Genetic basis of cancer

This session centres on Genetic Basis of Cancer, offering a structured look at the genetic foundations of cancer, focusing on how mutations in oncogenes and tumour suppressor genes disrupt normal cell regulation. We will explore sources of these mutations, including both inherited predispositions and environmental factors, and examine how failures in DNA repair contribute to genomic instability. Finally, we will discuss the multistep process of tumour progression, highlighting the role of driver mutations and the resulting genetic diversity in shaping cancer development and therapy challenges.. Cancer is fundamentally a disease of the genome. While many factors contribute to cancer, it primarily arises from accumulated genetic mutations that disrupt normal regulation of cell growth, survival, and differentiation. These mutations occur in two main classes of genes: oncogenes, which promote cell proliferation, and tumour suppressor genes, which restrain division or promote cell death. When the balance between these genes is disturbed by mutations, cancer can develop. Examining the types of mutations and their effects on cell function is essential to understanding the genetic basis of cancer. Cell division is tightly regulated by cellular machinery. Oncogenes are mutated proto-oncogenes that become hyperactive, driving unchecked cell division through dominant mutations—one mutated copy is enough. Tumour suppressor genes act as brakes, halting division or triggering cell death;