Dear Colleagues,

The cell cycle undergoes distinct modifications during embryo development and cancer, reflecting different biological functions and deviations from the classical cell cycle of somatic cells.

In early embryonic development of numerous organisms, cell cycles are remarkably rapid and simplified. Following fertilization, embryos undergo cleavage divisions characterized by shortened or absent gap phases (G1 and G2), allowing cells to alternate quickly between DNA synthesis (S phase) and mitosis (M phase). These early embryonic cycles lack the stringent checkpoint controls present in somatic cells, enabling rapid cell division without growth. As development progresses, gap phases gradually lengthen, and checkpoint mechanisms become more robust, allowing cells to respond to developmental signals and differentiation mechanisms.

In contrast, cancer cells exhibit aberrant cell cycle regulation that promotes uncontrolled proliferation. Key modifications include loss of checkpoint control, particularly at the G1/S restriction point, often through mutations in tumor suppressors such as p53 and Rb. Oncogenic activation of cyclins and cyclin-dependent kinases (CDKs) drives cells through cycle checkpoints regardless of DNA damage or growth signals. Cancer cells may also bypass senescence and ignore contact inhibition signals that normally halt division.

Interestingly, both contexts involve overriding normal cell cycle constraints - embryonic cells for necessary development, and cancer cells through pathological mutations. However, embryonic modifications are tightly regulated and temporary, reverting back to checkpoint-controlled cycling as development proceeds, while cancer cells sustain these alterations indefinitely, leading to tumor formation and progression.

In this Special Issue, we welcome original and review articles related to these various cell cycle modifications.

Jacek Kubiak
Guest Editor