No, it does not! That is the short answer. The rest of it requires me to get all sciency on you, so read on at your own risk!
Recently, I read yet another brilliant rocket scientist, stating that telomerase is turned off in most of our cells to protect us from cancer. The implication is, of course, that turning it on will increase your cancer risk, which would make TA-65 a cancer causing agent. The author then went on to cite some erudite scientific opinions in articles that were 2 and 6 years old respectively.
In this field, even when one is quoting Nobel Laureates, research that is 6 months old, is old news and over a year, is the dark ages, unless it has been recently repeated and updated.
The link between cancer and telomerase is embedded deeply in previous theory, but not actual fact.
The simple fact that 85% of human cancers appear to massively over express telomerase has been misinterpreted as proof that telomere shortening has something to do with protecting us from cancer and that telomerase is oncogenic. Short telomeres are definitively associated with cancer, not the other way around. If the cell regulatory mechanisms are intact, short telomeres (usually less than 5KB) will turn on cellular senescence mechanisms, or if they are “allowed” to grow shorter, apoptosis follows. Both mechanisms are mediated through the mitochondria and p53 – but telomeres “rule” this process.
If the cell undertakes, for whatever reason, to undergo the minimum of 4 “escape” steps to become cancerous, it may induce the very last step of telomerase over expression, which will effectively make the cancer cell line “immortal”. But telomerase is not the inciting factor any more than anaerobic metabolism, angiogenesis or Matrix Metalloproteinases are the causes of cancer and its subsequent spread. The disease, that is cancer, induces all these changes – and any attempts to fix them, without fixing the underlying causes, will not fix the cancer. This is why Ozone/oxygen therapy will not cure cancer. Cancer chooses to live in an anaerobic acidic environment and induces all kinds of things to make that possible. Dumping in oxygen or oxygen free radicals will not damage the cancer. It will simply wash those compounds away with its overdeveloped vascular system (the result of inducing angiogenesis using vascular stem cells) the way it washes away the toxins of its explosive growth and metabolism.
Blocking telomerase will not cure it either. The recent abject failure of telomerase inhibitors (like Imetelstat), cited in one of the answers as a potential cure for cancer, shows the flaw in this theory and this logic. Indeed, telomerase inhibition leads to only temporary suppression of cancer and then massive aggressive and treatment-resistant rebound, as the cancer “figures out a way around telomerase inhibition”. It is too early to say what will happen with the PinX mimics. It is possible that temporary suppression of tumors may be enhanced by telomerase inhibition via concomitant increased sensitivity to chemotherapeutic agents. In chemo-responsive tumors (without telomerase inhibition) however, telomere lengthening and a decrease in the variability of mean telomere length are positive signs, again pointing to some restoration of genomic stability. Aggressive malignancies replicate so rapidly, their telomere length remains short and the distribution of actual telomere lengths is very wide, within that parameter (e.g. short, very short and almost immeasurably short!)
But, once again, 15% of cancers do not rely on telomerase to lengthen their telomeres, but use the ALT mechanism instead, so telomerase expression is not a prerequisite for cancer either.
Early studies that used known oncogenic viruses to insert telomerase genes into the mouse genome in tert+/- and tert-/- mice are most likely the cause of the persistent misconception that telomerase is oncogenic and that turning it on will somehow foster cancer. When non-oncogenic strains are used, there is no increase in cancer and there is increase in life span and health span of the animals (see any of the recent studies by Maria Blasco). In humans, the mild telomerase activator, TA-65, initially an anti-HIV compound, has shown no increase in cancer (since 2005- Geron data), nor has it led to increased mortality in cancer patients either; and new human trials are due in the next 1-2 years. Finally, if telomerase were oncogenic, our species would not survive, since both stem cells and germ cells require “excess” telomerase expression to remain viable.
Cancer may use telomerase to stabilize its fragile genome and prevent its own destruction through genetic instability and reproductive failure, but telomerase does not cause cancer. Cancer causes over expression of telomerase, as it causes aberrations and over expression of many other enzymes.
I should point out a few things: The person asking the question states that “new drugs” have been developed, that lengthen telomeres. I am only aware of TA-65 as having human studies and it is a supplement, not a drug. Other supplements are being investigated and I am sure someone is working furiously on a drug somewhere, given the potential revenue it might generate. The Israeli’s reportedly are working on a telomerase activating drug for very specific use (not anti-aging), but it is not out of Stage 2 trials, as of yet.
My personal theory on why the telomerase gene is present, but inactivated in somatic cells, is the protection of evolutionary pressure on the species. During our past, there were not many of us and we were ill-equipped to capitalize on what has to have been even more enormous resources than we have now. Survival of the fittest dictated a rapid high pressure rise and demise of useful and unuseful traits, both genetic (slow and cumbersome) and epigenetic (far more rapid and “reflexive”). If people lived extremely long healthy lives, they would be better equipped to preserve their own static genomes and, unless they were able to reproduce much longer than we now do, some parts of their epigenomes as well. They would also have the experience and power to outcompete the young. So, simply put, telomerase suppression could exist simply to guarantee room and resources for the young of the species and to ensure evolutionary pressure remains meaningful. Since genetic engineering is likely to be a reality in the next decade, we will gain a measure of control over evolutionary pressure, as well as health and longevity, since they are all interrelated.
I fully admit this is just a theory, but when one looks at the evidence, it is certainly as viable as “to protect us from cancer”. If we look at current cancer rates, it’s not doing a very good job and it was unnecessary during all but our most recent existence, since we didn’t live past 50, on average, until a century ago, when the age-related disease we call cancer was not nearly as common as a cause of death. This would make the “to protect us from cancer” role of telomerase suppression a very recent evolutionary acquisition!
The ramifications of lengthening human life span and health span are many and can be summed up in this simple statement; we are stone aged genes in a space aged time. Meaning, people will remain subject to all the behavioral programming and perceived competition for resources that have plagued mankind since its inception. But, it also represents a tremendous opportunity to grow beyond and transcend those behaviors. It will certainly be interesting and could very well happen, on at least a small scale, in the lifetimes of many of the people reading this, thanks to the efforts of some of the aforementioned scientists.