You said: CF33 has been hyped as the virus that attacks all tumour types. Why have they not found optimal dose yet? Is this because the effectiveness of CF33 at the current dose levels isn’t meeting expected outcomes? Why do you need to keep escalating the current dose levels if it was showing signs of effectiveness?
Think of tumours as a bunch of wild breeding rabbits you want to control. So you introduce a specific number of foxes that only feed on rabbits. If the foxes multiply just a little faster than the rabbits they kill, then the rabbits will eventually disappear. Maybe that’s your optimal dose of foxes. If the foxes multiply at a similar rate to the rabbits, the rabbit population might stabilise. That’s analogous to stable disease. You can see that if the starting population of foxes is too low, the rabbit population will outgrow the fox population. That doesn’t mean foxes can’t do their job as expected - they can- it just means there aren’t enough of them to kill enough rabbits in your desired time frame.
Different types of cancer, like different kinds of animals, multiply at different rates. That’s why your starting population of oncolytic viruses might need to vary between different cancer types. Using the fox as CF33 virus analogy, you don’t want a situation where too many foxes destroy the environment (toxicity). That’s why a smaller number of viruses are initially trialled to establish safety parameters.
I hope my naive explanation is close to the truth. Believe it or not, I posed exactly the same questions to myself.
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