Final answer:
Loss of a tumor suppressor gene function can lead to uncontrollable cell division and cancer, as the cell lacks the necessary 'brakes' to stop proliferating despite DNA damage. Overactive tumor suppressors are not common, as their primary role is to inhibit cell growth. Mutations may lead to cancer by either producing non-functional suppressors or overly active oncogenes.
Step-by-step explanation:
When a tumor suppressor gene is lost or becomes non-functional, it can no longer control cell division, which is similar to a car without brakes. Without these critical 'brakes', cells can divide uncontrollably, a process that can lead to the development of cancer. The p53 protein, for example, which is a product of the p53 gene, normally acts to monitor DNA and prevent damaged cells from dividing. If p53 is mutated, it may fail to stop cell division in response to DNA damage. Conversely, an overactive tumor suppressor gene is not a typical scenario, since tumor suppressors work to inhibit cell division. The question usually pertains to the lack of activity rather than overactivation. Accumulation of damaged DNA without repair, due to a non-functional tumor suppressor gene, inevitably escalates the risk of cancer, as the cell skyrockets through the cell cycle without proper checks and balances.
The biological properties of tumor cells show an absence of regulation that normally governs healthy cell replication, due to mutations that either switch off tumor suppressor genes or turn proto-oncogenes into overly active oncogenes—promoting cancer cell properties.