Targeted Therapy and the Resistance That Follows It · seed 1 · A4, ink-friendly. The answer key prints on its own page for grown-ups.

Why targeted drugs stop working

Science · Organisms & Life Processes · ages 22-24
Name ______________________   Date ____________

  1. What is the therapeutic window?

    • The gap between the dose that stalls the tumour and the dose that poisons the patient
    • The number of pills in one bottle
    • The time a drug spends on the pharmacy shelf

  2. What does oncogene dependence mean?

    • The tumour leans entirely on one driver pathway for survival
    • Healthy cells need the drug to survive
    • Every pathway in the cell is equally essential

  3. Bypass resistance changes the drug binding pocket so the inhibitor no longer grips.

    Circle one:   True   False

  4. The original target stays suppressed but a parallel receptor is now active. What is it?

    • On target resistance in the binding pocket
    • Bypass resistance rerouting growth around the blockade
    • Complete cure with no remaining disease

  5. Relapse sequencing shows a fresh mutation in the drug binding pocket. What do you conclude?

    • Bypass resistance through a parallel pathway
    • The drug was never absorbed at all
    • On target resistance keeping the pathway essential

  6. Why does relapse often arrive faster than mutation rates predict?

    • Drugs directly write new mutations within hours
    • The resistant clone usually pre-existed and was selected
    • Tumours stop dividing during treatment

  7. How do you design for lasting control given pre-existing clones?

    • Single drug cycles with long breaks between
    • Combinations closing escape routes before selection opens them
    • Ever higher doses of the same inhibitor

  8. A colleague blames every relapse on poor dosing. What better hypothesis do you test first?

    • Whether sequencing shows on target or bypass evolution under the drug
    • Whether the patient drank enough water
    • Whether the tumour shrank too quickly
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Answer key

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

Why targeted drugs stop working W1-mt_HrU1DfZhGz-s1

  1. The gap between the dose that stalls the tumour and the dose that poisons the patient · Targeted drugs widen the gap by aiming at what the cancer uniquely needs.
  2. The tumour leans entirely on one driver pathway for survival · The cancer rewired itself around a single crutch that normal cells do not need.
  3. False · That describes on target resistance, while bypass reroutes around the blockade.
  4. Bypass resistance rerouting growth around the blockade · Growth switched routes while the target stayed blocked, so add a second blockade.
  5. On target resistance keeping the pathway essential · A changed pocket with the same essential pathway argues on target.
  6. The resistant clone usually pre-existed and was selected · A billion cells already harbor rare variants, so selection beats fresh mutation.
  7. Combinations closing escape routes before selection opens them · You block the target and the bypass route together, guided by repeat sequencing.
  8. Whether sequencing shows on target or bypass evolution under the drug · Tumours evolve under therapy, so you read the escape route from fresh data.
Worksheet · LightMySky