gene expression + cancer (incl oestrogen)

what are the 2 types of tumour

benign and malignant

4 treatments for cancer ?

chemotherapy, radiotherapy, monoclonal antibodies, surgery

how does chemotherapy work?

chemicals added to blood. prevents cell division, destroys fast dividing cells

risk of chemotherapy

affects all healthy rapidly dividing cells e.g. hairm, epithelial cells in intestine

how does radiotherapy work

kills cancer cells, localised

risk of radiotherapy

harms/destroys all cells in tissue surrounding tumour

when does a benign tumour pose risk?

when puts pressure on surrounding tissue e.g. organs

what are the 4 different types of tumour/cancer

precancerous- cells w potential to become cancerous. early tumour- small mass of cancerous cells. large tumour- tumour with blood and lymphatic supply. metastasis- secondary tumours

what do proto-oncogenes do?

promote cell division in controlled manner when growth factor present

how do proto-oncogenes become oncogenes?

if mutate, become permanently switched on, cause cell division in uncontrolled manner

what happens if a proto-oncogene mutates, becoming an oncogene? 2 things

receptor permanently activated, despite lack of growth factors, which normally start the signalling cascade. or, oncogene code for growth factor, leading to excessive production. both lead to tumour

how do mutations in proto-oncogenes occur? 3 ways

randomly, high energy damage to dna, inherited mutation of proto-oncogene

what does increased acetylation of oncogene do?

gene switched on, lots of transcription factors binding to receptors, uncontrolled cell division, tumour

what does decreased methylation of oncogene do?

gene switched on, lots of transcription factors binding to receptors, uncontrolled cell division, tumour

what does decreased acetylation on oncogene do?

gene switched off, normal cell divison

what does increased methylation of oncogene do?

gene switched off, normal cell divison

tumour suppressor genes are important for what? 3

slow cell division, repair cellular/dna mistakes, initiate apoptosis

what is apoptosis

programmed cell death

when tumour suppressor genes are inactivated, what is the result?

functionally and structurally different cells produced, most die- (immune system recognises as non-self and destroys by antibodies/cytotoxic T cells), cells that survive produce clones, leads to tumour

give 3 examples of tumour suppressor genes

T53, BRCA1 and BRCA2

T53 (tumour suppressor gene) produces what protein? what does it do?

P53 protein, regulated cell cycle + apoptosis. cells destroy themselves- needed when dna damaged beyond repair

what is the result of a failure of the T53 tumour suppressor gene?

no apoptosis, damaged cells can’t destroy themselves, mutant cells produced, uncontrollable cell division, cancer

what do the BRCA1 and BRCA2 tumour suppressor genes do?

code for protein involved in dna repair

what would result in a failure of the BRCA1 and BRCA2 tumour suppressor genes?

dna can’t be repaired, mutant cells produced, uncontrollable cell division, cancer

what does hypermethylation of tumour suppressor gene do?

switch off tsg, not expressed, increased cell division, tumour. no apoptosis/more mutation

what does hypomethylation of tumour suppressor gene do?

switch on tsg, expressed, normal cell division. no cancer/tumour