Lecture notes
First Class Lecture notes Cancer Biology (DNA and Disease)
- Module
- Cancer Biology
- Institution
- University Of Bath (UoB)
Metastasis lecture notes
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Metastasis!Migration of tumour cells from primary site to secondary sites – distant
locations within the body.
90% of cancer deaths occur due to spread.
Key concepts in metastasis:
1. Mechanism of the invasion and metastasis
cascade
2. Cancer cells activate Epithelial-mesenchymal
transition (EMT)
3. EMT is necessary for cell motility and
invasiveness
4. Metastasis is an inefficient process
5. Colonisation may depend on complex
interactions between the tumour cells and
the microenvironment
PET scan indicates presence of
metastasis – yellow shows glucose
uptake in the body.
Graph highlights the fact that
early detection is key, especially in
the case of solid tumours – the
sooner cancer is detected, the
sooner therapy can begin.
Invasion & Metastasis Cascade:
Metastatic efficiency is low
1. Formation of primary/ institute tumour located at first organ, followed
by localised invasion: tumour cells prise apart endothelial junctions and
move into circulation (blood vessels or lymphatic system).
2. Intravasation – tumour cells actively migrate into lumen of the nearest
blood vessel. Tumour cells interact with other components of the blood
(platelets, etc), in a very hostile environment. CTCs – circulating tumour
cells.
3. Transport through circulation - Transport is dependent on flow rates,
pressure and volume of the blood vessel. Secondary tumours are rare in
, the heart because there is no real capacity for tumour cells to become
trapped. Other organs have narrower capillaries, so higher chance of
trapped tumour cells. Arrest of tumour cells in organs such as lungs.
4. Extravasion – cancer cells move from blood vessel out into surrounding
tissue. Many things that could account for this.
5. Potential of colonisation
by forming
micrometastasis – small
lump/ institute tumour at
secondary site.
6. Macrometastasis: after
angiogenic switch is
activated. Tumour can
stay as micro or develop
into full blown
macrometastasis,
triggering angiogenesis
and allowing growth, etc.
Image: breast carcinoma
tissue – breast carcinoma
cells have broken past the blood basement membrane and invaded
surrounding tissue.
Some challenging questions:
How do cancer cells become metastatic?
How do cancer cells acquire the ability to form remote colonies
(colonisation to form micro or macrometastases)?
Intravasation to extravasation:
Vast majority of tumours are
carcinomas – epithelial in origin.
This is because they are more
exposed to DNA damaging agents
so there is a greater chance of
mutation.
Epithelial type of cancer cell must
move between endothelial cells –
have to digest/ push apart
adherens junctions that allow
endothelial cells to stick together.
Tumour vasculature is leaky anyway, so endothelial cells could already be loose.
Intravasation: Cancer cells push in between spaces and migrate into blood
vasculature.
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