6.3 Cancer and the Cell Cycle

Cancer develops when cells divide uncontrollably due to mutations in genes regulating the cell cycle. These mutations can occur in proto-oncogenes, tumor suppressors, or DNA repair genes, leading to tumor formation and potential metastasis.

Understanding cancer's link to the cell cycle is crucial. Normal cells have checkpoints ensuring proper division, while cancer cells bypass these controls. This chapter explores how genetic changes disrupt cellular processes, fueling cancer growth and spread.

Cancer and the Cell Cycle

Cell division and cancer development

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• Uncontrolled cell division and growth characterize cancer
  • Regulated cell cycles with checkpoints ensure proper division in normal cells
  • Mutations allow cancer cells to bypass checkpoints and divide uncontrollably
• Mutations in genes controlling the cell cycle can lead to cancer development (carcinogenesis)
  • Mutations can occur in proto-oncogenes, tumor suppressor genes, or DNA repair genes
• Uncontrolled cell division results in tumor formation
  • Benign tumors remain localized and do not invade surrounding tissues (lipomas, nevi)
  • Malignant tumors can invade nearby tissues and spread through metastasis (breast cancer, lung cancer)

Proto-oncogenes vs oncogenes

• Proto-oncogenes are normal genes regulating cell growth and division
  • Encode proteins promoting cell cycle progression (growth factors, receptors)
• Mutations convert proto-oncogenes into oncogenes
  • Oncogenes are altered proto-oncogenes causing uncontrolled cell growth and division
• Proto-oncogene activation mechanisms include:
  1. Point mutations altering protein function
  2. Gene amplification increasing proto-oncogene copy number
  3. Chromosomal translocations placing proto-oncogene under different promoter control
• Oncogenes contribute to cancer development by promoting excessive cell growth and division (RAS, MYC, BCR-ABL)

Function of tumor suppressors

• Tumor suppressor genes encode proteins inhibiting cell cycle progression and promoting apoptosis
  • Act as "brakes" on cell division, preventing uncontrolled growth
• Tumor suppressors regulate the cell cycle at various checkpoints
  • G1/S checkpoint ensures cell readiness to enter S phase and replicate DNA
  • G2/M checkpoint ensures complete DNA replication and cell readiness to divide
• Examples of tumor suppressor genes:
  • p53 induces cell cycle arrest or apoptosis in response to DNA damage
  • RB inhibits G1/S transition by binding transcription factors
  • BRCA1 and BRCA2 are involved in DNA repair and maintain genome stability

Normal vs mutated tumor suppressors

• Normal tumor suppressors prevent cancer by regulating cell division and promoting apoptosis
  • Ensure cells with damaged DNA do not progress through the cell cycle
  • Induce apoptosis in irreparable cells, eliminating potential cancer cells
• Mutated tumor suppressors lose ability to regulate the cell cycle and prevent cancer
  • Tumor suppressor gene mutations are typically recessive, requiring both allele inactivation
  • Loss of tumor suppressor function allows damaged cells to continue dividing
• Inherited mutated tumor suppressor genes can increase certain cancer risks (BRCA1/BRCA2 mutations increase breast/ovarian cancer risk)
• Somatic mutations in tumor suppressor genes can contribute to sporadic cancer development
  • Mutations accumulate over time due to environmental factors or random DNA replication errors

Cellular processes in cancer development

• Cell differentiation: Cancer cells often exhibit reduced differentiation, reverting to a less specialized state
• Telomerase: Activation of telomerase enzyme in cancer cells allows for unlimited replication potential
• DNA repair: Defects in DNA repair mechanisms contribute to the accumulation of mutations in cancer cells
• Cell signaling: Altered cell signaling pathways can lead to uncontrolled growth and division in cancer cells
• Genetic instability: Cancer cells often display increased genetic instability, facilitating further mutations