Because it has been commented over and over "oh, type 2 is because you are overweight"...
> We tend to think of type 2 diabetes as a disease that afflicts people who are overweight. But it can also appear in people with perfectly healthy weights—and be more deadly in them. A study published today in the Journal of the American Medical Association indicates that normal-weight people diagnosed with type 2 diabetes have double the risk of dying from heart disease and other causes than overweight people with diabetes.
(Yes, I know this post is about Type 1... but _all_ of the talk in it when I posted this was about Type 2; and basically blaming the people with it for their condition)
This is very encouraging, but will take a long time to get to any type of usable treatment because these cells are literally made to evade the immune system they run a whole bunch of other risks. Also cell therapies right now are one of the weakest markets in Biotechs due to the level of costs to develop. This is slightly different since it's Allogenic, but the market seems not very invested in cell therapy.
> This is very encouraging, but will take a long time to get to any type of usable treatment because these cells are literally made to evade the immune system they run a whole bunch of other risks. Also cell therapies right now are one of the weakest markets in Biotechs due to the level of costs to develop. This is slightly different since it's Allogenic, but the market seems not very invested in cell therapy.
If we're controlling the cells' genomes (which we are), we can add any sort of killswitch (see another comment https://news.ycombinator.com/item?id=45220068 ) that we would like, and this would function better than relying on host immune surveillance. The opposite could be done, making insulin release dependent on the presence of a harmless drug, e.g., insulin release can only happen if a designer steroid molecule is present in the blood.
There are already cell therapies that envisage permanent implantation of modified cells, so I am not sure why a long delay for 'any type of usable treatment' would occur. The structure of this need not be analogous to a stem cell transplant; you could imagine injecting new cells intramuscularly every few months.
The costs to develop this are incurred during development (unlike the autologous therapies that require extensive, expert-level analysis for each new patient). I'm not sure that we can compare the current levels of investment in autologous gene editing to this product.
This is great news. Any type of pancreatic function restoration is also potentially good for Type 1.5 (which constitute a sizable chunk of misdiagnosed T2Ds) where the body attacks more slowly (over the course of years) instead of acutely like traditional T1D and so doctors assume it's insulin resistance instead of pancreatic function decline since they both present with the same symptom - hyperglycemia.
This study's pretty wild -- but this approach has a major downside that they only mentioned in passing in the actual report in the New England Journal of Medicine (paywalled, unfortunately).
To gene-edit these cells, they had to use a lentivirus vector -- a (limited form of a) class of viruses that notably includes HIV. These viral vectors work by splicing themselves into random places in the host cell's DNA. Which is fine, except that there's a non-zero chance that in the process, the virus will initiate a cancer.
When you combine that with a cell deliberately engineered to hide from the immune system, you have the ticket to a very bad time.
> Although the research marks a milestone in the search for treatments of type 1 diabetes, it’s important to note that the study involved one one participant, who received a low dose of cells for a short period—not enough for the patient to no longer need to control their blood sugar with injected insulin. An editorial by the journal Nature also says that some independent research groups have failed in their efforts to confirm that Sana’s method provides edited cells with the ability to evade the immune system.
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[ 2.8 ms ] story [ 38.0 ms ] thread> We tend to think of type 2 diabetes as a disease that afflicts people who are overweight. But it can also appear in people with perfectly healthy weights—and be more deadly in them. A study published today in the Journal of the American Medical Association indicates that normal-weight people diagnosed with type 2 diabetes have double the risk of dying from heart disease and other causes than overweight people with diabetes.
- https://www.health.harvard.edu/blog/diabetes-can-strike-hard...
(Yes, I know this post is about Type 1... but _all_ of the talk in it when I posted this was about Type 2; and basically blaming the people with it for their condition)
If we're controlling the cells' genomes (which we are), we can add any sort of killswitch (see another comment https://news.ycombinator.com/item?id=45220068 ) that we would like, and this would function better than relying on host immune surveillance. The opposite could be done, making insulin release dependent on the presence of a harmless drug, e.g., insulin release can only happen if a designer steroid molecule is present in the blood.
There are already cell therapies that envisage permanent implantation of modified cells, so I am not sure why a long delay for 'any type of usable treatment' would occur. The structure of this need not be analogous to a stem cell transplant; you could imagine injecting new cells intramuscularly every few months.
The costs to develop this are incurred during development (unlike the autologous therapies that require extensive, expert-level analysis for each new patient). I'm not sure that we can compare the current levels of investment in autologous gene editing to this product.
To gene-edit these cells, they had to use a lentivirus vector -- a (limited form of a) class of viruses that notably includes HIV. These viral vectors work by splicing themselves into random places in the host cell's DNA. Which is fine, except that there's a non-zero chance that in the process, the virus will initiate a cancer.
When you combine that with a cell deliberately engineered to hide from the immune system, you have the ticket to a very bad time.
> Although the research marks a milestone in the search for treatments of type 1 diabetes, it’s important to note that the study involved one one participant, who received a low dose of cells for a short period—not enough for the patient to no longer need to control their blood sugar with injected insulin. An editorial by the journal Nature also says that some independent research groups have failed in their efforts to confirm that Sana’s method provides edited cells with the ability to evade the immune system.