8.2.3 gene expression and cancer

describe how cancer is form

mutations in DNA controlling mitosis can lead to uncontrolled cell division

describe how tumours are formed

if uncontrolled cell divison results in mass of abnormal cells

what are the two types of tumours

malignant - cancerous, can spready by metastasis

benign - non cancerous

what are the main characteristics of benign tumours

• grow slowly

• cells are differentiated/specialised

• cells have normal nuclei

• well defined borders and often surrounded by a capsule so don’t invade surrounding tissue

• do not spread by metastasis

• cells can be removed by surgery and then rarely return

main characteristics of malignant tumours

• grow fast

• cells are poorly differentiated/ unspecialised

• cells have irregular, larger 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 often return

describe function of tumour suppressor genes

codes for proteins that:

• inhibit/slow cell cycle

• or cause self destruction of potential tumour cells

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 a change in amino acid sequence which changes tertiary structure

decrease histone acetylation or increased DNA methylation - prevents production of protein

• by preventing RNA polymerase to promoter region, inhibiting transcription

both lead to uncontrolled cell division

describe function of proto-oncogenes

codes for proteins that stimulate cell division

explain the role of oncogenes in the development of tumours

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 or RNA polymerase to promoter region, stimulating transcription

both lead to uncontrolled cell division

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 can reverse epigenetic changes that caused cancer, preventing uncontrolled cell division

• increased DNA methylation or decreasing histone acetylation of oncogene

  to inhibit transcription

• decreasing DNA methylation or increasing histone acetylation of tumour suppressor gene

  to stimulate transcription

explain the role of increased oestrogen concentration in the development of some breast cancers

1. some breast cancer 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 of these genes increasing 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 preventing binding of oestrogen

so no/fewer transcription factors bind to promoter region of genes that stimulate cell cycle