OncologyTier 2Topic

Processes of - cell growth and ageing, cell injury, and apoptosis

Regulation of cell growth

Normal cell growth is tightly regulated by a balance between proliferation, differentiation, senescence, and programmed death - cancer arises when this regulation is progressively lost across multiple control points
Cellular ageing (senescence) and cumulative DNA damage over a lifetime underlie the sharply rising cancer incidence with age seen across almost all tumour types

Cell cycle checkpoints (G1/S, G2/M) normally arrest damaged cells for repair or trigger apoptosis if damage is irreparable - p53 ("guardian of the genome") is the central checkpoint regulator, and its loss (mutated in the majority of human cancers) removes this safeguard
Cellular senescence - a permanent, physiological growth-arrest state (distinct from apoptosis) that normally limits the replicative lifespan of damaged/aged cells (the Hayflick limit, linked to telomere shortening) - cancer cells characteristically reactivate telomerase to bypass this limit and achieve replicative immortality
Apoptosis (programmed cell death - controlled, non-inflammatory, cell shrinkage and fragmentation into apoptotic bodies) vs necrosis (uncontrolled cell death from injury - cell swelling, membrane rupture, inflammatory response) - cancer cells characteristically evade apoptosis despite accumulating damage that would normally trigger it

The "hallmarks of cancer" framework (sustained proliferative signalling, evasion of growth suppressors, resistance to apoptosis, replicative immortality, angiogenesis, invasion/metastasis, and more recently reprogrammed metabolism and immune evasion) describes the cumulative set of acquired capabilities that together define malignant transformation - no single mutation is sufficient

Explains why cancer is fundamentally a multi-step, multi-mutation process accumulating over years to decades, and why cancer risk rises with age and with cumulative carcinogen exposure (each exposure/replication cycle is an opportunity for another step toward malignancy)

Ageing, carcinogenesis, p53/Rb tumour suppressor pathways, telomerase reactivation

This framework underlies many modern cancer therapies - drugs targeting specific hallmarks (angiogenesis inhibitors, immune checkpoint inhibitors restoring immune surveillance, cell cycle checkpoint inhibitors) rather than simply targeting rapid proliferation indiscriminately, as older chemotherapy did

5 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.