Immunology and Immune Disorders - cancer and the immune system

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  • Created by: Rosa
  • Created on: 30-03-13 20:01

cancer cells ignore apoptosis cues and make their own proliferation cues

HMPCC hereditary nonpolyposis corectal cancer - insides of GI tract covered in small tumours - family history

6 seperate mutations to develope cancer?

exetrinsic factors:

  • tobacco smoke
  • pollution
  • radiation 
  • chemicals
  • viruses - Hep b and EBV

heamotological malignancies - 8% leukemia and lymophoma

sarcoma - 2% osteosarcoma

carcinoma - 80% breast lung colon

MAGE 1 - silent toumour antigen: germline cell in testes (normal), if found anywhere else it is indicativeof tomour

immune surveillance - cytotoxic t-lymphocytes

spontaneous solid tumours:

  • mutation causes protein to be potentially recognised and non-self by CTL's
  • naive t cells circulate in blood, lympoh and secondary organs
  • tumour cells lack co-stimulatory molecules, 
  • no circulation so cannot prevent

heamatological malignancies:

  • found where t-cells circulate
  • heam malignancies express high levels of B7 providing co-stimulation (not 100% fool proof)

Virus associated tumours:

  • viruses causing acute infections do not cause cancer, cells are quickly destroyed
  • viruses that cause cancer cause long term latent infections, so CTL's are no tgood

role of macrophages and NK cells

 Hyperactivated macrophages express TNF (tumour necrosis factor) which causes tumour cell necrosis

Abnormal expression of surface molecules eg phosphatidylserine enables macrophages to  differentiate between cancer and normal cells

 NK (natural killer) cells target cells with low MHC (major histocompatibility complex) class I expression and display unusual surface molecules 

Advantages-macrophage and NK are quick acting, recognize diverse targets, macrophages located in tissues where 92% tumours arise

 Disadvantage-both macrophages and NK cells are reliant on inflammatory reaction

Genomic instability keeps tumour cells one step ahead of CTL surveillance

 Tumour antigen mutate so no longer recognized 

 Tumour antigen mutate so no longer fit into MHC groove for presentation

 Lack MHC expression (15% of all tumours)

 Mutations of TAP transporters prevent tumour antigens being transported to MHC molecules

 Genomic instability keeps tumour cells one step ahead of CTL surveillance

 Tumour antigen mutate so no longer recognized 

 Tumour antigen mutate so no longer…

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