Talk:The Resilience Project

Merit of the project
What I don't get with this project is what the merit is. With people that carry a mutation on a gene that is known to cause a genetic disorder, it looks for mutations on other genes that prevent this first gene's mutation of developing into a severe disease (which causes the carrier harm in real life).

However, treating people that have this gene that is known to cause a genetic disorder using gene therapy (by hence simply overwriting the genetic code of this faulty gene with good code) would -as I understand it- already cause the disease to be eliminated. So why not do this instead of looking for a mutation on another gene to avoid this first gene of expressing itself ?

The only reason I could think of is that fixing this primary faulty gene would not solve the problem with the current person (and it would only make sure that the gene isn't passed on to later generations and cause problems with people in later generations -ie if the gene is used by the body only to build up tissue that hasn't yet been created-). So, otherwise put, having this gene correct or not would matter only for children that are still in growth, but would not matter for adults which already have a fullgrown body.

Finding and modifying a different gene could then still work for the adults, and so would give this project make sense.

Can someone look into this. If correct, it would be something we would need to mention on a wikipedia page somewhere.

KVDP (talk) 07:55, 24 June 2017 (UTC)


 * Found some clues for this --> see The the section of Stephen Friend I'll add in the article.

Sclerosteosis
Weird that this hasn't been added to their list. See Talk:Sclerosteosis KVDP (talk) 12:50, 25 June 2017 (UTC)

Proposed deletion
I deleted User:DGG's proposed deletion tag as per Proposed deletion. DGG felt that this article was non-notable.

My arguments are that: KVDP (talk) 17:42, 26 June 2017 (UTC)
 * I did some improvements on the page as requested by DGG, hereby also describing the reason why TRP used a workaround method rather than fixing the gene head on. (Initially, I didn't get this either, but I then found some articles about this as I improved the page later)
 * Industry leaders in this field, like Icahn Institute for Genomics at Mount Sinai, Sage Bionetworks, 23andMe, Beijing Genomics Institute, Broad Institute were behind the project, so calling it non-notable felt weird for me, even when I didn't yet understand why they used a workaround method.

Similar projects that used hospital data
The biggest problem this project seems to have is the source of its data. This comes from the general public, of which many hence don't have any gene that causes one of the 170 diseases. Aren't there any projects around that do this smarter ? For instance, in a family where there are several people known to have a specific (hereditary) disease, there may be people in this family that don't have this disease (but which are likely to still carry the faulty gene). The genetic code between relatives will also have less variations (than genetic code between 2 people not related to each other), so it would be much, much easier to find any mutations in a different gene that would cause the primary gene of not expressing itself. This way, there's less need of supercomputers to calculate this all out either. This data could be attained via hospitals, since they would already be treating people with the genetic diseases. People in the family that don't have the disease but are likely to still have the faulty gene and a mutation on a different gene avoiding it of expressing itself, could be contacted via the families -found via the hospitals/hospital data-. KVDP (talk) 18:35, 26 June 2017 (UTC)