4 ms·

All of these approaches are going to run into the reason why ageing is happening in the first place - to prevent cancer. Ageing is one of the original anti-onco

All of these approaches are going to run into the reason why ageing is happening in the first place - to prevent cancer. Ageing is one of the original anti-oncogenic systems and anything that messes with the rate of aging without doing something about cancer is doomed to failure. Interesting there are some human mutations that slow down the ageing rate [1]. These all cause an increased cancer rate, but if you manage to make it to old age you are physiologically much younger (20-30 years in the case of the Brazilian p53 mutation). 1. https://www.ncbi.nlm.nih.gov/pubmed/27663983 https://www.ncbi.nlm.nih.gov/pubmed/27663983

touringcomplete 9y ago
Exercise, sleep, socializing, sex, reducing stress and a carefully constructed diet clearly messes with the rate of aging. How would those be doomed? Also, perhaps the target and antitarget pathways of each could be isolated and modulated for maximum benefit?
nonbel 9y ago
>"if you manage to make it to old age you are physiologically much younger (20-30 years in the case of the Brazilian p53 mutation)." That sounds interesting, but I can't find it. Can you quote the part of that paper you are talking about?
- danieltillett 9y ago
  Have a look at this NIH talk [1]. 1. https://youtu.be/URKJ7LLXc3E https://youtu.be/URKJ7LLXc3E
  - nonbel 9y ago
    Are you saying that info was not in your original source? I'm not willing to spend 15 minutes watching a video to possibly get this info. I have low hopes since the speaker probably cannot cite their source in that format. Can you tell me what minute of the video I should watch?
    - danieltillett 9y ago
      The reference I provided was to the mutation, not the anti-ageing phenotype. The speaker is one of the PI’s on the project so it is worth watching the whole thing. I can’t find the paper again where the delayed ageing is mentioned, but the speaker does talk about it - far more offhand than it should be for my liking. It is pretty easy to ff through a scientific talk because of the slides, but if you are just interested in the Brazilian mutation then start from around 6 minutes.
reasonattlm 9y ago
Which is why the SENS portfolio includes a universal cure for cancer. This is not as hard as people have been made to think it is. The present mainstream approach of the past few decades is just not a good one. It is picking strategies that are very expensive to implement, and that attack vulnerabilities that are peculiar to tiny subtypes of cancer. There are hundreds of subtypes of cancer, most of which are cheerfully capable of evolving their way around many of the existing attacks on their biochemical vulnerabilities. There are only so many scientists, only so much funding. If it takes twenty man-years to produce a therapy to tackle transient vulnerability A in subtype 1 of 1000, we'll never see the end of it. Yet this is largely what is happening. What should be happening instead is the whole-hearted pursuit of vulnerabilities that are common to many, many types of cancer, or all cancers for preference. There is one very good one, which is that cancers must lengthen their telomeres, and there are only two ways for that to happen, neither of which should really be operating in somatic cells. So block telomerase, block ALT, and get that hooked up to some kind of cancer-cell-targeting-mechanism of the sort that has been under development for the past decade, and that will work to kill any cancer. A number of high profile groups are working on telomerase sabotage ( https://www.eurekalert.org/pub_releases/2015-01/usmc-rtt123114.php https://www.eurekalert.org/pub_releases/2015-01/usmc-rtt1231... ), and the SENS Research Foundation has been funding the necessary research to address ALT ( http://www.sens.org/research/introduction-to-sens-research/cancerous-cells http://www.sens.org/research/introduction-to-sens-research/c... ), still at comparatively early stages. There are other, prospective targets. The comparative biology crowd is reverse engineering naked mole rats to figure out what it is that makes them next to immune to cancer. There are a few leads there; p21, ARF, hyaluronan, alpha2-macroglobulin, etc. Another recent discovery relates to re-engaging the limitation on processing nutrients; apparently all cells have a food limiter, and all cancers abuse that limiter in order to enable rampant replication. Re-enable the limiter and cancers wither: https://www.salk.edu/news-release/salk-scientists-curb-growth-cancer-cells-blocking-access-key-nutrients/ https://www.salk.edu/news-release/salk-scientists-curb-growt... So there is no shortage of possibilities for people who want to kill all cancer. There is no excuse for continuing the wasteful business as usual of the past decades. This is an age of revolutionary progress in biotechnology - we should act like it and aim high.
- danieltillett 9y ago

touringcomplete 9y ago

Exercise, sleep, socializing, sex, reducing stress and a carefully constructed diet clearly messes with the rate of aging. How would those be doomed? Also, perhaps the target and antitarget pathways of each could be isolated and modulated for maximum benefit?

nonbel 9y ago

>"if you manage to make it to old age you are physiologically much younger (20-30 years in the case of the Brazilian p53 mutation)." That sounds interesting, but I can't find it. Can you quote the part of that paper you are talking about?

danieltillett 9y ago
Have a look at this NIH talk [1]. 1. https://youtu.be/URKJ7LLXc3E https://youtu.be/URKJ7LLXc3E
- nonbel 9y ago
  Are you saying that info was not in your original source? I'm not willing to spend 15 minutes watching a video to possibly get this info. I have low hopes since the speaker probably cannot cite their source in that format. Can you tell me what minute of the video I should watch?
  - danieltillett 9y ago
    The reference I provided was to the mutation, not the anti-ageing phenotype. The speaker is one of the PI’s on the project so it is worth watching the whole thing. I can’t find the paper again where the delayed ageing is mentioned, but the speaker does talk about it - far more offhand than it should be for my liking. It is pretty easy to ff through a scientific talk because of the slides, but if you are just interested in the Brazilian mutation then start from around 6 minutes.

reasonattlm 9y ago

Which is why the SENS portfolio includes a universal cure for cancer. This is not as hard as people have been made to think it is. The present mainstream approach of the past few decades is just not a good one. It is picking strategies that are very expensive to implement, and that attack vulnerabilities that are peculiar to tiny subtypes of cancer. There are hundreds of subtypes of cancer, most of which are cheerfully capable of evolving their way around many of the existing attacks on their biochemical vulnerabilities. There are only so many scientists, only so much funding. If it takes twenty man-years to produce a therapy to tackle transient vulnerability A in subtype 1 of 1000, we'll never see the end of it. Yet this is largely what is happening. What should be happening instead is the whole-hearted pursuit of vulnerabilities that are common to many, many types of cancer, or all cancers for preference. There is one very good one, which is that cancers must lengthen their telomeres, and there are only two ways for that to happen, neither of which should really be operating in somatic cells. So block telomerase, block ALT, and get that hooked up to some kind of cancer-cell-targeting-mechanism of the sort that has been under development for the past decade, and that will work to kill any cancer. A number of high profile groups are working on telomerase sabotage ( https://www.eurekalert.org/pub_releases/2015-01/usmc-rtt123114.php https://www.eurekalert.org/pub_releases/2015-01/usmc-rtt1231... ), and the SENS Research Foundation has been funding the necessary research to address ALT ( http://www.sens.org/research/introduction-to-sens-research/cancerous-cells http://www.sens.org/research/introduction-to-sens-research/c... ), still at comparatively early stages. There are other, prospective targets. The comparative biology crowd is reverse engineering naked mole rats to figure out what it is that makes them next to immune to cancer. There are a few leads there; p21, ARF, hyaluronan, alpha2-macroglobulin, etc. Another recent discovery relates to re-engaging the limitation on processing nutrients; apparently all cells have a food limiter, and all cancers abuse that limiter in order to enable rampant replication. Re-enable the limiter and cancers wither: https://www.salk.edu/news-release/salk-scientists-curb-growth-cancer-cells-blocking-access-key-nutrients/ https://www.salk.edu/news-release/salk-scientists-curb-growt... So there is no shortage of possibilities for people who want to kill all cancer. There is no excuse for continuing the wasteful business as usual of the past decades. This is an age of revolutionary progress in biotechnology - we should act like it and aim high.

danieltillett 9y ago