The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis.

Cancer meiomitosis is defined as the concurrent activation of both mitotic and meiotic machineries in neoplastic cells that confer a selective advantage together with increased genomic instability. MeiCT (meiosis-specific cancer/testis) genes that perform specialized functions in the germline events required for the first meiotic division are ectopically expressed in several cancers. Here we describe the expression profiles of meiCT genes and proteins across a number of cancers and review the proposed mechanisms that increase aneuploidy and elicit reduction division in polyploid cells. These mechanisms are centered on the overexpression and function of meiCT proteins in cancers under various conditions that includes a response to genotoxic stress. Since meiCT genes are transcriptionally repressed in somatic cells, their target offers a promising therapeutic approach with limited toxicity to healthy tissues. Throughout the review, we provide a detailed description of the roles for each gene in the context of meiosis and we discuss proposed functions and outcomes resulting from their ectopic reactivation in cancer.