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.
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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 kills the cell at once
    • One good copy still builds a brake
    • Both copies fail at the same time

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

    • It locks one growth relay on
    • It deletes the whole relay gene
    • It pauses the cycle until orders return

  3. Activating oncogene mutations are commonly inherited through families.

    Circle one:   True   False

  4. A family shows early bilateral eye tumours across generations, and allele tracking names the lost copy as the healthy one. What fits best?

    • An acquired relay fault in one cell
    • A harmless passenger change here
    • An inherited brake loss

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

    • The normal sample failed outright
    • Marker heterozygosity was lost
    • A third copy was inherited at birth

  6. In the classic suppressor case taught here, one brake copy is disabled completely. Do you predict dominance or recessiveness?

    • Dominant, as with a stuck relay
    • Recessive until copy two is lost
    • Silent, so no second hit can follow

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

    • It pushes growth orders directly
    • It freezes the current genome sequence
    • It raises the mutation rate

  8. A tumour carries an activating relay variant, but no matched normal was sequenced. A colleague calls the variant acquired. What is wrong?

    • Origin needs a matched normal check
    • The variant must be a passenger
    • Family history alone settles origin
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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. One good copy still builds a brake · In the classic model, one copy leaves a working brake, so both must go in the taught case.
  2. It locks one growth relay on · The stuck relay fires without orders, which can drive division; it alone does not guarantee cancer.
  3. False · These activating changes are usually acquired in body cells; rare inherited cases exist, so commonly inherited is false.
  4. An inherited brake loss · Family pattern plus tracked loss of the healthy copy fits an inherited brake loss; pedigree alone would not settle it.
  5. Marker heterozygosity was lost · Tumour versus normal comparison shows marker loss there; naming a deleted healthy copy needs allele proof.
  6. Recessive until copy two is lost · In the classic case, you predict from mechanism: one working copy covers until the second hit.
  7. It raises the mutation rate · Repair loss contributes as harmful combinations accumulate faster.
  8. Origin needs a matched normal check · Tumour-only data cannot prove acquired origin; a matched normal or germline check is needed, and family history alone is not the decider.
Worksheet · LightMySky