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Summary Cancer and Chronic Inflammation
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Summary on cancer and how it forms as well as its link to inflammation.
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Cancer and InflammationExample:
You’re driving a car and you want to break but the break doesn’t work.
The hand break doesn’t stop the car either.
It accelerates.
And neither does turning off the car using the keys.
Coming off roads doesn’t stop the car.
The only way to stop it is to hit a wall.
But the car goes through the wall.
The mechanic didn’t pick up on this when they checked the car.
The only way it will stop is if it runs out of petrol.
But the car uses other forms of petrol.
Self-sufficient growth signals
The car accelerates.
mutations in growth-promoting genes
autocrine signalling: cancer cells make and respond to their own growth signals
tumour suppressor genes are mutated. Normally they act as breaks on cell growth.
but mutations mean cells can continue to replicate.
microenvironment: neighburing cancer cells release their own growth factors to
recruit immune cells to be cancerous and replicate.
Limitless replicative potential
Imagine this as petrol. It can never run out.
Cells can only replicate 30 times before they die.
Telomeres: DNA at the end of a chromosome that codes for replication.
Abnormal telomeres: This is elongated to increase the number of times the cell can
replicate.
Adding a 6-base pair repeatedly to allow unlimited replication.
Insensitivity to growth signals
The car cannot break and the mechanic checks the car like the cell checks itself during cell
cycle. But cannot find any faults.
Tumour suppressor genes (p53) act as the breaks normally on the car.
If a change is detected: P53 halts the cell cycle at the G1 phase giving time for the cell
to repair. And activates DNA repair proteins.
Cancer can cause a mutation in these tumour-suppression genes to stop them
detecting changes.
So, the cell can continue to replicate, and a tumour can continue to form.
Evading apoptosis
When a car hits a wall you’d assume it stops and crashes, but it keeps going and doesn’t
crash.
Cancer grows cell growth>cell death.
, P53 can trigger apoptosis if a change is detected during the G1 checkpoint of the cell
cycle.
So by causing a mutation in the p53 you also evade apoptosis.
Sustained angiogenesis
The car makes its own petrol (blood vessels) to keep it driving (the tumour keeps growing).
Angiogenesis: development of a blood vessel in new tissue areas
To provide oxygen and nutrients to the cell
A cell must be within 150-200 micrometres of a blood vessel to receive these.
Normal cells:
o tightly regulated angiogenesis
o by pro-angiogenic and anti-angiogenic factors.
o How much of these is secreted depends on tissue damage, oxygen deficiency
and wound healing.
o When healed anti-angiogenic factors are produced to stop this and cause a
balance.
o Example: during tissue damage vascular endothelial growth factor is released
(VEGF). This attracts and activates endothelial cells to form blood vessels.
o LOOK BELOW!
Cancerous cells:
o Excessive production of VEGF
o Or high levels of pro-angiogenic factors
o So continuous signalling or angiogenesis occurs.
o Suppressed release of anti-angiogenic factors to stop it.
Tissue Invasion
The car can drive off roads too and isn’t limited to the roads it drives on. So, when the roads
run out it can continue driving.
Tumour cells invade beyond the tumour.
Enters the blood system.
Invades the local area.
Carcinoma: cancer cells divide and take up more space in the tissue. Partial blockage.
Invasive carcinoma: total blockage of an area.
Metastasis:
Formation of secondary tumours from primary tumours
Cancer cells enter blood vessels.
It sends signals for the blood cell to open to let it enter.
Circulates around the body until it finds a pre-metastatic niche (space and nutrients)
Micro metastasis: cancer cells replicate in the new niche.
Immunity mediators:
o The immune system tries to defend itself against the abnormal cells.
o Macrophages and neutrophils are attracted to the site of the tumour by
chemokines.
Extracellular matrix
Proteins, glycoproteins and other molecules.
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