Gene expression and cancer Flashcards
Describe how tumours and cancers form
● 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
the main characteristics of benign tumours
Usually grow slowly (cells divide less often
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 (as cell adhesion
molecules stick cells together)
Can normally be removed by surgery
and they rarely return
Malignant tumours
Usually grow faster (cells divide more often)
Cells become poorly differentiated / unspecialised
Cells have irregular, larger / darker nuclei
Poorly defined borders and not encapsulated so can
invade surrounding tissues (growing projections)
Spread by metastasis- cells break off and spread to
other parts of the body, forming secondary tumours
(due to lack of adhesion molecules)
Can normally be removed by surgery combined with
radiotherapy / chemotherapy but they often return
Describe the function of tumour suppressor genes
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)
Explain the role of tumour suppressor genes in the development of tumours
● 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 protein
○ By preventing binding of RNA polymerase to promoter region, inhibiting transcription
● Both lead to uncontrolled cell division (cell division cannot be slowed)
Describe the function of (proto-)oncogenes
Code for proteins that stimulate cell division
(eg. through involvement in signalling pathways
that control cell responses to growth factors)
Explain the role of oncogenes in the development of tumours
(An oncogene is a mutated / abnormally expressed form of the corresponding proto-oncogene)
● 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 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
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 divisio
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
Some breast cancers 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 cancer
● 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
