I should note that not all cancer cells exhibit KRAS mutations, so if this ARS1620 can get cancer cells to express more KRAS mutations (if biopsy shows KRAS mutations exist), now we have something to target.
Reminds me of other therapies that need some type of expression on the cancer cells to enhance inhibotrs, like using the cowpea mosaic virus, TROP2, PIK3 expressions. I think this is where immunotherapy is going next, to take an expression, force cells to over express it (specific mutations that healthy cells rarely have), then bind inhibitors to target the cell for apoptosis.
If someone has a lung tumor and the immune system is coaxed into killing/eating the cancerous cells, what happens after that? Is the lung able to fill in the gap with new healthy cells, or can the patient end up with a big hole in their lung?
I would suppose that maybe it turns into scar tissue of some sort, with maybe some regeneration of healthy lung cells? Maybe stem cells could be part of the post-treatment options after this type of procedure?
Many researchers have tried for many years to find a drug for cancer, but I believe no one has succeeded. They treat only early-stage cancer patients who are surviving, but many patients who are not diagnosed in the early stages are not surviving. I hope this is useful for all patients at all stages. Thank you, God and researchers.
Stopping the metastatic surge cancer cells undergo, forming new tumor micro-environments (TME, angiogenesis), are probably the main areas research should focus on to radically boost long-term survival. We need to move cancer from a fatal condition to a chronic condition.
We're sloooowly getting there with antibody drug conjugates like pembrolizumab (https://en.wikipedia.org/wiki/Pembrolizumab), but what truly causes metastatic spread (epithelial–mesenchymal transition) is still a mystery!
I know of at least one patient for stage 4 metastatic melanoma who's been in complete remission for several months on a cocktail of two different immunotherapies. Neither "stage 4" nor "metastatic" suggest early stages.
I should note that not all cancer cells exhibit KRAS mutations, so if this ARS1620 can get cancer cells to express more KRAS mutations (if biopsy shows KRAS mutations exist), now we have something to target.
Reminds me of other therapies that need some type of expression on the cancer cells to enhance inhibotrs, like using the cowpea mosaic virus, TROP2, PIK3 expressions. I think this is where immunotherapy is going next, to take an expression, force cells to over express it (specific mutations that healthy cells rarely have), then bind inhibitors to target the cell for apoptosis.
https://ucsdnews.ucsd.edu/pressrelease/researchers-shed-ligh...
https://en.wikipedia.org/wiki/Phosphoinositide_3-kinase_inhi...