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Diseases > Cancer
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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