Disease process of cancer Flashcards
1
Q
Causes of cancer
A
- Initiation
- Promotion
- Progression (metastasis)
2
Q
Initiation
A
- Chemical: alcohol, smoking, tar etc.
- Physical: ionising radiation, mechanism: chromosome translocation, gene amplification, oncogene activation
- Viral: Herpes virus, papillomavirus, hepatitis B
3
Q
Promotion
A
- Growth factors
- Oncogenes
4
Q
2 methods of stimulation for growth factors
A
- Autocrine: cell carries receptor and secretes growth factor (GF)
- Paracrine: GFs acting on a cell are produced locally by the cell or its immediate neighbours
5
Q
Growth factors
A
- Polypetide molecule
- Regulate cell growth and function
- Bind to cell membrane receptors
- Stimulate activation of intracellular signal transduction pathways
6
Q
Oncogenes
A
- Transforming genes
- Positive regulators of growth
- Represent a gain in function to transformed cells
7
Q
Tumour suppressor genes
A
- e.g. P53
- Most commonly altered gene in human tumours
- Normal function is as transcriptional regulator, promotes DNA repair, apoptosis, differentiation
- Induced by DNA damage and hypoxia
- G1/S checkpoint control gene
8
Q
Metastasis
A
- Not random
- Cascade of limited sequential steps
- Involves tumour-host interactions
- ‘Survival of the fittest’ pertains. So the healthier you are, the better the outcome
9
Q
Invasion and metastasis
A
- Tumour invades through basement membrane
- Moves into extracellular matrix/connective tissue/surrounding cells
- Invades blood vessels
- Tumours cells ‘arrested;’ in distant organ
- Enzymes involved from the ECM: plasmin, cathepsin
- Enzyme involved from cell adhesion: integrins and loss of cahedrins correlates with tumour invasion and metastasis
10
Q
Steps of invasion of metastasis
A
- Primary tumour -> intravasation -> circulating tumour cell in vessel -> extravsation -> metastases
11
Q
Angiogenesis
A
- Formation of new blood vessels is a key factor in the maintenance and progression of malignant tumours
- For tumour to grow >2mm there needs to be new blood vessels
12
Q
Example of understanding molecular biology can result in improved treatment methods
A
- Growth factors
- Anti-VEGF antbodies can prevent interaction of VEGF with its receptors
- Can prevent interaction with receptors
- Activation of downstream signalling pathways
- Can lead to vascular regression and a dormant tumour
13
Q
How the immune systems recognise ‘foreign’ cancer cells
A
- Cancer cells can ‘hide’ from T cells
- PD1 (programmed death receptors) is present on T lymphocytes
- Ligand (PGL-1) on tumour cells
- Interaction of these suppresses T cell action
- There is a therapeutic opportunity to block PD1 or PDL-1
