CANCER- Edmead Lecture Series

Question 0

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

Answer 0

None
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…

Question 1

Proto-oncogenes can be converted to oncogenes by a point mutation. What is this?

Answer 1

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

Question 2

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?

Answer 2

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

Question 3

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

Answer 3

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

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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

Answer 6

No
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

Question 7

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

Answer 7

IRESSA
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)