3.8.2.3 Gene expression and cancer

• The main characteristics of benign and malignant tumours.

  • Malignant tumours spread whereas benign tumours do not spread.
  • Benign tumours grow very slowly whereas malignant tumours grow quickly
  • Benign tumours tend to have localised effects on the body whereas malignant tumours tend to have systemic effects on the body
  • Benign tumours can usually be removed by surgery alone whereas malignant tumours usually require surgery, plus another treatment like chemotherapy
  • Benign tumours are much less likely than malignant tumours to reoccur after treatment
• Role of Tumour suppressor genes

  • slow down or prevent cell division
  • Repair mistakes in DNA
  • Code for proteins that 'tell' abnormal cells to die
• (Proto)- oncogenes

  • Normal function

  • Code for proteins involved in control of cell division

  • In particular, stimulating cell division (when growth factors attach to receptors on cell membrane, so cell division is required)

  
  

  • Role in development of tumours

  • Mutation could turn it into permanently activated oncogene

  • Decreased methylation / increased acetylation causes excess transcription

  • Cell division permanently activated; rapid / uncontrolled cell division

  • Note – only need 1 mutated allele
• Role of Increased oestrogen concentrations in the development of some breast cancers in development of tumours:

  • Areas of high oestrogen conc. such as adipose (fat) tissues in breasts, cell division is uncontrolled + women after menopause
  • Oestrogen initiates transcription of genes that stimulate cell division
  • ++ Growth of cancer minimised with drugs blocking the production / action of oestrogens in the breasts e.g. Tamoxifen prevents oestrogen binding to receptor
• A mutation of a tumour suppressor gene can result in the formation of a tumour. Explain how [2 marks]

  1. (Tumour suppressor) gene inactivated not able to control / slow down cell division (Ignore: references to growth)
  2. Rate of cell division too fast / out of control. 1 and 2 Accept: mitosis

  MP1: Role of the tumour suppressor gene

  MP2: What is a tumour
• What is a tumour? [1]

  • Mass of cells dividing/growing out of control

  What is a cancer? [1]

  • When cells from tumour have spread to other parts of body/metastasis has happened
• What effect might mutation 2 (single base substitution in intron) on protein produced?

  • 1 Intron non-coding (DNA)/only exons coding - EXPLAINING THAT INTRON IS NON CODING
  • 2 (So) not translated/no change in mRNA produced/no effect (on protein)/no effect on amino acid sequence
• Suggest why tumours require mutations in both alleles of a tumour suppressor gene but only one allele of an oncogene

  ● One functional allele of a tumour suppressor gene can produce enough protein to slow the cell cycle

  OR cause self-destruction of potential tumour cells → cell division is controlled

  ● One mutated oncogene allele can produce enough protein to lead to rapid / uncontrolled cell division
• Explain the relevance of epigenetics in cancer treatment

  Drugs could reverse epigenetic changes that caused cancer, preventing uncontrolled cell division.

  For example:

  ● Increasing DNA methylation OR decreasing histone acetylation of oncogene

  ○ To inhibit transcription / expression

  ● Decreasing DNA methylation OR increasing histone acetylation of tumour suppressor gene

  ○ To stimulate transcription / expression
• Explain the role of increased oestrogen concentrations in the development of some (oestrogen receptor-positive) breast cancers

  1. Some breast cancers cells have oestrogen receptors, which are inactive transcription factors

  2. If oestrogen concentration is increased, more oestrogen binds to oestrogen receptors, forming more oestrogen-receptor complexes which are active transcription factors

  3. These bind to promoter regions of genes that code for proteins stimulating cell division

  4. This increases transcription / expression of these genes, increasing the rate of cell division
• Suggest how drugs that have a similar structure to oestrogen help treat oestrogen receptor-positive breast cancers

  ● Drugs bind to oestrogen receptors (inactive transcription factors), preventing binding of oestrogen

  ● So no / fewer transcription factors bind to promoter regions of genes that stimulate the cell cycle
• Students should be able to evaluate evidence

  • showing correlations between genetic and environmental factors and various forms of cancer
  • AND interpret information relating to the way in which an understanding of the roles of oncogenes and tumour suppressor genes could be used in the prevention, treatment and cure of cancer.