Question
Which of the following statements is incorrect regarding oncogenes and tumour suppressor genes?
(A) Proto-oncogenes are normal cellular genes that promote cell growth
(B) Mutation of proto-oncogene to oncogene causes uncontrolled cell division
(C) p53 is an oncogene that accelerates cell cycle progression
(D) Loss of tumour suppressor gene function leads to cancer
Source: NEET 2024
Solution — Step by Step
We need to find the incorrect statement. This is a classic NEET trap — students read quickly and miss the “incorrect” part. Take 5 seconds before reading options.
Proto-oncogenes are perfectly normal genes in healthy cells. They code for growth factors, receptors, and cell cycle regulators. Think of them as car accelerators working fine at normal speed.
This statement is correct. Cross it out.
When a proto-oncogene mutates (point mutation, chromosomal translocation, gene amplification), it becomes an oncogene. The oncogene now produces a hyperactive protein or too much protein — the accelerator gets stuck down.
This statement is correct. Cross it out.
p53 is the guardian of the genome. It is a tumour suppressor gene, not an oncogene. When DNA is damaged, p53 either pauses the cell cycle (for repair) or triggers apoptosis.
Calling p53 an oncogene is factually wrong — it does the exact opposite of accelerating the cell cycle. Option C is the incorrect statement.
Tumour suppressor genes (like p53, Rb) act as brakes. When both copies are lost or mutated (Knudson’s two-hit hypothesis), there is no check on cell division. This is confirmed cancer biology.
Option D is correct. Our answer stands — Option C.
Why This Works
The key concept here is the two-class model of cancer genes. Oncogenes are dominant drivers — one mutated copy is enough to push cells toward uncontrolled division (like a stuck accelerator). Tumour suppressor genes are recessive guards — you usually need both copies disabled before cancer develops (like losing both brakes).
p53 specifically monitors DNA integrity at the G1/S checkpoint. Cells with damaged DNA that slip past this checkpoint accumulate mutations rapidly, which is exactly why p53 mutations are found in over 50% of all human cancers. It is the most commonly mutated gene in human cancer.
Metastasis happens when cancer cells acquire additional mutations — they detach from the primary tumour, invade the basement membrane (using enzymes like collagenase), enter blood/lymph, and establish secondary tumours at distant sites. This multi-step progression from a single mutated cell to metastatic cancer is why NEET asks about oncogenes alongside metastasis.
Alternative Method
Use the accelerator vs. brake analogy to classify quickly in the exam hall:
| Type | Normal Role | Mutated Effect | Example |
|---|---|---|---|
| Proto-oncogene → Oncogene | Promotes growth (controlled) | Uncontrolled growth | ras, myc |
| Tumour suppressor | Inhibits growth / triggers repair | Growth goes unchecked | p53, Rb |
If an option calls p53 a “promoter of cell cycle” or an “oncogene,” it is automatically incorrect. p53 = brake, always.
In NEET, remember this shortcut: p53 = guardian, Rb = gatekeeper. Both are tumour suppressors. Any option that flips their function is the answer to “find the incorrect statement.”
Common Mistake
Students confuse oncogenes with proto-oncogenes and lose marks. Proto-oncogenes are normal, healthy genes present in every cell. They only become dangerous oncogenes after mutation. Writing “proto-oncogenes cause cancer” in a short-answer question is wrong — the correct statement is “mutation of proto-oncogenes to oncogenes causes cancer.” NEET 2024 and NEET 2022 both tested this exact distinction.
A second common error: students apply Knudson’s two-hit hypothesis to oncogenes. It applies only to tumour suppressor genes (like Rb in retinoblastoma). Oncogenes follow a dominant gain-of-function model — one mutated copy is enough.