[20.5] gene expresssion and cancer Flashcards
what are cancerous and non-cancerous tumours called?
- cancerous = malignant
- non-cancerous = benign
comparison of benign and malignant tumours: size
both can grow to a large size
comparison of benign and malignant tumours: rate of growth
- B = grow very slowly
- M = grow rapidly
comparison of benign and malignant tumours: cell nucleus
- B = cell nucleus has a relatively normal appearance
- M = cell nucleus is often larger and appears darker due to an abundance of DNA
comparison of benign and malignant tumours: differentiation
- B = cells are often well differentiated (specialised)
- M = cells become de-differentiated (unspecialised)
comparison of benign and malignant tumours: spreading
- B = cells produce adhesion molecules that make them stick together so they remain in the tissues where they arose (primary tumours)
- M = cells don’t produce adhesion molecules so tend to spread to other regions of the body (metastasis), forming secondary tumours
comparison of benign and malignant tumours: capsule
- B = tumours are surrounded by a capsule of dense tissue so remain as a compact structure
- M = tumours are not surrounded by a capsule so can grow finger-like projection into the surrounding tissue
comparison of benign and malignant tumours: life-threatening
- B = much less likely to be life-threatening, but can distrupt functioning of a vital organ
- M = more likely to be life-threatening, as abnormal tumour tssue replaces normal tissue
comparison of benign and malignant tumours: effects on body
- B = tend to have localised effects on the body
- M = often have system effect eg. weight loss, fatigue
comparison of benign and malignant tumours: treatment
- B = can usually be removed by surgery alone
- M = removal usually involves radiotherapy and / or chemotherapy as well as surgery
comparison of benign and malignant tumours: reoccurence
- B = rarely recocurs after treatment
- M = reoccurs more frequently after treatment
describe how a cancerous tumour forms (7)
- cell is stimulated to rapidly divide
- cancerous cell does not respond to signals from other cells so continues to divide by mitosis
- cancerous cell not removed by immune system
- rapid mitosis, so tumour gets bigger
- tumour is supplied with blood and lympathic vessels
- if malignant, tumour cells spread in blood and lymph to other parts of the body
- metastasis - tumour cells invade other tissues, secondary cancers form
4 examples of carcinogens
- UV light
- tar in tobacco smoke
- asbestos
- x-rays
what 2 groups of genes interact to be responsible for nomal division?
- proto-oncogenes - stimulate cell division
- tumour suppressor cells - slow down cell division and control apoptosisw
what are oncogenes?
- mutated proto-oncogenes
- permanently stimulate cell division
how can oncogenes permanently stimulate cell division? (2)
- receptor protein on CSM can be permanently activated so cell division is switched on even in the absence of growth factors
- oncogene may code for a growth factor that is then produced in excessive amounts, stimulating excessive cell division
what happens if tumour suppressor genes mutate?
- stops inhibiting cell division
- cell grows out of control, forming a tumoour
what happens if tumour suppressor genes become inactivated by excessive methylation?
- hypermethylation in promoter region of TSGs
- TSG becomes inactivated
- transcription of promoter region of TSGs is inhibited
- TSG is silenced
- inactivation of TSG leads to increased cell division and the formation of a tumour
where might hypomethylation be a problem?
- if found in oncogenes, they will become activated
- cell division becomes permanently stimulated
- tumour forms
how does increased oestrogen concentrations lead to the development of breast cancer? (3)
- locally produced oestrogens trigger breast cancer in menopausal women
- once a tumour has developed, it further increases oestrogen concentrations
- WBC drawn to the tumour increase oestrogen production
how can oestrogen cause a tumour to develop?
- oestrogen activates a gene which promotes transcription
- oestrogen causes proto-oncogenes in cells of breast tissue to develop into oncogenes
- oncogenes will be activated and continue division to produce a tumour
