation, have been identified as crucial factors for balancing the supply of proteins contributing to mitosis. Genetic alterations affecting these mechanisms can lead to mitotic anomalies and the occurrence of various degrees of aneuploidy, as can be observed in the majority of cancers.

This special topic aims to improve our understanding of genetic changes leading to mitotic anomalies and how these alterations and the resulting aneuploidy contribute to cancer onset, progression, and metastasis. In line with the general direction of the journal, we especially encourage experimental and computational studies applying high-throughput molecular screening methods or the combination of molecular screening data with original functional studies.

In this context, we welcome original research and review articles related, but not limited, to

• Experimentally validated de novo genetic alterations and associated pathways functioning as drivers of malignancy through impact on mitotic processes
• Genetic regulation of mitosis, including the role of chromatin structure modification
• Genomic factors influencing post-translational regulation of mitotic proteins
• Experimental evidence for genetic changes leading to resistance for drug(s) targeting cell division