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Cell cycle dysregulation

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Virology

Definition

Cell cycle dysregulation refers to the abnormal control of the cell cycle, leading to uncontrolled cell division and growth. This phenomenon is a key feature in the development of cancer, where the normal checkpoints and regulatory mechanisms that ensure proper cell division are disrupted. In the context of viral infections, certain viruses can hijack these regulatory pathways to promote cell proliferation, contributing to oncogenesis.

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5 Must Know Facts For Your Next Test

  1. Cell cycle dysregulation is often caused by mutations in genes that regulate the cell cycle, such as cyclins, cyclin-dependent kinases (CDKs), and their inhibitors.
  2. Certain viruses, like Human Papillomavirus (HPV) and Epstein-Barr Virus (EBV), encode proteins that interfere with host cell cycle regulators, promoting uncontrolled cell division.
  3. The dysregulation of the G1/S checkpoint is particularly significant because it allows cells with DNA damage to continue dividing instead of undergoing repair or apoptosis.
  4. Viral oncogenes can mimic or bind to cellular proteins involved in the cell cycle, effectively tricking the host into disregarding normal growth control mechanisms.
  5. Cell cycle dysregulation not only contributes to cancer development but also affects cancer treatment responses, making it a critical area of study for therapeutic strategies.

Review Questions

  • How do viruses influence cell cycle dysregulation to promote oncogenesis?
    • Viruses influence cell cycle dysregulation by encoding proteins that disrupt normal regulatory pathways. For instance, viral oncoproteins can bind to host proteins such as p53 or Rb, which are crucial for controlling cell division. This interference bypasses checkpoints in the cell cycle, leading to uncontrolled proliferation and potentially resulting in cancer development.
  • Discuss the role of tumor suppressor genes in relation to cell cycle dysregulation and viral oncogenesis.
    • Tumor suppressor genes play a critical role in maintaining normal cell cycle regulation by inhibiting excessive cell division. In cases of viral oncogenesis, viruses can disrupt these genes' functions through their encoded proteins. For example, HPV E7 protein can bind to Rb, a tumor suppressor that prevents progression from G1 to S phase, leading to dysregulation of the cell cycle and increased risk of tumor formation.
  • Evaluate the implications of cell cycle dysregulation for cancer therapy in the context of viral infections.
    • Cell cycle dysregulation poses significant challenges for cancer therapy, particularly when viral infections are involved. Understanding how viruses manipulate cell cycle control can inform therapeutic approaches. For example, targeting specific viral oncoproteins or restoring normal function to tumor suppressor genes might improve treatment outcomes. Additionally, therapies that induce apoptosis in dysregulated cells could be more effective if they specifically address the altered pathways caused by viral influences.

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