The graph illustrates that cancer cells fail to:

Answer: Show density-dependent inhibition Normal cells stop dividing when they fill the available area (density-dependent inhibition / contact inhibition); cancer cells lose this regulation and keep dividing.

Why is CDK activity cyclic when CDK protein levels are roughly constant?

Answer: CDK requires binding to cyclin, whose levels rise and fall CDKs are present throughout the cycle but only active when bound to cyclins. Cyclic accumulation and destruction of cyclins drives the cyclic activity of CDKs.

Cancer cells differ from normal cells in that they

Answer: Lose normal cell-cycle regulation, divide uncontrollably, and ignore checkpoints Mutations in genes regulating the cycle (proto-oncogenes, tumor suppressors) free cancer cells from normal growth controls.

AP Biology · Topic 4.7

Regulation of Cell Cycle Practice

Part of Cell Communication and Cell Cycle.(IST-1.B)

Practice questions

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Sample questions

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Sample 1difficulty 2/5
$The graph illustrates that cancer cells fail to:$
- A
  $Express any cyclins$
- B
  $Form a contractile ring$
- C
  $Synthesize DNA$
- D
  $Show density-dependent inhibition$
  check_circle
Why
$Normal cells stop dividing when they fill the available area (density-dependent inhibition / contact inhibition); cancer cells lose this regulation and keep dividing.$
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Sample 2difficulty 2/5
$Why is CDK activity cyclic when CDK protein levels are roughly constant?$
- A
  $CDK loses phosphates during S phase$
- B
  $CDK is degraded each cycle$
- C
  $CDK enters the nucleus only at metaphase$
- D
  $CDK requires binding to cyclin, whose levels rise and fall$
  check_circle
Why
$CDKs are present throughout the cycle but only active when bound to cyclins. Cyclic accumulation and destruction of cyclins drives the cyclic activity of CDKs.$
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Sample 3difficulty 2/5
$Cancer cells differ from normal cells in that they$
- A
  $Always trigger apoptosis when DNA damage is detected at checkpoints$
- B
  $Die after a single division due to telomere shortening$
- C
  $Lose normal cell-cycle regulation, divide uncontrollably, and ignore checkpoints$
  check_circle
- D
  $Cannot replicate their DNA, so they accumulate in G₁ phase$
Why
$Mutations in genes regulating the cycle (proto-oncogenes, tumor suppressors) free cancer cells from normal growth controls.$
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Sample 4difficulty 2/5
$In a culture dish, normal cells stop dividing when they form a monolayer. This is called$
- A
  $Apoptosis (programmed cell death)$
- B
  $Density-dependent inhibition (contact inhibition)$
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- C
  $Anchorage dependence (attachment-required division)$
- D
  $Cytokinesis (cytoplasmic division)$
Why
$Cell-cell contacts arrest the cell cycle; cancer cells lose this and pile up in multiple layers.$
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Sample 5difficulty 2/5
$A "hallmark of cancer" not typical of normal cells is$
- A
  $Sustained proliferative signaling and resistance to apoptosis$
  check_circle
- B
  $Density-dependent inhibition of cell division at confluence$
- C
  $Apoptosis triggered when DNA damage is detected$
- D
  $Chromosome stability maintained across many divisions$
Why
$Cancer cells gain growth signals, ignore apoptosis triggers, invade tissues, and induce angiogenesis — among other hallmarks.$
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