4 ms·

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 appro

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
What we really need is to look at is elephants and bowhead whales in detail. These animals have a large number of extra anti-oncogene systems that prevent them getting cancer despite their large size and long life span.
nonbel 9y ago
>"there is no shortage of possibilities for people who want to kill all cancer." Your posts in this thread make me think you have a different view of what is going on regarding aging and cancer than I do... As mentioned below, it seems that after each division more and more "genetic errors and other junk" accumulate in tissue stem cells. After a certain number of these divisions the stem cell needs to stop replenishing the tissue because the risk of generating a cancer cell is too high. Thus the turnover of terminal cells must slow and eventually stop as each tissue stem cell becomes "exhausted". So the options upon exhaustion (of safe divisions) of the stem cells are either: 1) Continue replenishing the tissue at a high risk of cancer. Even the non-tumorgenic new terminal cells are also becoming less and less functional due to the accumulated erros/junk. - high cancer risk, slow organ failure 2) Stop replenishing the tissue and let whatever cells are there survive as long as possible (these are the senescent cells). - low cancer risk, slow/intermediate rate organ failure 3) Stop replenishing the tissue and remove the senescent cells, replacing the space with connective tissue. In this case the tissue will become less and less functional eventually leading to organ failure. - low cancer risk, fast organ failure All of your ideas proposed here seem to be #1 or #3. Nature's solution is #2, and probably for good reason. Also, obviously the ultimate solution needs to be either reducing the number of cell divisions or the rate of junk/error accumulation per division. This all seems to follow very easily from the premise that errors/junk accumulate after each division, so I would be interested to know what you are reading that makes you think it is incorrect.
- danieltillett 9y ago
  The other solution is as suggested which is increase the robustness of the anti-oncogene systems. This way the stem cells will still accumulate mutations (hard to solve this problem), but they won’t progress to cancer. This approach is how evolution has solved the problem of cancer in large animals with long lifespans.

danieltillett 9y ago

What we really need is to look at is elephants and bowhead whales in detail. These animals have a large number of extra anti-oncogene systems that prevent them getting cancer despite their large size and long life span.

nonbel 9y ago

>"there is no shortage of possibilities for people who want to kill all cancer." Your posts in this thread make me think you have a different view of what is going on regarding aging and cancer than I do... As mentioned below, it seems that after each division more and more "genetic errors and other junk" accumulate in tissue stem cells. After a certain number of these divisions the stem cell needs to stop replenishing the tissue because the risk of generating a cancer cell is too high. Thus the turnover of terminal cells must slow and eventually stop as each tissue stem cell becomes "exhausted". So the options upon exhaustion (of safe divisions) of the stem cells are either: 1) Continue replenishing the tissue at a high risk of cancer. Even the non-tumorgenic new terminal cells are also becoming less and less functional due to the accumulated erros/junk. - high cancer risk, slow organ failure 2) Stop replenishing the tissue and let whatever cells are there survive as long as possible (these are the senescent cells). - low cancer risk, slow/intermediate rate organ failure 3) Stop replenishing the tissue and remove the senescent cells, replacing the space with connective tissue. In this case the tissue will become less and less functional eventually leading to organ failure. - low cancer risk, fast organ failure All of your ideas proposed here seem to be #1 or #3. Nature's solution is #2, and probably for good reason. Also, obviously the ultimate solution needs to be either reducing the number of cell divisions or the rate of junk/error accumulation per division. This all seems to follow very easily from the premise that errors/junk accumulate after each division, so I would be interested to know what you are reading that makes you think it is incorrect.

danieltillett 9y ago
The other solution is as suggested which is increase the robustness of the anti-oncogene systems. This way the stem cells will still accumulate mutations (hard to solve this problem), but they won’t progress to cancer. This approach is how evolution has solved the problem of cancer in large animals with long lifespans.