Oncogenes and Tumour Suppressors: Why One Allele Is Sometimes Enough · seed 1 · A4, ink-friendly. The answer key prints on its own page for grown-ups.

Why one bad copy can be enough, or not

Science · Genetics & Evolution · ages 22-23
Name ______________________   Date ____________

  1. Why are suppressor defects recessive at the cellular level?

    • One lost copy always kills the cell instantly
    • The remaining good copy still builds a working brake
    • Suppressors never suffer second hits

  2. What does an activating oncogene mutation do to growth signaling?

    • It locks a growth relay in the on position
    • It deletes every growth receptor from the cell
    • It freezes the cell cycle permanently

  3. Activating oncogene mutations are commonly inherited through families.

    Circle one:   True   False

  4. A family shows early bilateral tumours across generations. What gene class do you argue?

    • An acquired dominant oncogene event
    • A harmless variant with no role
    • An inherited suppressor or repair defect needing one further hit

  5. Normal tissue shows two marker variants, the tumour only one. What happened?

    • The sequencer failed on the normal sample
    • Loss of heterozygosity deleted the healthy region
    • The patient inherited a third copy

  6. A mutation disables a brake protein completely. Do you predict dominance or recessiveness?

    • Dominant, because any mutation is dominant
    • Recessive at the cell level, until the second copy is lost
    • Neither, because brakes never mutate

  7. Repair gene loss raises the mutation rate without driving growth itself. Why does it still predispose to cancer?

    • It directly forces division without signals
    • It prevents any mutation from ever occurring
    • It supplies raw material that accelerates every later malignant step

  8. A single sporadic tumour carries an activating relay mutation. A colleague calls it inherited. What is wrong?

    • Sporadic single tumours fit an acquired dominant event, not an inherited defect
    • Oncogenes can never mutate in tumours
    • Single tumours always prove inheritance
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Answer key

For grown-ups. Fold this page away before handing over the rest.

Why one bad copy can be enough, or not W1-mt_7WTgv1dLNx-s1

  1. The remaining good copy still builds a working brake · Losing one copy leaves a working brake, so both must go.
  2. It locks a growth relay in the on position · The stuck relay fires without orders, so the cell divides on its own.
  3. False · A body wide stuck accelerator would be lethal early, so these changes are somatic.
  4. An inherited suppressor or repair defect needing one further hit · Carriers start one hit down in every cell, so tumours come early and often.
  5. Loss of heterozygosity deleted the healthy region · Comparing tumour with normal reveals the deleted healthy copy directly.
  6. Recessive at the cell level, until the second copy is lost · You predict from mechanism: lost brakes keep one working copy until the second hit.
  7. It supplies raw material that accelerates every later malignant step · Broken repair speeds the search for the combinations that transform.
  8. Sporadic single tumours fit an acquired dominant event, not an inherited defect · Familial clustering argues inherited suppressor, while sporadic singles fit somatic oncogenes.
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