The Biology of Cancer

  • Created by: rosieevie
  • Created on: 19-05-17 19:18

What is Cancer?

Cancer breaks rules of self-sacrifice and cooperation = uncontrollable proliferation w/ time-dependent replication turned off and apoptosis doesn't occur

Apoptosis - programmed cell death (PCD)

Neoplasia - abnormal growth of tissue

Two forms of tumour growth:

  • Increased cell division + Normal apoptosis = Tumour
  • Normal cell division + Decreased apoptosis = Tumour 

Cancer tends to come from single precursor cell thats incurred genetic damage due to clonal expansion

However, multiple mutations in same cell must occur for cancer = accumulation of mutations over a period of years 

- Natural selection for increased proliferation/invasiveness and against programmed cell death

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(Proto-) Oncogenes

Proto-oncogene - normal gene when altered by mutations, becomes and oncogene

Oncogene - gene that has the potential to cause cancer

Oncogenes contribute to cancer when overexpressed/overactive

Example - Ras pathway

Ras GTPase - monomeric enzyme that hydrolyses GTP

Hydrolysiation = conformational change between GTP-bound and GDP-bound states = change controls signalling pathway

Missense mutation - point muation 

Ras missense mutations in codons 12, 13 and 61 alter product activity = MAP kinase cascade = increased cell proliferation

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Tumour Suppressor Genes

Discovered as recessive mutations that cause cancer - contribute when inactivated or inhibited

Autosomal recessive disorder - two copies of abnormal gene must be present for disease/trait to develop

Example - Tp53

  • Normally senses cellular stress - causes changes to minimise damage
  • HPV E6 protein resembles E6-AP from humans 
  • Usual E6-AP role - addition of ubiquitin to p53, targeting for degradation
  • Expression of HPV E6 causes loss of p53
  • = inactivation of p53 tumour suppressor gene = cancer
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