Telomerase does Not Cause Cancer

I am one of a growing minority of life extension scientists who believe that telomerase may be our most promising, near-term path to a major boost in the human life span.  Notably, almost all the scientists who specialize in telomere biology have come to this opinion (e.g., Andrews, Blasco, de Pinho, Fossel, Harley, West, Wright).  But research investment in this strategy has been limited and the main obstacle has been fear of cancer.  Back in 1990, a young Carol Greider was the first to float the idea that the reason that man and most other mammals have evolved with short telomeres is to help protect against cancer.   Independently in 1991, senior geneticist Ruth Sager proposed the same hypothesis with more detail, citing circumstantial evidence.  Inference of evolutionary purpose is of necessity indirect.

The idea that lengthening telomeres poses a danger of cancer took a life of its own, based on marginal experimental data and firm grounding in a theory that is fundamentally flawed.  It is now taken for granted in publications, and only token documentation and no reasoning is provided when this view is asserted.  (e.g., “The senescence response is widely recognized as a potent tumor suppressive mechanism.” [ref])  I believe that this concern is misplaced, that activating telomerase will actually reduce net cancer risk, and that the fear of cancer is damping the enthusiasm that telomere science so richly deserves.  I have written a technical article on this subject, and in this and next week’s columns, I’ll take the opportunity to summarize the situation as I see it.

Relationship of Telomerase to Cancer

There are forces at work here in opposite directions:

(Bad #1) Once a cell becomes cancerous, it can only continue to grow if it has telomerase. So giving the cell telomerase removes one barrier to malignancy.
(Bad #2) Secondary to its role in growing telomeres, the telomerase component hTERT also functions as a kind of growth hormone, that can promote malignancy.

(Good #1) The body’s primary defense against cancer is the immune system. As we get older, our blood stem cells slow down because their telomeres are too short. Telomerase rejuvenates the immune system, and helps the body fight cancer before it gets started.
(Good #2) When telomeres in a cell get too short, the cell goes into a “senescent” state, in which it spits out hormones (called “cytokines”) that raise inflammation throughout the body and damage cells nearby. Telomerase protects against this.
(Good #3) When telomeres in a cell get too short, the cell’s chromosomes can become fragmented and unstable, and this can lead to cancer. Telomerase protects against this.

I believe that the three “goods” far outweigh the risk from the two “bads”. In animal experiments this seems to be the case, and I think that the “theoretical” reasons for concern are based on discredited theory. Of course, we won’t know for sure until we have more experience with humans.

The topic is timely, as last week a Danish study appeared in the Journal of the National Cancer Inst, tracking a huge population for the first time, and relating their telomere length to their mortality risk. Because of its size, this study gave a sound foundation to the thesis that longer telomeres portend a longer life.

Background

In the late 1980s, the story of cellular senescence took shape:  The gradual loss of viability that comes from multiple cell replications (the Hayflick Limit) was explained by shortening telomeres.  The process was reset by an enzyme, telomerase, first reported in a paper by Blackburn and Greider, the importance of which the Nobel Prize committee took 25 years to recognize.

Every eukaryotic cell knows how to make telomerase—it’s an ancient and ubiquitous piece of the genome.  (It has to be as old as DNA replication, because without telomerase, DNA can’t be copied for long.)  It was natural to ask the question:  with the remedy so widely and easily available, why should cells ever have to become senescent?  Why isn’t the telomere maintained with application of a little telomerase every time the cell divides?

Withholding telomerase looked like a kind of programmed death, and standard evolutionary theory said that programmed death is impossible.  “More survival, more reproduction” was the standard definition of Darwin’s fitness, and programmed death was just the opposite.  How could programmed death be, in some way, pro-life?

The answer that seemed obvious was:  death of cancer cells = life of the animal.  Maybe cellular senescence was permitted to occur as part of a protection against cancer.  It was known that cancer cells do not senesce; they can go on reproducing forever.  So cancer cells must have learned how to unlock telomerase.  Later, different human cancers were surveyed, and it was confirmed that well over 80% express telomerase.

Normal cells go through many transformations in order to become malignant.  One of these is to unlock telomerase.  Perhaps telomerase is the bottleneck, and the lockdown of telomerase helps to protect us from cells that otherwise might go rogue and turn into cancers.

This explanation was consistent with the standard evolutionary theory, but it was a very human-centric answer.  It was soon learned that cells senesce for want of telomerase in all kinds of animals, including those that don’t get cancer at all.  This might have been an early warning that the simple answer was not the whole story.  Even some protozoa withhold telomerase and suffer cellular senescence (ciliates). The very notion of cancer does not apply to single-celled protozoa.

The truth is that telomere attrition is an ancient mode of programmed death.  It functions that way in protozoans, and it functions that way in mammals.  Evolutionary theorists are going to have to expand the simplistic, one-gene-at-a-time theory about how natural selection works.

 

What really causes cancer?

It’s true that acquiring telomerase is one necessary step in the progression from a normal cell to a cancer cell.  But this only really matters if it is the rate-limiting step.

In every multi-step process, there are fast and slow steps, and the rate of the process as a whole is controlled entirely by the rate of the slowest step.  Adding telomerase capacity to a cell will only cause the cell to progress toward cancer more rapidly if telomerase was the slowest step, the rate-limiting step.  The best evidence we have is that some other step is rate-limiting, because in practice, adding telomerase does not seem to increase cancer risk.  Already in 1999, a study from the UTexas lab of Woody Wright and Jerry Shay demonstrated that

(What is the rate-limiting step?  My money is on evasion of the immune system.  I believe that of the trillions of cells in our bodies, a few become malignant every day, and that the immune system is constantly looking out for cancers and nipping them in the bud.)

 

Limited evidence for the hypothesis

Some studies in mice have found an increase in cancer incidence when telomerase was overexpressed. Female mice with extra (transgenic) copies of the telomerase gene developed breast tumors, while control mice had cancers in other organs, but not breast [ref].  Transgenic telomerase targeted to thymocytes (stem cells of the thymus) resulted in an increased incidence of T-cell lymphoma [ref].  Similarly, telomerase overexpression in skin stem cells increased the rate of skin cancer [ref].  In a mouse model genetically engineered to be prone to endocrine cancers, disabling telomerase dramatically reduced the frequency of tumor formation [ref].

All authors of the mouse studies note a puzzling aspect of their results: telomerase is already abundantly expressed in mice, and telomeres are never critically short.  According to the standard hypothesis, telomerase rationing should serve the body by halting tumors when they reach a size determined by beginning telomere length.  Any association of telomerase with initiation of cancer must be by a different mechanism, not yet understood.

Lab mice are not among the species whose life spans are limited by telomere attrition, so the evolutionary theory about telomerase rationing ought not to apply to them at all.  These results are interesting, and suggestive that telomerase plays other roles in metabolism, perhaps as a growth promoter; but results in mice cannot be cited as evidence for the standard hypothesis that applies to humans, dogs, horses, etc, (but not to mice).

A surprising line of research has indicated that telomerase has other functions besides maintaining telomeres.  A telomerase component called TERT can act like a growth hormone [ref, ref, ref], and in fact, all the credible pro-cancer activity of telomerase comes from the hormonal activity of TERT, and not from “immortalization” via telomere extension.

 

Cellular senescence is toxic

When human cells become senescent, usually because their telomeres have eroded with too many replications, they do not simply languish and die (like senescent protozoans).  Instead, they become toxic and send powerful signals out into the body that promote inflammation and further increase cell senescence.  This is called SASP, for Senescence-Associated Secretory Phenotype.  Not to mince words, the cells become toxic monsters that have a powerful pro-aging effect.  Van Deusen has shown that life span of mice can be extended 25% just by inducing senescent cells to die [ref].

There is no metabolic logic behind this toxicity, so I think it is probable that it is an evolutionary adaptation, and it must be seen as a pro-death adaptation.  I cite this as evidence that the reason for cell senescence in mammals is the same as the reason for cell senescence in protozoans:  it is an evolved mode of regulated life span.

Once you realize this, it resolves the paradox that led to Greider and Sager’s hypothesis in the first place.  They had been thinking within a limited evolutionary model in which evolution of programmed death has no place.  The inertia of that model continues to be the driving force behind the idea that “there can be no free lunch”, that evolution has already done her best to maximize human life span, and that we tinker with her choices at our peril.  If we are willing to discard that model, then a lot of the “big picture” in evolution starts to fall into place, including adaptations that favor the community at the expense of the individual, and programmed death in particular.

And the possibility opens up that lengthening telomeres may indeed be a “free lunch”.

 

Animal experiments in which life span was increased with telomerase

Lab worms would be the last place you’d expect telomere length to effect life extension.  This is because adult worms are endowed with a set of cells that last them through their short lifetimes of 15-20 days.  There is no cell replacement in adult worms, hence no telomere shortening, hence no cellular senescence, nothing for telomerase to do.  So it was quite a surprise in 2004 when a Korean study showed, using not telomerase but a different means of lengthening telomeres, that life span was extended 19%.

Using a cancer-resistant strain of mice in a 2008 study, Maria Blasco’s Madrid laboratory was able to extend life span of mice by 40% by adding an extra copy of the telomerase gene.  Again, this is surprising because it was thought that mice already have plenty of telomerase, and that their telomeres never shortened to a critical level during a lifetime.

An updated study from the same group showed that their care in using cancer-resistant mice was unnecessary.  Introducing an extra telomerase gene increased life span in normal mice as well, and cancer rates did not go up.  Blasco expresses her enthusiasm for the potential of telomerase therapy in this article.  She writes explicitly about the relationship between cancer and telomerase here, in an article that has been a source for my own views.

In a 2011 study from the Harvard laboratory of Ronald dePinho, mice were deprived of their usual abundance of telomerase by knocking out the telomerase gene.  The mice were followed until they experienced dramatic age-associated deterioration, including muscle atrophy, brain atrophy, and cognitive impairment.  Restoring telomerase, they found that both muscle and brain tissues were remarkably rebuilt, not merely preserved.

 

A New Survey of Telomere Length and Mortality

Last week, a Danish study was published that tracked 65,000 people over 15 years.  The bottom line was that telomere length robustly predicts longevity, even after factoring out the effect of age, smoking, exercise, blood cholesterol, BMI, and alcohol consumption. People with the longest telomeres had the lowest cancer rates.  This is a rich new source of statistical inferences, and  I’ll write a full column on the study next week.

35 thoughts on “Telomerase does Not Cause Cancer

  1. Do notice that the study you quoted from nearly sixteen years ago showed that telomere length in peripheral blood leukocytes predicted mortality – but they, being the descendants of hematopoietic progenitor cells might not have the same telomere length as cycling cells and stem cells – which are the cells that matter.
    I hope you are right – having telomerase brought in by virus would be not all that difficult I think – its been done with mice with good results. Telomerase has many functions as you point out – including functions in the mitochondrion. Over expression of ectopic telomerase actually helped cells reduce the ROS production and made them less likely for apoptosis – but they were cancer cells. Though I’d like to see the human results. We’ll see I hope.

  2. Interesting article – thank you.

    What do you believe is the source of the mice’s 40% lifespan extension upon telomerase overexpression, if their life spans are not limited by telomere shortening?

    I’m trying to rectify this with the idea of senescent cell purging. If mice truly do express high levels of telomerase, wouldn’t this mean they have very few senescent cells? Then wouldn’t Van Deusen’s experiments have yielded little to no lifespan increase? I’m assuming the answer here is that there is another major source of senescent cells that is not related to telomere shortening. If that is the case, shouldn’t clearance of senescent cells in humans have even more of an effect than in mice?

    • Yes – I agree with your reasoning on all counts. There is something going on that we don’t understand, and I can only speculate. Maybe even though mice have plenty of long telomeres, there are a few short ones. The distribution in telomere lengths is harder to measure than the average, and it is the short ones that cause senescent cells, regardless of how long the long ones are. Or maybe telomerase has new benefits that have yet to be discovered, in addition to the pro-growth activity of TERT that I mentioned, and in addition to the basic function of telomere elongation.

      • Telomere shortage is one way cells enter Senescence but ROS damage can also cause them to shut down considerably earlier than before they reach critical length. ROS causes a DNA damage response (DDR) which can cause cell cycle arrest.

        Also Telomere length is influencing gene expression via the TPE (telomere positioning effect) so optimal length is encouraging more favourable genes and silencing ones expressed in old age(TPE – Shay et al). This is why I believe we are seeing tissue regeneration.

        I don’t know but also suspect these changes to gene expression may be changing the phenotypes of Stem Cell niches thus causing quiescent Stem Cells to return to duty thus boosting tissue regeneration. This is also seen in Parabiosis/Plasma where blood signals encourage TERT and return Stem cells to service.

        Dr Katcher linked an interesting study on GRG that confirmed that factors (in this case Hormones) do influence telomere length at least in hematopoietic cells.

        http://www.bloodjournal.org/content/114/11/2207

        It is very odd that bar this single study no one has measured telomere changes via factoral changes. It suggests to me that factors regulate Telomerase expression but as we age these factors reduce causing loss of repair mechanisms and homeostasis. On the other hand Telomeres also have a hand in regulating gene expression and ergo what factors are expressed. A bit like the chicken and the egg I think.

        We should find out shortly about TERT anyway if Bioviva go ahead with their testing in Mexico this year. I suspect it will rejuvenate as you suggest Josh.

        • Josh : (What is the rate-limiting step? My money is on evasion of the immune system. I believe that of the trillions of cells in our bodies, a few become malignant every day, and that the immune system is constantly looking out for cancers and nipping them in the bud.)

          This could be right, we get Cancers when young and the T-Cells destroy them most of the time. As we age the Thymus, Thyroid and Spleen etc… function increasingly poorly leading to a drop in the immune response. Now if we could rejuvenate these parts of the Endocrine system that could in theory mitigate the problem somewhat.

          Would Telomerase therapy in fact return these organs to efficient function and thus mitigate this?

    • That was the question that I formulated immediately as I read this article.

      Telomerase expression is the first derivative of telomere length itself.
      Telomerase expression and not telomere length might be in itself a signal to gene expression control within cells.
      Telomerase expression might turn back the epigenetic clock of the cells – the clock that is ticking even in non dividing cells.
      http://genomebiology.com/2013/14/10/R115/
      That can explain the effect in worms.
      There are many reports that hematopoietic stem cell aging and renewal is based on the epigenetic signature, for example
      http://www.bloodjournal.org/content/121/21/4257.short?sso-checked=true

      • As Dr Katcher informed me, Hematopoietic cells are definitely influenced by signals/hormones that can control telomerase:

        http://www.bloodjournal.org/content/114/11/2207

        No doubt about it the body can be Epigenetically controlled using factors, Parabiosis has shown that. The problem is working out the exact mix of factors you need to control every cell type then synthesising that mix.

        Exercise is also shown to fluctuate telomere length, likely due to the release of hormones so again there is every reason to believe the body is quite capable of producing its own factors but it choses not to as the Epigenetic program progresses and the damage builds up.

        Young blood plasma is the obvious way to do this but there is no way demand could be met by supply and working out all the factors would be the work of decades. The only possibility with young blood is IF sufficient exposure to it could “reset” the system so it resumes producing its own positive factors again via the Endocrine/Paracrine system. I believe that Telomerase would be expressed as a side effect of youthful factors as the above article eludes to.

        Only Alkahest is trying this in the human model and only to a very limited degree. Yet again the problem is funding and how broken the medical system currently is. Dr Katcher has been saying for years how factors can reprogram the body but I am yet to see any serious work being done bar the Conboys work on mice.

  3. Life has evolved to be evolvable. Go back 3 billion years and life was evolving in millions of little ponds. Life that had unlimited lifespan would keep all the old generations and use up all the food and slow down on making new offspring. Life that killed off the older generation would be making new offspring at a faster rate and therefore could evolve (optimize) faster than the rest. The most highly evolved life would eventually take over the planet. Of course the first life probably had circular DNA so when eukaryotes came along it too would evolve limited lifespan.

    If you think that having long telomeres makes you more likely to get cancer then you have to explain why old people with short telomeres get cancer way more than young people with long telomeres.

    I’m thinking that when cells go bad they get a signal to self destruct (apoptosis). If all the nearby cells have long telomeres then one of them can divide to replace the one that killed itself. If all the nearby cells have short telomeres then maybe they are signalling the bad cell to stay alive because sometimes a bad cell may be better than no cell at all. This is consistent with old people getting cancer more than young people.

  4. Hm, What a coincidence. Today I was writing for my graduation license work about the relation between cancer and aging with a special part about telomers and telomerase. I learned that cancer cells are desperate to hijack the genetic control of telomers so they can keep them in shape for their immortality quest. I was reading.also some sf aproaches like the SENS strategy to actually delete/shutdown in all the body the genes controling telomerase and ALT mechanism so future cancer cells will not have any way to become immortal. And to avoid the decline of tissues and cells to have every 10 years new stem cells introduced in our body. Doesn t this sounds a little too over the top? 🙂

    • I think that externally replenishing stem cells and progenitors with might be the only viable solution. I am somehow very reluctant to believe that fiddling the mass of trillions of aging cells all with divergent genotypes and expression profiles can lead to much results.
      Although one might not be that strict like shutting down all oncogenes.
      You might need to introduce an extra copy of p53 or fiddle a bit with the mTor complex.
      But you need to have your rejuvenated cells tested and sorted. With in situ shotgun approach (like activating hTERT by CRISPR) you get a lot of unknown quality cells transfected with hTERT leading to a million outcomes.
      In the lab you can assay your rejuvenated stem cells.
      One big problem with this approach might probably be grafting (after we have overcome the problem of reprogramming, testing and expansion of poorly differentiated cells).

      • That will not work, putting young cells into an old environment causes their function to be inhibited by the Stem Cell niche phenotype. Irina Conboy has identified this problem in her Parabiosis/Plasma studies. Basically you need to make the Stem Cell niche young otherwise new cells will not work. It seems there is little option but to tackle the niche and that probably means via systemic signals.

        As Dr Katcher has said numerous times the mix of signals is in plasma and has been shown by various studies to rejuvenate.

        • Thanks. I try to read something from Conboys tonight.
          However it might happen what they find is not true rejuvenation in the sense of turning back the epigenetic or telomere clock, but alleviating the symptoms of aging phenotype (e.g. thickening of ventricular wall).

          • See studies by Rando, Conboy, Wagers etc…

            Rejuvenation is seen and the cells appear to return to a more youthful level of function. I suspect blood factors are epigenetically re-programming histone/methylation patterns and telomeres are also likely benefitting from this too with renewed signals encouraging telomerase. It is certainly the case with at least one type of cell that expresses telomerase when hormones reach it.

            I think younger blood encourages a younger phenotype, returns stem cells to action and possibly on top of that is encouraging telomerase expression and thus telomere repair.

  5. I just wonder why these researches won’t be organized in a kind of ‘trial, then acceptance or elimination’ fashion. It is obvious that rejuvenation ideas are close to a breakthrough. The scientific community needs to consider all the viable researches like SENS, hTert therapy and studies on Cholinergic anti-inflammatory pathways. I agree with Josh on this, ideology is holding back this fight of all fights. I mean we are talking about fighting aging, and yet we do not even agree on a general plan to attain such an important goal. This will definitely keep affecting the funding for researches. Man landed on the moon, I don’t think such a feat was achieved without some kind of ‘agreed upon’ general plan of action by both the Government and the scientists involved.

  6. I’m a 75 year old blue-eyed descendent of ancestors who evolved in sun-deprived northwestern Europe. My ancestors evolved to have very little pigment in their skin. While allowing for sufficient vitamin D to be synthesized under low light levels, this characteristic of people like me allows ultraviolet light to reach and damage the chromosomes of our skin cells when we move to sunnier locales, including California where I have lived for 52 years. This genetic background leaves me unusually susceptible to skin cancer.

    I experienced the first of many basal cell carcinomas of the sun damaged skin on my face or neck at age 41. By age 71 I had experienced eight of them. In this period of 30 years the rate at which I experienced a basal cell carcinoma accelerated from once per 10 years to once per year. At the end of this period I was seeing a dermatologist every 4 months; at each visit he would discover about 5 actinic keratoses (precursors to basal cell carcinoma) and kill the cells by freezing them with liquid nitrogen. If he missed one it was liable to turn into a basal cell carcinoma and I’d be off to a surgeon once again.

    At this point I began taking the telomerase activator cycloastragenol (20 mg per day) in the hope of reversing some of the ravages of old age. Consequently, the sun damaged skin on my legs, arms, face and scalp became a laboratory in which I could watch what happened to basal cell carcinoma prone skin cells when their telomerase was activated. Would their susceptibility to evolving into basal cell carcinomas be exacerbated, as suggested by a theory then being espoused by a group of telomere biologists that included the illustrious Carol Greider?

    Within weeks I began to observe bumps on my sun damaged skin which were of a character that I had not previously seen. My dermatologist classified them as “seborrheic keratoses.” I searched on the term and found they were collections of senescent cells in G-2 arrest of their mitosis.. The number of actinic keratoses that were discovered by my dermatologist at each visit began to decline toward zero. The number of new seborrheic keratosis on my sun-damaged skin increased with time for a while then decreased toward zero.Today I have gone two years without the need for surgery to remove a basal cell carcinoma because none have been discovered.

    My seborrheic keratoses tend to live on until I have my dermatologist kill the cells with liquid nitrogen. Thus the main effect from telomerase activation has been to halt mitosis of cancer-prone cells. Through this halt on mitosis, the basal cell carcinoma that had plagued me since age 41 has been cured.

  7. The Danish study (http://jnci.oxfordjournals.org/content/107/6/djv074.full) measured: 1) telomere length sampled from blood cells, and 2) genetically determined telomere length. They found that the former was associated lower mortality (including cancer), but the latter was associated with an increased risk of cancer.

    In their discussion, they seem to argue that longer telomeres are simply a proxy for good health (as they get shorter due to various lifestyle and environmental factors). But having the genes for maintaining longer telomeres may be counterproductive, because cancer cells would proliferate as a result of being able to maintain longer telomeres.

    This seems to suggest that processes that promote telomere length may in fact promote cancer. How would you respond to this?

    • Josh is basically saying that processes that promote telomere length are less likely to give you cancer to begin with, which itself is the product of a short telomere.

      • http://www.bloodjournal.org/content/114/11/2207

        It shows that factors (in this case hormones) in fact do restore Telomeres via encouraging telomerase. This suggests to me that Telomeres shorten and are damaged by ROS etc…, gene expression changes via the TPE effect and epigenetic drift begins. This then leads to a reduction of youthful factors being transmitted which causes further telomere attrition and further dysfunction ultimately leading to the stem cells shutting down and a fall in new cell production. At least in Hematopoietic cells and likely is the case for other Stem cells.

        If longer telomeres promote youthful gene expression via TPE and the Epigenetic drift is reversed that suggests that it would not cause cancer. A number of studies have indicated cancer is not increased so its a worthy avenue to explore. The linked paper shows therapy improved telomere length without promoting Cancer suggesting efficient function may be restored if telomeres are lengthened.

  8. Pingback: SAGE Review: Game-changing discoveries in cancer and neuroinflammation | SAGE

  9. John, I really admire you for writing this blog. I am a Marine Science & Genetics student and have been studying telomerase on my own for years now. I agree with all points mentioned. Maintaining telomerase long enough = protecting the cell from mutation = no chance of developing cancerous cells. Telomerase activation in organisms without any actively developing cancerous cells will overcome the Hayflicks limit and lower the chances of dying from diseases as the immune system will be stronger. There will be other possible threats but we will achieve biological immortality. I am devoted to this study and eager to learn even more. Thank you for writing this blog.

    • Olivia do you know much about Starfish cloning and their use of Telomaris to boost Telomerase?

      It seems that the starfish born via cloning live longer compared to the ones created via sexual production. No doubt as they have longer telomeres and better gene expression.

      Is the lifespan significantly more for the clones I wonder?

  10. So – bottom line – would you recommend taking Cycloastragenol and/or Astragaloside IV and if so how much per day? Would it be best to cycle on/off?

    • The bottom line is that we’re guessing. There’s better evidence for TA65 than for other telomerase activators, but we don’t even know for sure that it’s made of cycloastragenol and astragaloside.

  11. I suspect that cytokines are senecent cells’ way of signaling “eat me” to the immune system, but with age our immune system becomes more and more ineficiente at clearing them.

  12. Based on what I am understanding from this article and other resources, I have a quick question for this audience. First, I am neither a medical or research professional, nor am I promoting any product or program. I am the son of a great dad who is in a fierce fight with cancer, and I am looking for solutions.

    It seems possible to lengthen, or at least slow down the rate of shortening, telomeres through diet, exercise and some supplements. This sounds like a great plan before cancer because your cells are stronger. However, once you have cancerous cells, is it a bad or good idea to try and lengthen telomeres through diet, exercise and supplements?

    If you do nothing to lengthen the telomeres, it seems only the cancerous cells create telomerase, remain strong and grow. The gap between the healthy cells weakening and the cancer cells developing widens. But, if you lengthen the telomeres of all your cells, malignant and benign, it looks like the healthy cells have an improved chance to fight and you at least close the gap. Wouldn’t the increased number of healthy cells gain the advantage over the cancer cells?

    I appreciate your responses.

    • Rob – I agree that lengthening telomeres might put the immune system in a better position to fight the cancer (which probably already has all the telomerase it needs). But there are probably more effective ways to support your Dad’s immune system in this time of crisis.
      – Josh

Leave a Reply

Your email address will not be published. Required fields are marked *