Why can failures in apoptosis contribute to cancer?

In healthy organisms, apoptosis serves as a vital surveillance mechanism that triggers programmed cell death in damaged, infected, or potentially malignant cells to prevent them from proliferating. Failures in this process contribute to cancer because they allow abnormal tumor cells to evade destruction and survive.12

This evasion typically occurs through specific genetic mutations:

• Inactivation of the p53 gene: This gene normally functions to trigger apoptosis in response to cellular damage; its loss removes a critical safeguard against tumor development.2
• Alteration of the BCL-2 gene: This gene codes for proteins that block cell death. Mutations, such as chromosomal translocations, can keep this gene in a permanent "on" position, leading to an overproduction of anti-apoptotic proteins that prevent the cell from committing suicide.12

By blocking the apoptotic pathway, these mutations enable cancer cells to resist both natural physiological regulation and many clinical treatments, such as radiation and chemotherapy, which rely on inducing apoptosis to eradicate tumors. Restoring the body's ability to identify and eliminate these cells is a primary goal of modern cancer research.21