Molecular Basis of Cancer
Start with the big picture
The lesson frames cancer as a disease shaped by the stepwise accumulation of changes in growth-regulatory genes. Gain-of-function alterations can turn proto-oncogenes into oncogenes, where one altered allele may be sufficient; tumor suppressor genes generally contribute to cancer when both alleles are inactivated. Examples include RAS, MYC, and BCR-ABL among oncogenic drivers, and TP53, RB1, APC, and PTEN among tumor suppressors. The topic also connects gene regulation and genome maintenance to cancer development, covering epigenetic silencing, mismatch-repair defects, chromosomal instability, and mechanisms that support continued replication, angiogenesis, apoptosis evasion, and altered metabolism. Together, these themes provide a framework for understanding how molecular changes contribute to tumor behavior.
What you'll learn
- Distinguish proto-oncogenes from tumor suppressor genes by function and mutation pattern.
- Identify representative oncogene and tumor suppressor gene products and their roles.
- Describe mechanisms that activate oncogenes or silence tumor suppressor genes.
- Explain how DNA repair defects and genomic instability contribute to cancer.
- Relate cellular immortality, angiogenesis, apoptosis evasion, and metabolic change to tumor development.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
