3.8.2.3 - Gene expression and cancer

Question 1

Describe how tumours 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 grow more slowly (cells divide less often),
• Malignant tumours Usually grow faster (cells divide more often)
• Benign tumour Cells are well differentiated / specialised,
• Malignant tumour Cells become poorly differentiated / unspecialised
• Benign tumour Cells have normal, regular nuclei,
• Malignant tumour Cells Cells have irregular, larger / darker nuclei
• Benign tumours have Well defined borders and often surrounded by a
  capsule so do not invade surrounding tissue,
• Malignant tumours have Poorly defined borders and not encapsulated so can
  invade surrounding tissues (growing projections)
• Benign tumours Do not spread by metastasis (as cell adhesion
  molecules stick cells together),
• Malignant tumours Spread by metastasis - cells break off and spread to other parts of the body, forming secondary tumours (due to lack of adhesion molecules)
• Benign tumours Can normally be removed by surgery and they rarely return,
• Malignant 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 (eg. if DNA damage detected)
● OR cause self-destruction (apoptosis) of potential
tumour cells (eg. if damaged DNA can’t be repaired)

Question 4

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

Answer 4

● Mutation in DNA base sequence
→ leads 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 protein
○ By preventing binding of RNA polymerase to promoter region, inhibiting transcription

● Both lead to uncontrolled cell division (cell division cannot be slowed)

Question 5

Describe the function of (proto-)oncogenes

Answer 5

Code for proteins that stimulate cell division
(eg. through involvement in signalling pathways
that control cell responses to growth factors)

Question 6

oncogene

Answer 6

An oncogene is a mutated / abnormally expressed form of the corresponding proto-oncogene

Question 7

Explain the role of oncogenes in the development of tumours

Answer 7

● Mutation in DNA base sequence
→ leads to 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 acetylation → increases production of protein
○ By stimulating binding of RNA polymerase to promoter region, stimulating transcription

● Both lead to uncontrolled cell division (cell division is permanently stimulated)

Question 8

Suggest why tumours require mutations in both alleles of a tumour
suppressor gene but only one allele of an oncogene

Answer 8

● 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 9

Explain the relevance of epigenetics in cancer treatment

Answer 9

> 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

Question 10

Explain the role of increased oestrogen concentrations in the development
of some (oestrogen receptor-positive) breast cancers

Answer 10

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

Question 11

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

Answer 11

● 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