Molecular Basis of Cancer: Oncogenes and Tumor Suppressor Genes
Start with the big picture
Proto-oncogenes normally help regulate growth and differentiation. A gain-of-function change can convert one into an oncogene, producing a persistently active protein; a single altered allele may be sufficient. Examples include RAS and BRAF signaling changes, BCR-ABL fusion, and MYC or cell-cycle gene alterations. Tumor suppressor genes generally require loss of both functional copies to remove growth restraints. RB regulates the G1-to-S transition, TP53 coordinates responses to cellular damage, and APC limits β-catenin signaling. Other suppressors affect pathways such as PI3K/AKT, hypoxia signaling, and DNA repair. Together, these mechanisms show how cancer can develop through increased growth signals, weakened safeguards, or both.
What you'll learn
- Distinguish proto-oncogenes, oncogenes, and tumor suppressor genes by their mechanisms of action.
- Explain why oncogenes can act dominantly while tumor suppressor gene loss typically requires two hits.
- Relate selected oncogenes to their altered signaling mechanisms and associated cancers.
- Describe key roles of RB, TP53, APC, and DNA repair tumor suppressors.
- Connect loss of tumor suppressor function with selected inherited cancer syndromes.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
