Function of pRb
pRB carries out its gatekeeping function by binding E2F, a protein which triggers the cell's DNA replication machinery. As long as pRb and E2F are bound, the cell cannot pass the restriction point and begin copying its DNA. Of course, there is a way in which pRb can lose its grip, and tumor cells are able to use this to their advantage, even without a direct mutation of pRb.
The grip between pRb and E2F, and control of DNA replication, is in turn managed by proteins known as cyclins, and their partners, called cyclin-dependent kinases (CDKs). Specifically, pRb is monitored by cyclin D1, and CDK 4 or 6. These proteins are activated as part of a chain reaction that starts when growth factors outside the cell interact with receptors on the cell surface. Once active, they cause a chemical change in pRb, caused phosphorylation, which forces it to release E2F. Then E2F is able to signal to the cell that it can copy its DNA and prepare to divide.
Tumor cells can short-circuit this process by increasing the activity of the cyclins and CDKs holding pRb in check. Common ways of doing so are by substantially increasing the cell's production of growth factors, which in turn are taken up by the receptors. The receptors themselves may also be mutated and "stuck in the on position" without growth factors being present. However, pRb itself can also be disabled directly through mutation.