I don’t get why is possible to regrow a lot of stuff (skin, muscles, broken bones etc.), but only to a certain extend. At one moment you are suddenly not able to rebuild things.

Why is that and what determines what we can regrow?

  • Shou@lemmy.world
    1·
    22 hours ago

    This is not true.

    It’s not about cancer, it’s about senescence. Mammals’ and many other animals’ only way to adapt to an ever changing enviroment, is: remix genes + mutations + epigenetic factors. And hope for the best.

    In order for parents to not compete with their offspring for food or sex, they have to die. Which can simply be a limited lifespan by cells getting sloppy in their maintenance, or by choosing to starve yourself to death.

    If you get injured badly, you have failed to survive. It is more energy and evolutionarily speaking to let you die, than expend energy on your recovery. Energy is limited in every enviroment. Depression and lethargy are interesting aspects to self-elimination (not suicide) as well.

    Senesence is also why cancer is far more common in older people than in children. Our repair functions stop doing their job well as part of senescence. Increasing the chance and speeding up the development of tumors.

    • deranger@sh.itjust.works
      2·
      21 hours ago

      Our repair functions stop doing their job well as part of senescence. Increasing the chance and speeding up the development of tumors.

      Those repair functions working better than normal is one of the hallmark signs of cancer, specifically telomerase being reactivated. Senescence is anti cancer, not pro cancer. You know those HeLa cells that are immortal? Cancer cells. Having a time limit or replication limit on cells through senescence is a great way of limiting tumors.

      The two barriers to proliferation—senescence and crisis/apoptosis—have been rationalized as crucial anticancer defenses that are hard-wired into our cells, being deployed to impede the outgrowth of clones of preneoplastic and frankly neoplastic cells. According to this thinking, most incipient neoplasias exhaust their endowment of replicative doublings and are stopped in their tracks by one or the other of these barriers. The eventual immortalization of rare variant cells that proceed to form tumors has been attributed to their ability to maintain telomeric DNA at lengths sufficient to avoid triggering senescence or apoptosis, achieved most commonly by upregulating expression of telomerase or, less frequently, via an alternative recombination-based telomere maintenance mechanism. Hence, telomere shortening has come to be viewed as a clocking device that determines the limited replicative potential of normal cells and thus one that must be overcome by cancer cells.

      https://www.cell.com/cell/fulltext/S0092-8674(11)00127-9