Question
What are the key characteristics of cancer cells? Differentiate between oncogenes and tumor suppressor genes with examples. What is metastasis?
(NCERT Class 12 — frequently asked in NEET)
Solution — Step by Step
Cancer cells differ from normal cells in several ways:
- Uncontrolled proliferation — they divide continuously, ignoring normal growth signals
- Loss of contact inhibition — normal cells stop dividing when they touch neighbouring cells; cancer cells don’t
- Immortality — cancer cells avoid programmed cell death (apoptosis) and can divide indefinitely
- Angiogenesis — they stimulate new blood vessel formation to supply the growing tumour
- Metastasis — they can break away, travel through blood/lymph, and establish new tumours at distant sites
- Altered metabolism — cancer cells often rely on glycolysis even in the presence of oxygen (Warburg effect)
| Feature | Oncogenes | Tumor suppressor genes |
|---|---|---|
| Normal form | Proto-oncogenes (promote cell growth) | Active tumor suppressors (inhibit cell growth) |
| How cancer happens | Gain of function mutation — gene becomes overactive | Loss of function mutation — gene stops working |
| Analogy | Stuck accelerator pedal | Failed brake pedal |
| Examples | ras, myc, HER2 | p53, Rb (retinoblastoma), BRCA1 |
| Inheritance pattern | Usually dominant (one mutant copy enough) | Usually recessive (both copies must be lost) |
Proto-oncogenes are normal genes that promote cell division. When mutated, they become oncogenes — permanently “switched on,” driving uncontrolled division.
Tumor suppressors are the cell’s brakes. They check for DNA damage and halt division or trigger apoptosis. When both copies are lost (Knudson’s two-hit hypothesis), the brakes fail.
Metastasis is the spread of cancer cells from the primary tumour to distant organs through blood or lymph vessels. This is what makes cancer lethal.
The process: cancer cells lose cell adhesion molecules → detach from the primary tumour → enter blood/lymph → travel to distant organs → exit blood vessels → colonise new tissues → form secondary tumours.
A benign tumour stays localised and doesn’t metastasise. A malignant tumour (true cancer) invades surrounding tissue and can metastasise.
Why This Works
Cancer is fundamentally a disease of gene regulation. Normal cells have a balance between growth-promoting signals (proto-oncogenes) and growth-inhibiting signals (tumor suppressors). Cancer develops when this balance tips — either the accelerator gets stuck (oncogene activation) or the brakes fail (tumor suppressor loss), or usually both.
The p53 gene is called the “guardian of the genome” because it monitors DNA damage. If damage is detected, p53 either halts the cell cycle for repair or triggers apoptosis. Mutations in p53 are found in over 50% of all human cancers — making it the most commonly mutated gene in cancer.
Alternative Method — Cancer Causes Summary
For NEET, know the three categories of carcinogens (cancer-causing agents):
- Physical: UV radiation, X-rays, ionising radiation
- Chemical: Tobacco smoke (benzopyrene), asbestos, vinyl chloride, aflatoxin (from Aspergillus)
- Biological: Oncogenic viruses — HPV (cervical cancer), EBV (Burkitt’s lymphoma), Hepatitis B (liver cancer)
NEET often asks which virus causes which cancer — memorise HPV → cervical and HBV → liver at minimum.
Common Mistake
Students confuse benign and malignant tumours. A benign tumour is localised, slow-growing, and non-invasive (e.g., uterine fibroids). A malignant tumour is invasive, fast-growing, and can metastasise. Only malignant tumours are called “cancer.” Also, don’t say “oncogenes cause cancer” — mutated proto-oncogenes (i.e., oncogenes) cause cancer. Normal proto-oncogenes are essential for healthy cell growth.