Abstract

All three factors of apoptosis and angiogenesis and metastasis work together in creating tumour growth pathways that result in cancer progression. Cell survival depends on apoptosis which functions to maintain homeostasis. The deregulation of apoptosis enables cancer cells to resist death processes allowing tumour survival. Uncontrolled cellular growth results from two key factors - mutations in p53 regulators together with increased expression of BCL-2 and other related anti-apoptotic genes. Tumours gain the essential nutrients and oxygen through angiogenesis which leads to their expansion. The tumour vascularization process depends on vascular endothelial growth factor (VEGF) which activates the necessary vascular endothelial cells. Existing anti-angiogenic VEGF blocking therapies show potential to control tumour spread yet their long-term effectiveness remains uncertain. The principal cause of death from cancer owes to metastasis which describes cancer cells colonizing distant body sites. Cellular invasion precedes intravasation and circulation while extravasation and colonization complete this process through tumour angiogenesis and anoikis-resistance functions. The discovery of targeted therapies depends on our ability to understand the complex interplay between these processes. A review explores disease mechanisms at the molecular level as well as therapeutic interactions together with treatment requirements for better cancer management results.

Key words: Cancer pathogenesis, apoptosis, angiogenesis, metastasis, p53, BCL-2, VEGF, tumour microenvironment, therapeutic targeting, cancer progression.