• Disruptions to cell cycle or inability to carry out apoptosis can lead to cancer

Cancer Cells

  • Cancer: unregulated/out of control cell division, results from genetic changes affecting genes whose proteins regulate the cell cycle
    • Normal cells become cancer cells by the accumulation of mutations affecting proto-oncogenes and tumor-suppressor genes
    • If gene mutates, protein product (often enzyme) changes which changes its function and causes improper regulation
  • Abnormalities of cancer cells:
    • Do not move through cell cycle in a regulated way; if stop dividing, only at random checkpoints
    • Can divide forever with given nutrients
    • Do not display anchorage dependence of density-dependence (divide past one layer)
    • Evade signals that trigger apoptosis when something goes wrong
  • Proto-oncogenes: normal version of genes that code for protein that stimulate cell growth (growth-stimulating)
  • Oncogenes: dysfunctional, cancer-causing genes
    • Transformation: When gene becomes oncogene

Causes for Oncogenes

  1. Gene Translocations: Chromosome broken and rejoined incorrectly; Errors may place gene close to control regions and then expression of wrong gene products can make cancer worse                                                                                                         
  2. Gene Amplification: too many copies of gene → excess growth-stimulating proteins
  3. Epigenetic: abnormal chromatin condensation → proto-oncogene expressed at the wrong time or amount
  4. Point Mutations:
  • In promoter, enhancer/control element → could increase expression → excess growth-stimulating proteins
  • Within gene → could code for protein that is more/less to degradation


  • Cannot directly inherit cancer cuz need more than one oncogene but can be predisposed by being passed down a couple
    • Major difference between the two tumors/cancers is a number of mutations
  • Benign: ~5 mutations, generate mass, abnormal but NOT cancerous cuz do not spread→ stay at the original site due to specificity of structure
  • Malignant: impairs the function of organ it’s in, cancerous ~7 mutations,
    • Can metastasize: part breaks off, enters the bloodstream, divides and creates a tumour elsewhere in the body
    • Release their own growth factors and cause blood vessels to grow towards it so it can nourish and spread
  • Causes for changes in malignant tumours: excessive buildup, altered metabolism, cell surface changes, secrete sig. molecules


  • Radiation that harms localized tumours more than normal cells
  • Chemotherapy: a toxin that kills all dividing cells by destroying spindle fibres that splits cell


  • *Each cancer is caused by a different set of mutated genes, so there is no possible cure-all

Genetic Alterations and Cancer

  • Tumor-suppressor genes: genes that can inhibit cell division and prevent cancer from developing (growth-inhibiting)
    • Most mutated → stimulated cell division
    • Protein products repair DNA, control adhesion, and regulate cell signalling pathways that inhibit cell cycle
  • Defective version of a protein in an inhibitory pathway (p53) fails to act as a tumour-suppressor.

Interference with Normal Cell Signaling Pathways factor

With P53 Transcription Factor:

  • Activated by signal transduction pathway when DNA is damaged from external factors and promotes transcription of cycle-inhibiting proteins

Without P53 Transcription Factor:                                                                                                                 

  • If gene mutates, damaged cells can proliferate and spread, becoming tumor
  • Increased cell division

Ras gene:

  • Gene that codes for G protein that relays growth factor message

When gene is mutated, causes ras protein to be overexpressed and cell cycle overstimulated