Cancer Self-Sufficiency in Growth Signals
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Questions and Answers

What is the primary reason a cell might become cancerous?

  • Enhanced apoptosis
  • DNA mutations that disrupt growth regulation (correct)
  • Reduced cell signaling ability
  • Increased nutrient supply
  • How do cancer cells achieve self-sufficiency in growth signals?

  • Through upregulation of anti-growth receptors
  • By producing abnormal ligands and increasing receptor levels (correct)
  • By relying solely on external signals
  • By decreasing the availability of growth factors
  • What effect do mutations in the Ras protein have on cancer development?

  • They lock Ras in its inactive state
  • They can keep Ras active by blocking regulatory interactions (correct)
  • They have no effect on cancer cells
  • They enhance anti-growth signaling
  • What is a common characteristic of tumors related to the p53 tumor suppressor gene?

    <p>They commonly contain mutations or deletions of p53</p> Signup and view all the answers

    What defines the hallmark of insensitivity to anti-growth signals in cancer cells?

    <p>Ability to evade both internal and external growth restriction</p> Signup and view all the answers

    What is the role of the Rb tumor suppressor protein?

    <p>To bind to cyclins and inhibit cell cycle progression</p> Signup and view all the answers

    Which mutation is MOST commonly associated with constitutive signaling in Ras?

    <p>G12V mutation that prevents binding of regulatory proteins</p> Signup and view all the answers

    What is the main mechanism by which cancer cells resist anti-growth signals?

    <p>Through alterations in signaling pathways that regulate cell proliferation</p> Signup and view all the answers

    Study Notes

    Cancer: Self-Sufficiency in Growth Signals

    • Cancer is a condition where cells grow uncontrollably, bypassing normal regulatory mechanisms.
    • Normal cell growth requires pro-growth signals, which can be disrupted in cancer.
    • Pro-growth molecules bind to receptors, activating intracellular signaling pathways.
    • This leads to the transcription of pro-growth proteins.
    • Cancer cells can achieve self-sufficiency through various mechanisms:
      • Abnormal Ligand Production: Cancer cells may produce excessive pro-growth signaling molecules, activating their own receptors (autocrine signaling) or those of surrounding cells (paracrine signaling).
      • Upregulated Receptor Expression: Increased receptor levels on the cell surface can amplify the response to pro-growth signals.
      • Mutations in Signaling Pathways: Mutations can lead to constitutive activation of signaling pathways, even without external pro-growth signals.
    • Ras is a key protein in cellular signaling, often mutated in cancer.
    • Mutations in Ras are present in 20-30% of cancers.
    • Specific mutations like G12V and Q61K lock Ras in an active state, promoting continuous cell growth.

    Cancer: Insensitivity to Anti-Growth Signals

    • Normal cells require a balance between pro-growth and anti-growth signals to maintain controlled growth.
    • Anti-growth signals can be both internal and external, and can be normal or induced.
    • Key tumor suppressor genes play a role in regulating cell growth and preventing uncontrolled proliferation.
    • The p53 gene:
      • p53 is a tumor suppressor protein that acts as a "guardian of the genome".
      • It plays a critical role in the cell cycle control, preventing uncontrolled cell growth.
      • Mutations in p53 occur in more than 50% of all human cancers.
    • The Rb gene:
      • Rb inhibits cell cycle progression, ensuring controlled growth.
      • Mutated Rb leads to uncontrolled cell growth, as the brakes are removed.

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    Description

    This quiz explores the mechanisms by which cancer cells achieve self-sufficiency in growth signals. It covers abnormal ligand production, upregulated receptor expression, and mutations in signaling pathways. Test your understanding of how these factors contribute to uncontrolled cell growth in cancer.

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