8.2.3 Gene expression and cancer Flashcards
(22 cards)
What causes tumours and cancers to form?
Mutations in DNA or genes controlling mitosis can lead to uncontrolled cell division.
What is a tumour?
A tumour is formed if uncontrolled cell division results in a mass of abnormal cells.
What is a malignant tumour?
A malignant tumour is cancerous and can spread by metastasis.
What is a benign tumour?
A benign tumour is non-cancerous.
What do tumour suppressor genes code for?
Proteins that inhibit or slow the cell cycle, or cause self-destruction of potential tumour cells.
How do tumour suppressor genes respond to DNA damage?
They inhibit or slow the cell cycle if DNA damage is detected, or cause apoptosis if damaged DNA can’t be repaired.
What is the role of tumour suppressor genes in tumour development?
Tumour suppressor genes help regulate cell division and prevent uncontrolled growth.
Mutation in these genes can lead to tumour formation.
What happens when there is a mutation in the DNA base sequence of tumour suppressor genes?
It results in the production of a non-functional protein due to changes in the amino acid sequence, affecting the protein’s tertiary structure.
How does decreased histone acetylation or increased DNA methylation affect protein production?
It prevents the binding of RNA polymerase to the promoter region, inhibiting transcription.
What is the consequence of mutations in tumour suppressor genes?
Both mutations lead to uncontrolled cell division, meaning cell division cannot be slowed.
What do (proto-)oncogenes code for?
Proteins that stimulate cell division
Example: Involvement in signalling pathways that control cell responses to growth factors.
What is an oncogene?
An oncogene is a mutated or abnormally expressed form of the corresponding proto-oncogene.
How do mutations in DNA base sequence affect oncogenes?
They can lead to overproduction of protein or a permanently activated protein.
What is the effect of decreased DNA methylation or increased histone acetylation on oncogenes?
It increases the production of protein by stimulating binding of RNA polymerase to the promoter region, which stimulates transcription.
What is the result of oncogene activation?
- mutation in DNA base sequence
- overproduction of protein or permanently activated protein
- by leading to a change in amino acid sequence which changes protein tertiary structure - decreased DNA methylation or increased histone acetylation
- increased production of protein
- by stimulating the binding of RNA polymerase to the promoter region, stimulating transcription
Both mechanisms lead to uncontrolled cell division, as cell division is permanently stimulated.
Why do tumours require mutations in both alleles of a tumour suppressor gene?
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, thus controlling cell division.
Why do tumours require mutations in only one allele of an oncogene?
One mutated oncogene allele can produce enough protein to lead to rapid or uncontrolled cell division.
What is the relevance of epigenetics in cancer treatment?
Drugs could reverse epigenetic changes that caused cancer, preventing uncontrolled cell division.
How can increasing DNA methylation or decreasing histone acetylation affect oncogenes?
It can inhibit transcription / expression.
How can decreasing DNA methylation or increasing histone acetylation affect tumor suppressor genes?
It can stimulate transcription / expression.
Explain the role of increased oestrogen concentration in the development of some (oestrogen receptor-positive) breast cancer
- some breast cancer cells have oestrogen receptors, which are inactive transcription factors
- if oestrogen concentration is increased, more oestrogen binds to oestrogen receptors, forming more oestrogen-receptor complexes which are active transcription factors
- these bind to promoter regions of genes that code for proteins stimulating cell division
- 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
