I have been doing some research on how CF33 will most probably work differently in humans compared to mice. In humans we may have to temper our expectations because there are quite a few barriers that CF33 will encounter that make a more difficult pathway to success.
CF33 works well in mice, but when we try to use it in humans, it faces more challenges.
In mice, tumours are small, and CF33 can easily break through the walls to attack the cancer cells inside. But in humans, solid tumours are considerably bigger and have thicker walls, making it harder for CF33 to get in and spread effectively.
Solid tumours in people have more dense connective tissue, which makes it harder for CF33 to move around. Tumours in humans have areas with very little oxygen, which can make it difficult for CF33 to survive and spread.
In mice, CF33 can spread easily because their immune system doesn’t react as strongly. But in humans, the immune system is better at recognising and attacking CF33. So, before it even gets a chance to attack the tumour the body may try to destroy it.
CF33 needs to travel through the bloodstream to reach the tumour. In mice, the tumours blood vessels allow the virus to enter more easily. But mans, these blood vessels are often abnormal and may prevent CF33 from spreading effectively in the tumour
Even though CF33 works well in mice human tumours are larger, and have stronger defences.
I am not trying to be negative, just realistic.
I would appreciate others to comment and pick holes in what I have learned. @davybabyk and others please chime in.
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