Cell Cycle — Cellular Division Process

The cell cycle comprises four distinct ordered phases: Gap 1 (G1), Synthesis (S), Gap 2 (G2), and Mitosis (M). During G1, the cell increases in size and synthesises proteins. In the S phase, it duplicates its DNA to ensure identical genetic copies. In G2, further growth and repair occur as the cell prepares for division. Finally, during mitosis (M phase), the chromosomes separate and the cell divides into two daughter cells.

Non-dividing cells exit into a resting state known as G0. Crucially, molecular checkpoints monitored by cyclins and cyclin-dependent kinases (CDKs) verify genomic integrity before letting the cycle advance. Tumour suppressor genes, such as TP53 and RB1, halt the cycle if DNA damage is detected, triggering repair or programmed cell death (apoptosis). In cancer, these protective barriers fail.

Understanding the cell cycle is fundamental to how cancer treatments are planned. Many traditional chemotherapies and newer targeted agents are designed to attack cells at precise moments during division. For example, some drugs damage DNA during replication, while others freeze the cell during mitosis. Knowing how rapidly your cancer cells cycle helps your oncology team select the right combination and scheduling of drugs, maximising damage to cancer cells while giving healthy, slower-dividing tissues time to recover.

While the cell cycle itself is not a blood test, pathology laboratories measure cellular division rates in biopsy specimens. The Ki-67 proliferation index uses immunohistochemistry to evaluate the percentage of actively dividing cells. Flow cytometry measures cellular DNA content to determine what proportion of cells are in the S phase. Molecular panels also test for mutations in regulatory genes such as TP53, CDKN2A, or RB1.

Cell cycle dysregulation is a universal hallmark of all human cancers. It is particularly prominent in rapidly dividing malignancies, including acute leukemias, aggressive non-Hodgkin lymphomas, and small cell lung cancer. It also plays a key role in solid tumours such as hormone-receptor-positive breast cancer, where aberrant cell cycle activity is often driven by cyclin D-dependent pathways that can be targeted therapeutically.

Many oncology therapies depend directly on the cell cycle. Cell-cycle-specific chemotherapies, such as antimetabolites (e.g., methotrexate, fluorouracil) and taxanes (e.g., paclitaxel), act during the S phase and M phase, respectively. Targeted therapies known as CDK4/6 inhibitors (such as palbociclib, ribociclib, and abemaciclib) selectively halt the cell cycle in G1, preventing breast cancer cells from replicating and significantly improving progression-free survival.