What are the differences of the Cancer cell cycle and the Normal cell cycle?
The cell cycle has several phases. In G0, or the resting stage, the cell has finished divided and is now at "rest". During the G1 phase, the cell begins a period of growth. Remember, that after cell division, the daughter cells were half the size of the parent after the cytoplasm divided? Now, it is time for the cell to grow to a larger size. New organelles are also manufactured during this phase, so that important enzymes and structural proteins are made. There is the G1 restriction point which makes sure the DNA is intact and the cell has what it needs to function. Genes responsible for DNA synthesis are activated as are S phase CDK proteins. These proteins regulate the cell cycle. The S phase is next and the DNA replicates. Next is G2 phase where the cell experiences another period of growth. G2 checkpoint makes sure that the cell can enter the M phase. The M phase is the mitosis phase. The cell divides into two identical daughter cells. A checkpoint during metaphase checks that the chromosomes aligned at the equator of the cell so that it can then enter anaphase. If everything is okay, the cell completes telophase and cytokinesis and the daughter cells begin interphase once again. In patients with cancer, sometimes a mutation occurs causing uncontrolled mitotic division. It is a loss of cell cycle control. Usuallly, mitosis is the shortest part of the cell cycle and interphase usually takes the longest. In tumor cells, the percent of cells in active cell divsion is much higher than in normal cells. That is due to mutations in cell cycle inhibitors. There is a protooncogene called RAS and its protein RAS is part of a signal pathway that turns on cell division. The protein is activated and changes its shape and becomes switched on transferring its signal to another protein to begin cell division. Once it transfers its signal, it changes its shape again and becomes inactive. In a mutation of the RAS gene, the protein stays switched on, leading to uncontrolled cell division. This leads to the formation of various types of cancer. There are tumor suppressor proteins that when mutated, lead to the formation of cancer when for example, the pRB protein is mutated, its function is to inhibit cell cycle progression until a cell is ready to divide, and if an oncogene binds to it, this can lead to cancer. Tumor suppressor proteins are supposed to destroy cancerous cells and when the genes that code for them are mutated, these proteins can no longer do their job. Eventually, a tumor can form. When the cell cycle is no longer regulated, cancer can occur as daughter cells divide uncontrollably.