8.2.3 Gene expression and cancer

Question 1

Describe how tumors and cancers form

Answer 1

• mutations in DNA / genes controlling mitosis can lead to uncontrolled cell division
• tumour formed if this results in mass of abnormal cells
  • malignant tumour = cancerous , can spread by metastasis
  • benign tumour = non cancerous

Question 2

compare the main characteristics of benign and malignant tumours

Answer 2

benign tumours :
- usually slowly growing
- cells are well differentiated/ specialised
- cells have normal , regular nuclei
- well defined borders and often surrounded by a capsule so do not invade surrounding tissue
- do not spread by metastasis
- can normally be removed by surgery and they rarely
return
Malignant tumours :
- usually grow faster
- cells become
poorly differentiated / unspecialised
- cells have irregular , larger / darker nuclei
- poorly defined borders and not encapsulated so can invade surrounding tissues
- spread by metastasis => cells break off and spread to other parts of the body forming secondary tumours
- can normally be removed by surgery combined with radiotherapy / chemotherapy but they often return

Question 3

describe the function of tumour suppressor genes

Answer 3

code for proteins that :
- inhibit / slow cell cycle
- or cause self
destruction of potential tumour cells

Question 4

explain the role of tumour suppressor genes in the development of tumours

Answer 4

• mutation in DNA base sequence => production of non functional protein
  • by leading to change in amino acid sequence which changes protein tertiary structure
• decreased histone acetylation or increased DNA methylation => prevents production of proteins
  • by preventing binding of RNA polymerase to promoter region, inhibiting transcription
• both leading to uncontrolled cell division

Question 5

describe the function of (proto-)oncogenes

Answer 5

code for proteins that stimulate cell division

Question 6

explain the role of oncogenes in the development of tumours

Answer 6

• mutation in DNA base sequence => overproduction of protein or permanently activated protein
  • by leading to change in amino acid sequence which changes protein tertiary structure
• decreased DNA methylation or increased histone acetlyation => increases production of protein
  • by stimulating binding of RNA polymerase to promoter region , stimulating transcription
• both lead to uncontrolled cell division

Question 7

suggest why tumours require mutation in both allele of a tumour suppressor gene but only one allele of an oncogene

Answer 7

• 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

Question 8

explain the relevance of epigenetics in cancer treatment

Answer 8

• increasing DNA methylation or DECREASING histone acelyatiom of oncogene
  • to inhibit transcription/ expression
• decreasing DNA methylation or increasing histone acetylation of tumour suppressor gene
  • to stimulate transcription / expression

Question 9

explain the role of increased oestrogen concentration in the development of some (oestrogen receptor - positive ) breast cancers

Answer 9

1) some breast cancers have oestrogen receptors , which are inactive transcription factors
2) if oestrogen conc is increased , more oestrogen binds to oestrogen receptors , forming more oestrogen - receptors 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 , increaseinf the rate of cell division

Question 10

suggest how drugs that have similar structure to oestrogen help treat oestrogen receptor
- positive breast cancers

Answer 10

• drugs bind to oestrogen receptors , preventing binding of oestrogen
• so no / fewer transcription factors bind to promoter regions of genes that simulates the cell cycle