Cancer begins at the cellular level when DNA damage accumulates beyond the cell's repair capacity. The human body produces approximately 3.8 million new cells per minute, and each cell division carries a small risk of replication errors. Over a lifetime, these errors accumulate—which is why cancer risk increases significantly with age, with approximately 60% of all cancers diagnosed in patients over 65.
Tumor suppressor genes like TP53 and BRCA1/2 normally detect and repair DNA damage or trigger programmed cell death (apoptosis) when damage is irreparable. Mutations in these protective genes—whether inherited or acquired—disable the body's quality control system, allowing damaged cells to replicate unchecked and eventually form tumors.
Telomere biology provides another window into cancer risk. Telomeres—protective caps on chromosome ends—shorten with each cell division. Critically shortened telomeres cause genomic instability, a hallmark of cancer development. Telomere length analysis can reveal accelerated biological aging that may correlate with increased cancer susceptibility.
