Lecture 19
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Questions and Answers

What is the fundamental principle that lies at the heart of carcinogenesis?

  • Non-lethal genetic damage (correct)
  • Accumulation of mutations over time
  • Viral infections only
  • Environmental agents only
  • What type of mutations confer a growth advantage on cells?

  • Driver mutations (correct)
  • Passenger mutations
  • Proto-oncogenes
  • Oncoproteins
  • What is a characteristic of normal cells in terms of growth factors?

  • Uncontrolled proliferation
  • Independence from growth factors
  • Dependence on growth factors (correct)
  • Sensitivity to apoptosis
  • What happens to normal somatic cells after a limited number of divisions?

    <p>They enter senescence</p> Signup and view all the answers

    What is a characteristic of oncogenes?

    <p>They promote uncontrolled cell growth autonomously</p> Signup and view all the answers

    What is a hallmark of cancer?

    <p>Sustaining proliferative signaling</p> Signup and view all the answers

    What is a mechanism of self-sufficiency in growth signals in cancer cells?

    <p>Stimulus-independent secretion of growth factor</p> Signup and view all the answers

    What is the result of the accumulation of mutations over time in a cell?

    <p>Development of a malignant tumor</p> Signup and view all the answers

    What is the function of tumor suppressor genes?

    <p>To inhibit cellular proliferation by regulating the cell cycle</p> Signup and view all the answers

    What is the term for the normal genes that promote cell proliferation and differentiation?

    <p>Proto-oncogenes</p> Signup and view all the answers

    What is the result of mutations in cyclin genes?

    <p>Uncontrolled cell proliferation</p> Signup and view all the answers

    What is the function of the RAS gene?

    <p>To encode signaling proteins from receptor to nucleus</p> Signup and view all the answers

    What is the result of overexpressing nuclear transcription factors?

    <p>Promoting cell cycle progression</p> Signup and view all the answers

    What is the result of mutations in the Her2/NEU receptor?

    <p>Uncontrolled cell proliferation</p> Signup and view all the answers

    What is the result of the BCR-ABL fusion gene?

    <p>Growth autonomy and impaired apoptosis</p> Signup and view all the answers

    What is the function of the MYC gene?

    <p>To promote cell cycle progression</p> Signup and view all the answers

    What is the characteristic of tumor suppressor genes in terms of carcinogenesis?

    <p>Both copies of the gene must be lost</p> Signup and view all the answers

    What is the result of inheriting one defective copy of a tumor suppressor gene and losing the second one through somatic mutation?

    <p>Familial predisposition for tumor development</p> Signup and view all the answers

    What is the role of the RB gene in retinoblastoma?

    <p>It causes both alleles to be lost</p> Signup and view all the answers

    Why does familial transmission of retinoblastoma follow an autosomal dominant inheritance pattern?

    <p>Because only one somatic mutation is required for expression of the disease</p> Signup and view all the answers

    What is the role of the TP53 gene?

    <p>It senses DNA damage and assists in DNA repair</p> Signup and view all the answers

    What is the result of activating the DNA damage checkpoint?

    <p>The cell cycle is arrested and DNA repair or apoptosis occurs</p> Signup and view all the answers

    What is the role of the APC gene?

    <p>It is a tumor suppressor gene lost in Adenomatous polyposis coli</p> Signup and view all the answers

    What is the result of P53 inducing DNA repair genes?

    <p>The cell cycle is arrested</p> Signup and view all the answers

    Study Notes

    The Molecular Basis of Cancer

    • Oncogenesis is the formation or induction of tumors, involving mutant forms of normal genes called proto-oncogenes, which code for oncoproteins.
    • Genetic damage, acquired through environmental agents or inherited, is the fundamental principle of carcinogenesis, resulting in a single progenitor cell that has incurred genetic damage and undergoes clonal expansion.
    • Carcinogenesis involves the accumulation of mutations over time, as well as one-off catastrophic events.

    Mutations in Cancer

    • Driver mutations confer a growth advantage on cells and are located in cancer genes.
    • Passenger mutations do not confer a growth advantage.

    Normal Cellular Processes

    • Dependence on growth factors and cell/tissue-specific signals is a normal characteristic of cells.
    • Loss of these signals leads to apoptosis.
    • Anchorage-dependent proliferation requires interaction with the extracellular matrix (ECM) through transmembrane proteins (integrins).
    • Contact inhibition occurs when cells are in contact with each other, inhibiting proliferation and movement.
    • Normal somatic cells have a limited number of divisions before entering senescence.

    The Hallmarks of Cancer

    • Sustaining proliferative signaling: oncogenes promote uncontrolled cell proliferation through mechanisms such as stimulating independent growth factor secretion, mutated growth factor receptors, and over-expressed nuclear transcription factors.

    Oncogenes and Tumor Suppressor Genes

    • Oncogenes are mutated forms of proto-oncogenes that promote cancer cell growth autonomously.
    • Oncoproteins (products of oncogenes) promote uncontrolled cell proliferation.
    • Mechanisms of self-sufficiency in growth signals include:
      • Stimulus-independent secretion of growth factors
      • Mutation/over-expression of growth factor receptors
      • Mutation in genes encoding signaling proteins from receptor to nucleus
      • Over-expression of nuclear transcription factors promoting cell cycle
      • Mutations in cyclin genes resulting in uncontrolled cell proliferation
    • Tumor suppressor genes encode proteins that inhibit cellular proliferation by regulating the cell cycle.
    • Mutation in tumor suppressor genes leads to uninhibited cell proliferation.

    Tumor Suppressor Genes

    • Both copies of the gene must be lost for carcinogenesis to occur (autosomal recessive).
    • In cases with familial predisposition, affected persons inherit one defective copy of a tumor suppressor gene and lose the second one through somatic mutation.
    • Examples of tumor suppressor genes include:
      • RB gene in retinoblastoma
      • P53 in human cancers
      • APC in Adenomatous polyposis coli

    Cell Cycle Regulation

    • The RB gene prepares for mitosis and controls the cell cycle.
    • DNA damage checkpoint arrests the cell cycle, allowing for DNA repair or apoptosis.
    • P53 is a tumor suppressor gene that maintains the integrity of the genome and senses DNA damage, assisting in DNA repair by arresting the cell cycle and inducing DNA repair genes.

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    Description

    Learn about the fundamental principles of oncogenesis, including the role of oncogenes, proto-oncogenes, and genetic mutations in carcinogenesis.

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