In cancer, disruptions in the regulation of cell division can occur at various cell cycle checkpoints, leading to uncontrolled cell proliferation. Mutations in genes involved in cell cycle control, such as tumour suppressor genes (e.g., p53) or oncogenes (e.g., Ras), can contribute to these disruptions. Additionally, defects in DNA repair mechanisms can result in the accumulation of genetic abnormalities, further promoting cancer development. Understanding the aberrations in the cell cycle regulation and identifying key molecular targets involved in cancer cell division are crucial for developing targeted therapies to treat cancer. In normal cells, the cell cycle is tightly regulated to ensure proper growth and maintenance of tissues. However, in cancer cells, cell cycle regulation becomes disrupted, leading to uncontrolled cell division and tumour formation. In the first phase of the cell cycle, the G1 phase (Gap 1 phase) the cell grows (via a co-ordinated increase in biosynthesis) and carries out its normal maintenance functions. The G1 phase also involves monitoring of any DNA damage and initiation of repair mechanisms. However, in cancer cells: 1) the G1 phase is often markedly shortened, allowing cells to quickly progress to the next cell cycle phase without fully repairing DNA damage; 2) in S Phase (Synthesis phase) DNA replication occurs, resulting in the synthesis of identical copies of the cell's genetic material. In cancer cells, the S phase may be further dysregulated, leading either to excessive DNA replication or to errors in DNA replication, which can then contribute to genomic instability; 3) G2 phase (Gap 2 phase), the cell continues biosynthesis and prepares for cell division by ensuring proper DNA replication and repair. Again, cancer cells may have a markedly shorter G2 phase than normal cells, leading to inadequate DNA repair before entering mitosis; 4) M phase (Mitosis phase), the stage of active cell division, during which the replicated DNA, now in reformed chromosomes, is equally distributed into two daughter cells. Mitosis consists of several distinct steps: prophase, prometaphase, metaphase, anaphase, and telophase. Cancer cells often exhibit abnormal mitotic activity, such as an increased frequency of mitotic divisions or abnormal chromosomal segregation; 5) G0 Phase (Resting Phase): After completing the cell cycle, normal cells can enter the G0 phase, a non-dividing state. In normal cells, this phase allows cells to temporarily or completely exit the cell cycle, perform specialized functions, or undergo differentiation. However, cancer cells tend to bypass the G0 phase and continuously proliferate. We provide a wide product catalogue of research reagents for studying cell division, including Ki67 antibodies, PCNA antibodies, Ku70 antibodies, Cortactin antibodies, and Cdk5 ELISA Kits. Explore our full cell division product range below and discover more, for less.