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MCAT Cancer, Oncogenes, Tumor Suppressors and Apoptosis Practice Questions

By StudyStore · Published 2026-11-04 · 8 original questions · about 12 min

Eight free MCAT-style practice questions on proto-oncogenes, p53, Rb, apoptosis, caspases, telomerase and the cell cycle checkpoints, with explanations.

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Quick concept primer

Cancer arises when the cell cycle escapes control. Proto-oncogenes promote normal growth; a gain-of-function mutation turns one into an oncogene, which needs only one mutated allele to act (dominant at the cellular level). Ras and Myc are examples. Tumor suppressors such as p53 and Rb restrain the cycle and typically require loss of both alleles (Knudson two-hit hypothesis) before control is lost.

p53 senses DNA damage, halts the cell at the G1/S checkpoint by inducing p21, and triggers repair or apoptosis. Rb binds the E2F transcription factor and blocks entry into S phase until phosphorylated by cyclin-CDK complexes. Apoptosis is programmed cell death carried out by caspases, with cell shrinkage and no inflammation, unlike necrosis. Most cancer cells reactivate telomerase and so avoid replicative senescence.

8 practice questions

Try each question before opening the explanation. Click "Show answer and explanation" to check yourself. All questions are original and written for study practice.

Question 1

A mutation changes a proto-oncogene so that it is permanently active. How many mutated alleles are generally enough to promote uncontrolled growth?

  1. Two, because both alleles must be mutated
  2. One, because the mutation is gain of function
  3. Zero, because proto-oncogenes are never involved in cancer
  4. Three, one for each checkpoint
Show answer and explanation

Answer: B. One, because the mutation is gain of function

An oncogene arises from a gain-of-function mutation, so a single mutated copy can drive growth even if the other allele is normal. Tumor suppressors typically behave in the opposite way and require loss of both functional copies.

Question 2

Which statement correctly describes tumor suppressor genes?

  1. Loss of function of both alleles is typically needed to remove their effect
  2. A single gain-of-function mutation activates them
  3. They stimulate the cell cycle
  4. They are found only in cancer cells
Show answer and explanation

Answer: A. Loss of function of both alleles is typically needed to remove their effect

Tumor suppressors act as brakes. One working copy is usually enough to keep the brake on, so both alleles must be lost for control to fail, as in Knudson's two-hit hypothesis. Oncogenes, not tumor suppressors, are the accelerators.

Question 3

DNA damage is detected in a cell in G1. Which protein is most likely to halt the cell cycle and promote repair or apoptosis?

  1. p53
  2. Ras
  3. Myc
  4. Telomerase
Show answer and explanation

Answer: A. p53

p53 is activated by DNA damage and induces p21, an inhibitor of cyclin-dependent kinases, which arrests the cell at the G1/S checkpoint. If repair fails, p53 promotes apoptosis. Ras and Myc are proto-oncogenes that promote growth.

Question 4

In a normal cell, hypophosphorylated Rb prevents progression from G1 to S by

  1. activating telomerase
  2. phosphorylating cyclin D
  3. binding and inhibiting the E2F transcription factor
  4. cleaving caspase 3
Show answer and explanation

Answer: C. binding and inhibiting the E2F transcription factor

Active (hypophosphorylated) Rb sequesters E2F so S-phase genes are not transcribed. When cyclin-CDK complexes phosphorylate Rb, it releases E2F and the cell enters S phase. Loss of Rb function therefore removes a key brake on the cell cycle.

Question 5

Which feature distinguishes apoptosis from necrosis?

  1. Apoptosis is programmed and does not trigger inflammation
  2. Apoptosis releases cell contents and triggers inflammation
  3. Apoptosis occurs only in cancer cells
  4. Apoptosis is caused by physical injury
Show answer and explanation

Answer: A. Apoptosis is programmed and does not trigger inflammation

Apoptosis is a controlled process using caspases, in which the cell shrinks and is packaged into membrane-bound fragments that phagocytes remove without inflammation. Necrosis follows injury, with swelling and rupture that spills contents and causes inflammation.

Question 6

Most cancer cells divide indefinitely. Which change contributes to this?

  1. Increased expression of caspases
  2. Increased activity of p53
  3. Shortening of telomeres after each division
  4. Reactivation of telomerase to maintain telomere length
Show answer and explanation

Answer: D. Reactivation of telomerase to maintain telomere length

Normal somatic cells lose telomere length with each division and eventually become senescent. About 85 to 90 percent of cancers reactivate telomerase, which adds telomeric repeats and allows unlimited replication. High p53 activity and caspases would limit growth instead.

Question 7

A person inherits one defective copy of a tumor suppressor gene. Why is this person at higher risk of cancer than the general population?

  1. Only one additional mutation is needed to lose all function
  2. The defective copy acts as an oncogene
  3. The defective copy is dominant negative in all cells
  4. The normal copy is silenced in every cell
Show answer and explanation

Answer: A. Only one additional mutation is needed to lose all function

In every cell, one hit is already present, so one somatic mutation in the remaining allele eliminates function. Someone with two normal copies needs two separate hits in the same cell, which is far less likely. This explains the early onset of familial retinoblastoma.

Question 8

Cytochrome c released from mitochondria during apoptosis activates which group of enzymes?

  1. DNA polymerases
  2. Caspases
  3. Cyclin-dependent kinases
  4. Helicases
Show answer and explanation

Answer: B. Caspases

In the intrinsic apoptotic pathway, cytochrome c release helps assemble the apoptosome, which activates initiator caspase 9 and then executioner caspases such as caspase 3. These proteases dismantle cellular proteins and lead to cell death.

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Written by StudyStore from standard scientific facts as a study aid. These are not official exam questions and are not affiliated with or endorsed by any testing organization. Always check values against the reference provided with your exam or course.

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