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Flashcards in CANCER- Edmead Lecture Series Deck (8)
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Proto-oncogenes can be converted to oncogenes by a point mutation. What is this?

Results in a protein always being active
Replication protein slips and copies the gene again:
You end up with twice as much protein


Which cells in our body are more likely to be mutated and cause cancer?

It's thought that Each cell is just as likely to mutate as any other
But it doesn't necessarily mean that all cells are therefore likely to cause cancer: take stem cells- we know these are more prone...


Cancer is caused by an accumulation of how many mutations?
How many cells do these mutations have to occur in?
Can they effect different pathways?

Accumulation of 3+ mutations
All have to occur in a single cell
But they can effect a number of different pathways involved in growth and survival


What happens if you put adult stem cells straight into a tissue?

They will form tumours.
Proliferation of stem cells is usually very tightly controlled. If you don't suppress their growth they become tumourgenic.


Why do only some cells that break off tumours re grow to from a secondary growth/ tumour?

If fully differentiated cells in the tumour break off and metastasise: these won't recolonise and grow in another location.
If undifferentiated cells break off: these can grow and form a secondary tumour.
This is because they have to retain the ability to proliferate in order to grow elsewhere: undifferentiated (stem cells) have this ability


What are the main different types of mutations seen in cancers?

Gain of function in protooncogenes: to make them Oncogenic

Loss of function of tumour suppressor genes: makes them loose expression or lack function of tumour suppressor proteins

Changes to chromosomes


A patient has an oestrogen-driven breast cancer. Can I treat them with Herceptin?

Herceptin only effective in patients with HER-2 driven breast cancer, so will only treat patients who are HER2 positive.
Not those driven by oestrogen


What's the small molecule inhibitor drug that patients can show variability to?

It's an inhibitor of EGFR
Only effective in patients carrying a particular mutation that makes EGFR hyperactive
It's not effective in patients with mutated Ras
(Can often mistake patients for being resistant but really it's due to patient variability)

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