Indeed, in gametes (sperm and egg cells) the cells use enzymes that rebuild telomeres.
Telomeres "shorten" when DNA is copied for cell replication; the benefit of this is that it means telomeres quickly whittle down to nothing, and kill the resulting cells, when a rogue cell line has started replicating an unnecessary number of times- e.g., in cancer.
However, people die of cancer (especially if untreated...)
So does this mean that without this shortening of the telomeres, the incidence of cancer would be much larger? That the cancers that actually manifest are a small fraction of the potential cancers aborted by this defense mechanism?
Absolutely. You have 'rogue' cells that go on independent replication programs all the time. But there are a few checkpoints which are no-go if a cell passes them - they are immediately forced to die. These include, short telomeres, lack of proper DNA repair, and ability to respond to induced-suicide signals. In order for an otherwise 'cancerous' cells to be a problem, it really has to have developed processes that ignore ALL of these (few) checkpoints. The chance that the particular mutation in that cell includes a mutation to overcome ALL of those hurdles simultaneously in a single cell is the chance you develop (a harmful) cancer. A change to nearly any other gene will cause one of those checkpoints to kick in and force the cell to die.
The DNA damage checkpoint is interesting all the way through public health policy in 2 cases: 1) The BRCA gene is a DNA repair protein. Women with a mutated brca gene are missing one of those 3 checkpoints. 2) HPV (for which we have a complete vaccine) is of a type of virus that is generally destroyed by your DNA-repair machinery. However HPV, being evolutionary wily, has a specific mechanism to shut down your own DNA repair machinery that would otherwise catch the foreign invader. Hence, HPV 'causes cancer' by deliberately disabling one of those checkpoints.
I can't name the research on this topic off of the top of my head, but yes to both questions. Cancer is a common occurence in all mammals and we have evolved many self defense mechanisms, including telomeres, to fight it as animals started living longer and longer. One of the most promising areas of oncology research is immunotherapy, for example, which guides your immune system to attack cancer cells that havent been recognized as targets.
Indeed- and there's many other, separate defence mechanisms that also quash cancers before they become a problem. If a tumour has grown enough to threaten, it has evolved workarounds to at least several of these.
"I think that before we have immortality, we need to understand and cure cancer."
I'd be happy with toenail fungus. Or mild eczema. Or, really, any medical condition whatsoever.
You realize people are still arguing over why your joints make a "pop" sound when you crack them, right ? Like, they've sort of settled on the air bubbles rapidly escaping the joint, but ... there's still a debate.
I assume that this is far from unique to humans, but not quite universal. I wonder whether the "immortal jellyfish" turritopsis dohrnii has some telomere rebuilding mechanism for all cells that provide its age-defying abilities.
I also wonder whether there is a second advantage to telomere depletion; reducing the instances of organisms from different generations carrying the same genes competing for resources. After all, we're here for the benefit of our genes, not the other way round.
Some scientists consider ageing to be a disease. They're trying to rebuild telomere length to keep us young, so this sounds like a step towards that goal.
That's probably exactly what the article was talking about- though its very short on details, aside from that the treatment was a form of "gene therapy." But my guess would be that the therapy involved the addition of a gene for this very enzyme (telomerase) in a form that it would become active in adult somatic cells.
Of course whether this would actually meaningfully extend life is uncertain- aging is complicated.
Telomeres "shorten" when DNA is copied for cell replication; the benefit of this is that it means telomeres quickly whittle down to nothing, and kill the resulting cells, when a rogue cell line has started replicating an unnecessary number of times- e.g., in cancer.