A plain language summary about a cell cycle-based, new surveillance mechanism against cancer.

What is this summary about? This is a plain language summary about a new mechanism on how our body selectively looks for any unusual cells that might turn into cancer. It was presented in a paper published in a scientific journal. The paper reviewed the relevant existing literature but importantly, defined a new anti-cancer surveillance system that is different from what was previously known. Our immune system has specialised cells that can detect certain proteins on the surface of cancer cells and induce an immune response to eliminate them before they can form tumours. In this way, it acts as our body's "anti-cancer immune surveillance" system. The new mechanism is a cell cycle-based surveillance against cancer. This mechanism supports our bodies' natural defence by selectively checking for any abnormal or tumour cells and directly altering their growth cycle, or cell cycle, and causing them to lose the ability to form tumors before they can turn into a cancer. At the same time, the normal cells are largely not impacted.What did the research find out? The author of the paper presented a theory with supporting evidence that a cell cycle-based anti-cancer surveillance system exists in our body. When a normally-functioning cell is about to become a tumor cell due to viral infection, genetic mutations or other changes, a tumor-suppressing protein called interferon-beta (IFN-ß) can directly work on the cell to slow its growth at a specific phase of its growth cycle, the S (synthesis) phase, a phase of the cell cycle when DNA is replicating. Accompanied by the slow S phase progression, the cell ages and declines (senescence) and is no longer capable of forming a tumor. This process takes place in most cases when normally-functioning cells are transforming into cancer cells. However, IFN-ß can also stop the growth of certain cancer cell types in the G1 phase (the phase before the S phase) so the cells are no longer cancerous at this stage. Whether the IFN-ß effect is growth arrest in G1 or slowing growth at the S phase is dependent on whether or not the cell has permanently lost the function of another tumor-suppressing protein called retinoblastoma protein-1 (RB1). If the cell has lost RB1 permanently or irreversibly, as in most cases during cancer formation, IFN-ß induces signals to activate proteins related to RB1 (such as a cell cycle regulating protein called p107) to slow its growth at S phase and to trigger cell aging, so it is no longer has the ability to form a cancer. In this process, a barrier or checkpoint within the S phase consisting of activated proteins, such as p107, is in place to slow the S phase progression. If RB1 function can be restored as observed in certain lymphoma or leukaemia cells, IFN-ß signals can activate RB1 directly to stop the cell growth in the G1 phase. The IFN-ß action has little effect on normal cells since they have functional RB1. In normal cells, RB1 function is properly present and it tightly regulates the cell cycle so they are not significantly impacted by the IFN-ß-induced cell cycle effect. Therefore, two proteins IFN-ß and RB1 together with the relevant proteins such as p107, form a network or system for a new anticancer surveillance mechanism to keep watch selectively for and remove cancer cells in our body, i.e., the cell cycle-based anticancer surveillance system. The publication further illustrates the molecular basis underlying the cell cycle change and senescence. The research has implications for future cancer treatment.