Cancer Biology
Core concepts
Cancer arises from accumulated genetic and epigenetic changes producing uncontrolled proliferation, evasion of apoptosis, replicative immortality, angiogenesis, invasion, and metastasis. Understand oncogenes (gain of function, e.g., HER2, RAS, MYC), tumor suppressor genes (loss of function, e.g., TP53, BRCA1/2, RB), and DNA mismatch repair defects. Know the hallmarks of cancer and how they map to treatment targets: HER2 to trastuzumab, EGFR to tyrosine kinase inhibitors, PD-L1 to checkpoint inhibitors, BRCA to PARP inhibitors.
Traps in questions
- Oncogene versus suppressor: oncogenes are activated by mutation or amplification; suppressors require loss of both alleles in classic models.
- Benign versus malignant: benign tumors do not invade or metastasize; they can still cause harm by location or hormone secretion.
- Metastasis routes: lymphatic spread is common for carcinomas; hematogenous spread favors liver, lung, bone, and brain.
- Tumor markers: markers such as CEA or CA-125 support monitoring but are not diagnostic alone.
Rule of thumb
Target the driver, not the symptom. If a stem names a molecular alteration, the answer usually concerns a therapy directed at that pathway or a resistance mechanism.
Worked example
A breast tumor overexpresses HER2. Because HER2 is an amplified oncogene driving proliferation, trastuzumab-based therapy is indicated - the biology explains the drug choice, not the other way around.