There are more than 200 different types of cancer. Tumor cells normally multiply rapidly. Cancers commonly require at least five distinct mutations in the same cell before it becomes a cancer. Such mutations take time, so that cancers occur more frequently as people become older. For example, Trisomy 21 (Down syndrome, and not a cancer) increases greatly as mothers approach the age of 40. In a similar manner, the likelihood that offspring will have neural defects increases with the age of fathers in a survey in Iceland. Description of the cell cycle and checkpoints in that sequence of events: cells in the G0 stage have left the cycle and can differentiate to achieve their special function. Cells in the G0 stage can re-enter the cell cycle for replication only in response to some specific signal to activate this process. This normally involves cyclin-dependent protein kinases (Cdks). Most cancers result from mutations to and subsequent improper function of tumor suppressors or oncogenes. Rb was the first tumor suppressor identified in children with retinoblastoma. A transcription factor known as E2F (early region 2 binding factor) acts to attract RNA polymerase to the TATA box, leading to the synthesis of proteins needed for cell division, and this is blocked by the Rb suppressor. Cdks phosphorylate Rb, making it inactive. The p53 tumor suppressor is the most important for regulating cell division. Explanation of western blots: some viruses can cause cancer.