How do mutations in tumour suppressor genes differ from oncogenes in their effect on cancer development?

• A. Tumor suppressor genes must be inactivated to promote cancer; oncogenes are activated to promote cancer progression.
• B. Tumor suppressor genes must be activated; oncogenes inactivated.
• C. Oncogenes must be deleted from the genome to cause cancer.
• D. Tumor suppressor genes and oncogenes are never involved in cancer.

Answer: (B)

Mutations that influence cancer development show two opposing effects: tumor suppressor genes normally brake cell growth or promote DNA repair, while oncogenes promote cell division and survival.

For tumor suppressor genes, their job is to keep cell growth in check. When such a gene is inactivated by mutation, that brake is released, allowing cells to divide more freely. In cancer, you usually need both copies of the gene to be inactivated (the two-hit scenario) so no functional protein remains. A single mutated copy can predispose to cancer, but loss of both copies is typically what unleashes unchecked growth.

Oncogenes, by contrast, are normal growth-promoting genes (proto-oncogenes) that become overactive through activating mutations or other changes. A single activating mutation can make the protein continually push cells to divide, driving cancer progression. These mutations act dominantly because one copy is enough to promote uncontrolled growth.

So cancer commonly arises from inactivation of tumor suppressor genes and activation of oncogenes. The statement that tumor suppressor genes must be activated and oncogenes inactivated would run opposite to what actually drives cancer. The other options likewise don’t align with how these gene types contribute to cancer.