06/06/2025
Not all cells with cancer-linked mutations turn into tumors—so what makes some vulnerable while others stay normal? A new study from researchers at Sinai Health in Toronto has found that the key may lie in how fast a cell divides. They discovered that cells with a shorter total cell cycle duration (Tc)—the time it takes to complete a full division—are much more likely to develop into tumors. This insight could help explain why cancer arises in some tissues but not others, even when the same dangerous mutations are present.
The team started with retinoblastoma, a childhood eye cancer caused by mutations in the Rb gene. They found that mice with mutated Rb genes developed tumors only in specific areas—like the pituitary gland—even though the same mutated cells were present throughout the body. When researchers looked deeper, they noticed that the cells that turned cancerous all had shorter division cycles. This trend was consistent across multiple tissues and various mutations, including ones commonly seen in lung and skin cancers.
Even more interesting, slowing down a cell’s cycle—even without triggering cell death or immune clearance—was enough to stop tumors from forming. Blocking the SKP2–p27–CDK2/CDK1 pathway slowed division and prevented cancer, without changing the cell’s other behaviors. This finding shifts the focus away from only genetic mutations or immune evasion, and toward the role of a cell’s behavior after mutation—especially how fast it divides.
The researchers believe this discovery could change how we think about cancer’s origins and even help identify the specific “cell of origin” in various cancers. It also opens the door to new ways of preventing cancer by targeting cell division speed, offering a fresh approach beyond traditional treatments.