RE: Question5 Jul 2021 18:31
Burble
Posts: 521
Price: 21.50
No Opinion
RE: QuestionToday 09:19
Bojo.
So it depends highly on the cancer, the mechanisms for tumourogenesis and a number of other factors. Cancer is unfortunately an evolving beast and one that can be difficult to stay ahead of.
Some cancers have proteins/glycans on their surface which are relatively stable and remain upregulated in cancer initiation and progression. However for a large proportion, the molecular targets may change as the disease progresses.
An example of this may for instance be HER2 positive breast cancer. This is a cancer which has high levels of human epidermal growth factor receptor 2 displayed on the surface of the cell. This protein promotes the growth of the cancer cells and is an aggressive cancer type. HER2 treatments (herceptin for example) are effective and so progonsis is good.
Cancers can however escape treatments, such as if cancer relapses or spreads and in the case of HER2 positive BC, patients would be rescreened as the cancer may stop expressing this target on its surface. A lack of target means a therapy such as herceptin becomes ineffective.
If you can 'go hard and go fast' on a cancer, you don't give it the chance to mutate. As such, many treatments aim to do just that. They aim to remove 100% of the tumour through chemo, radio or immunotherapy to prevent the chance of escape and relapse. When a patient does relapse, this tumour tends to be different from the original one and so new therapies are needed.
Scancell's platforms have a number of different benefits. Immunobody - targetted treatment against a particular molecular target which is present or upregulated on the cancer cell surface. The benefit to T-cells is that they act like molecular scouts, so if the cancer has started seeding elsewhere across the body, if it has the target molecule on it's surface, the T-cell repertoire will mop up these seeds before they properly start growing. Immunobody is also adaptable, so in the future we may see new 'flavours' of this, targetting different commonly upregulated targets. So you may have a HER2 +ve immunobody construct, an estrogen receptor targetting construct, a GD2 targetting construct, etc. So you mix and match depending on the molecular profile of your cancer.
Moditope works slightly differently (I'm running out of space so will continue on a seperate post.)
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