Cancer

Lung cancer

• Tar in smoke contains several carcinogens (cancer causing agents)
  • Cause mutations in the genes which control cell division (oncogenes)
  • Divide uncontrollably to produce a mass of cells - tumour
• Tumour cells do not respond to signals from nerves and hormones
  • Continue to grow
  • No programmed cell death occurs
• A small group of tumour cells is called a primary growth. It may be
  • Benign - does not spread from its origin
  • Malignant - spread throughout the body invading other tissues and destroying them
• Cells breaking off malignant tumours from secondary growth cause cancer to spread - metastasis
  • Hard to find and remove them in this state
• Tumour may take many years to develop with few or no real symptoms
  • Well advanced when discovered
  • If the respiratory system is involved:
  • Symptoms like coughing up blood and blocked airways leading to diseases like pneumonia are common
  • Removing a whole or part lung may be effective provided metastasis is not well advanced

Smoking and lung cancer risk

• Risk increases if
  • Smokers start young
  • Inhale deeply
  • More cigarettes are smoked per day
  • The cigarettes are high tar
  • Smoking goes on over a long period of time
• Risk decreases if smoking stops
• Smokers 18x more likely to develop lung cancer than non-smokers
• One third of all deaths from cancer can be attributed to smoking

Genes and Cancer

• 3 types of evidence support a link
  • Tendency to develop cancer seems to be inherited
  • Tumour cells in some cancers have abnormal chromosomes
  • There is a positive correlation between mutations and carcinogens
• Genes causing cells to become cancerous are called oncogenes (oncology = study of cancer)
  • They are found when proto-oncogenes, normal versions of genes, mutate and become overactive
  • The RAS proto-oncogene codes for plasma membrane proteins called G-proteins
  • G-proteins enable cells to respond to growth factors
  • These G-proteins are normally activated by one of their own enzymes GTPase
  • The mutant ras gene produces GTPase deficient G-proteins / they remain active longer causing tumours
• Myc oncogenes (chromosome 8)
  • Myc proto-oncogenes produce proteins needed for transcribing genes required for normal cell division
  • Common mutation switches the myc proto-oncogenes to chromosome 14 where it acts as an oncogene / abnormal cell division / tumour
  • When both ras and myc oncogenes are present together, malignant cells will result
• Tumour suppressor genes
  • Associated with cell division
  • Converted to oncogenes by mutation and reduce normal activity by inhibiting cell division
  • Might inhibit transcription of the proto-oncogenes like myc
  • May become overactive → tumour