gene expression and cancer Flashcards
describe the development of secondary tumours from primary tumours (4 marks)
- random mutation results in formation of tumour cells
- as tumour enlarges it develops blood and lymph vessels
- tumour cells squeeze into blood and lymphatic vessels
- tumour cells circulate in the blood and lymph
- tumour cells adhere to blood vessel walls and squeeze through to form metastases
- metastases can form in the lymph nodes
what are the 3 roles of tumour suppressor genes
- decrease cell division
- apoptosis (cell death)
- “fix” DNA
Distinguish between benign and malignant tumours
Benign tumours are not cancerous, malignant tumours are cancerous
Explain the role of oncogenes and tumour suppressor genes in the development of tumours
Oncogens: mutations of proto-oncogenes,oncogenes are permanently activated and stimulate cell division causing tumours.
Tumour suppressor genes: slow cell division, if mutated become inactive and therefore cell division increases and tumours develop
define secondary tumour cell
a tumour that is formed in different tissues far away from primary tumours
what are the 2 ways that tumours travel around the body
- blood
- lymph
explain the role of tumor suppressor genes in prevention of tumours
when active tumour supressor genes cause decreased cell division preventing a tumour
when tumour supressor genes have a mutation they are inactive resulting in increased cell division and therefore a tumour
give the 11 characteristics of benign tumours (used to compare to malignant tumours)
benign tumours
- can grow to a large size
- grows very slowly
- cell nucleus has a relatively normal appearance
- cells are differentiated
- cells produce adhesion molecules that make them stick together so they remain within the tissue they arise in (primary tumours)
- tumours are surrounded by a capsule of dense tissue
- less likely to life threatening but can disrupt functioning of a vital organ
- localised effects on the body
- can be removed by surgery alone
- rarely reoccur after treatment
give the 11 characteristics of malignant tumours (used to compare to benign tumours)
- can grow to a large size
- grows rapidly
- cell nucleus is larger and appears darker due to abundance of DNA
- cell become dedifferentiated
- cells do not produce adhesion molecules so can spread to other regions of the body (a process called metastasis) forming secondary tumours
- tumours are not surrounded by a capsule so can grow finger like projections into the surrounding tissue
- more likely to be life threatening as abnormal tumour tissue replaces normal tissue
- systemic effects (e.g: weight loss and fatigue)
- removal involves radiotherapy or chemotherapy as well as surgery
- more frequently reoccur after treatment
what is the role of mutated protooncogenes in cell division
the oncogenes code for excess growth factor resulting in increased cell division
or oncogenes switch on receptors even if there is no increase in growth factor resulting in increased cell division
Explain the effects of abnormal methylation of tumour suppressor genes and oncogenes
Abnormal methylation of tumour suppressor genes: hypermethylation in promotor region of tumour suppressor gene inactivates the gene and transcription is inhibited
Tumour suppressor gene no longer reduces cell division
Abnormal methylation of oncogenes: hypomethylation leads to activation and increased cell division
suggest how hypermethylation of tumour suppressor genes can result in cancer (4 marks)
- hypermethylation occurs in the promotor region of tumour suppressor genes
- tumour suppressor gene is inactivated
- transcription of tumour suppressor gene is inhibited
- tumour suppressor gene is switched off (silenced)
- increase cell division and formation of tumours due to inactive tumour suppressor gene
explain how increased oestrogen levels can cause breast cancer
oestrogen causes transcription factor to become active and increase transcription
This can lead to increased cell division and therefore tumours if it acts on a gene that controls cell division
oestrogen can also turn protooncogenes into oncogenes
