2189 replies to this topic

[smithx]

The concern I've seen expressed is not that telomerase induction would itself cause a cell to become transformed into a cancer cell.

It's actually a more complex concern. There are a number of changes which usually have to occur before a cell can become a cancer cell. It is believed by many scientists that one reason that telomeres function as they do is because it is desirable to place a limit on the total number of divisions a cell can make, because this also limits the number of cells which can undergo all the changes necessary to become cancer cells before they run out of time.

Scientists with this view are concerned that by reactivating telomerase, and thereby allowing cells to divide more times, more cells will survive long enough to undergo the changes which transform them into cancer cells. So it's not the telomerase that's causing cancer in this view -- it's the fact that lengthened telomeres allow already damaged cells to continue to replicate, producing damaged daughter cells, some of which become more damaged and transform into cancer cells.

It may be that astragalus root, which induces telomerase and which doesn't appear to increase cancer rates, has some synergistic compounds which induce apoptosis in damaged cells before they can reproduce. If so, it would be better to take whole root or whole root extracts rather than one particular component. And that's what I've been doing.

[jettax]

Jettax,

again... transient telomerase happens when you are fighting off a cold, healing a wound, etc...
You tell me a single study where a cold (or getting a cut while chopping tomatoes) caused cancer, and I will agree with you.

Until then, I will agree to disagree with you.

Again, I believe you are confused about this issue, and maybe should ask Carol about transient telomerase in the course of a normal human lifespan.

Cheers
A

(To Mr. Loera)
Isn't it marvelous our body transiently activate and deactivate telemerase in the right place at the right time? Like The Terminator directs auxiliary power on-need basis?
We hardly understand how telomerase activation/deactivation is controlled endogenously, much less exogenously. And it will be only naive to assume exogenous telomerase would not disrupt the endogenous intricacy.

(To Mr. AlexB)
Before I let myself into a pedantic wrestle, please allow me to ask a question.
If mice have very long telomeres, why do they live so short?

[maxwatt]

The concern I've seen expressed is not that telomerase induction would itself cause a cell to become transformed into a cancer cell.

It's actually a more complex concern. There are a number of changes which usually have to occur before a cell can become a cancer cell. It is believed by many scientists that one reason that telomeres function as they do is because it is desirable to place a limit on the total number of divisions a cell can make, because this also limits the number of cells which can undergo all the changes necessary to become cancer cells before they run out of time.

Scientists with this view are concerned that by reactivating telomerase, and thereby allowing cells to divide more times, more cells will survive long enough to undergo the changes which transform them into cancer cells. So it's not the telomerase that's causing cancer in this view -- it's the fact that lengthened telomeres allow already damaged cells to continue to replicate, producing damaged daughter cells, some of which become more damaged and transform into cancer cells.

It may be that astragalus root, which induces telomerase and which doesn't appear to increase cancer rates, has some synergistic compounds which induce apoptosis in damaged cells before they can reproduce. If so, it would be better to take whole root or whole root extracts rather than one particular component. And that's what I've been doing.

The human body is a complex system. Lengthening telomeres could as well prevent the defects in DNA that prevent apoptosis, which also leads to cancer. Or it could maintain the integrity of the immune system cells, so they destroy those cells that do become cancerous. Or maybe not. It is very clever of TA Sciences to get wealthy individuals to fund studies by paying for the privilege of being test subjects, but at least we can be reasonably confident that Cycloastragenol does not induce cancer in the short or near term.

But astragalus as an herb seems to do much more than lenghten telomeres. It is used in Chinese medicine to treat anemia, and some papers suggest it increases hematocrit levels. But the amount of Cycloastragenol in the herb is so little, I doubt it the herb itself would lengthen telomeres. It has been claimed that it does not.

Edited by maxwatt, 19 March 2011 - 01:25 PM.

[Anthony_Loera]

Hi Max,

The only thing I have against whole astragalus root, is the fact that you have to take about 30 grams a day for it's equivalence to whats found in capsules such as Astral Fruit or TA.

Smith's argument also seems a bit fatalistic in nature, as that kind of thinking would have folks consider a heart operation not necessary because an increase in lifespan would give the person a higher chance to get run over by a bus...



Sorry, it's the first thing that came to mind when I read it. I know it is more complex than that, but it still reminds me of it...

Cheers
A

[AlexB]

Before I let myself into a pedantic wrestle, please allow me to ask a question.
If mice have very long telomeres, why do they live so short?

Mice become fertile a few weeks after they're born so the force of natural selection is very weak in mice.
Aging and Genome Maintenance: Lessons from the Mouse?
Developmental and tissue-specific regulation of mouse telomerase and telomere length

[AlexB]

Lengthening telomeres could as well prevent the defects in DNA that prevent apoptosis, which also leads to cancer.

Cancer and aging: the importance of telomeres in genome maintenance

[GregLong]

The only thing I have against whole astragalus root, is the fact that you have to take about 30 grams a day for it's equivalence to whats found in capsules such as Astral Fruit or TA.

I would agree as to your product, however in regards to Astragaloside IV, doesn't it depend on the extract concentration and polysaccharide content?
There are some web published calculations that show Solaray extract yielding about 4.6mg of Astralgaloside 4 per each 200mg capsule. This would seem to infer that an effective telomerase enhancing dosage can be obtained at much less than 30 grams, maybe at only 2 or 3 grams. I doubt this would be as effective as a cycloastragenol product, but, if the calculations are correct, it may be cost effective for some.

[jettax]

Before I let myself into a pedantic wrestle, please allow me to ask a question.
If mice have very long telomeres, why do they live so short?

Mice become fertile a few weeks after they're born so the force of natural selection is very weak in mice.
Aging and Genome Maintenance: Lessons from the Mouse?
Developmental and tissue-specific regulation of mouse telomerase and telomere length

Mr. AlexB,

You said,
"Mice become fertile a few weeks after they're born so the force of natural selection is very weak in mice."

Isn't this a circular reasoning? Had lifespan of mice been much longer in the first place, they would have reached puberty in years after birth, not in weeks. Now mice has a longer telomere than human, so why didn't mice outlive human in the first place? And thus reach puberty in scores of years after birth in the first place, which would have ensured an efficient natural selection for the species?

Are you now admitting that telomere length has little to do with an organism's lifespan thus supplementing telemerase will not help you live longer?

As to Astragaloside IV, Cycloastragenol, astral fruit and TA-65, I will take none of these because there is no credible evidence that they do any good, not to mention they may give you cancer.
I used to take Astragalus root but I am currently not since many of my East Asian friends tell me that Astragalus root is not really a "highly regarded" herb in China and East Asia.
I take Carnosine.

Edited by jettax, 19 March 2011 - 10:33 PM.

[maxwatt]

Lengthening telomeres could as well prevent the defects in DNA that prevent apoptosis, which also leads to cancer.

Cancer and aging: the importance of telomeres in genome maintenance

AlexB -

Do you think you could summarize your point? I am sure it's a very interesting paper, but help me out: give me the Cliff Notes version

[AlexB]

Maxwatt,

There's already a nice summary at the bottom of the document (p 986) :

In summary, functional telomeric structures help maintain the stability of the genome (prevent cancer)
and protect cells against telomere-induced apoptosis or senescence (postpone aging) (Fig. 4). On the other
hand, dysfunctional telomeres lead to genomic instability, which can promote cancer, but also lead to the
tumor suppressor mechanisms of apoptosis and senescence, which can promote aging (Fig. 4). Therefore,
telomeres act in context, and can balance their ability to prevent or promote complex organismal phenotypes
such as cancer and aging.

[AlexB]

Mr. Jettax,

Isn't this a circular reasoning? Had lifespan of mice been much longer in the first place, they would have reached puberty in years after birth, not in weeks. Now mice has a longer telomere than human, so why didn't mice outlive human in the first place? And thus reach puberty in scores of years after birth in the first place, which would have ensured an efficient natural selection for the species?

You're missing the whole point of 'force of natural selection'.

Besides, you tried to use the argument :

"By early 1996, she had created a mouse model in which she genetically“knocked out”the telomerase enzyme. The mouse showed no adverse effects."

for proving your point that telomerase is somehow not necessary. There are plenty of scientific articles to prove you wrong.

Are you now admitting that telomere length has little to do with an organism's lifespan thus supplementing telemerase will not help you live longer?

Google "centenarians and long telomeres".

[niner]

As to Astragaloside IV, Cycloastragenol, astral fruit and TA-65, I will take none of these because there is no credible evidence that they do any good, not to mention they may give you cancer.

You must not have read Harley et al., a link to which is posted somewhere upthread. Cal Harley was a colleague of Carol Greider's, so I think he knows what he's doing. They present credible evidence that TA-65 is quite helpful in remodeling immune systems that have been degraded by the very common CMV infection. You can claim that they "may give you cancer", but there is no evidence to date that supports you, and there are even reasons to suspect that it may do the opposite, preventing cancer.

We know that you are the same person as 'my conscious', 'ingrid', and several dozen other user names, and that you are on a vendetta against RevGenetics, attacking telomerase activation and resveratrol at every opportunity. You've been PM spamming other members, which all find highly annoying. Normally I wouldn't argue with you, but I feel a need to correct the misinformation that you've been spreading, and to make sure that the rest of our community knows what you're up to.

[smithx]

The only thing I have against whole astragalus root, is the fact that you have to take about 30 grams a day for it's equivalence to whats found in capsules such as Astral Fruit or TA.

True, but what about extracts? We don't know unless we pay to have them analyzed, but some extracts claim to be "10x", so depending on what specifically is being concentrated, it's possible that 3gm or less of these extracts would provide a useful amount of cycloastrogenol, astragaloside IV or other telomerase-inducers.

Smith's argument also seems a bit fatalistic in nature, as that kind of thinking would have folks consider a heart operation not necessary because an increase in lifespan would give the person a higher chance to get run over by a bus...

The idea that multiple changes to a cell are required to produce cancer, and that one function of the telomeres is to put a limit on the number of cell divisions which can take place, in order to reduce the occurrence of cancers is not my argument, it's an argument made by various cancer researchers.

In fact, one article stated that the maximum number of cell divisions in humans is slightly less than the number typically required for a cell to accrue enough damage to become a cancer cell.

Whether it's true or not is a question which can only be resolved through research.

[GreenPower]

As to Astragaloside IV, Cycloastragenol, astral fruit and TA-65, I will take none of these because there is no credible evidence that they do any good, not to mention they may give you cancer.

You must not have read Harley et al., a link to which is posted somewhere upthread. Cal Harley was a colleague of Carol Greider's, so I think he knows what he's doing. They present credible evidence that TA-65 is quite helpful in remodeling immune systems that have been degraded by the very common CMV infection. You can claim that they "may give you cancer", but there is no evidence to date that supports you, and there are even reasons to suspect that it may do the opposite, preventing cancer.

We know that you are the same person as 'my conscious', 'ingrid', and several dozen other user names, and that you are on a vendetta against RevGenetics, attacking telomerase activation and resveratrol at every opportunity. You've been PM spamming other members, which all find highly annoying. Normally I wouldn't argue with you, but I feel a need to correct the misinformation that you've been spreading, and to make sure that the rest of our community knows what you're up to.

Not to say that I agree with the reasoning of jettax (I do not), but I would be somewhat careful referring to the paper "A Natural Product Telomerase Activator As Part of a Health Maintenance Program" by Harley and Blasco (among others). Not only was it sponsored by TA Sciences and mostly written by people with competing interests, but it also contains some strange conclusions which I believe might lack conclusive data. Not that the conclusions are necessarily wrong, I just can't find the data presented in the report.

Regarding the positive remodeling of the immune system
The report says that "The most striking in vivo effects were declines in the percent senescent cytotoxic (CD8+/CD28- T cells".... and "natural killer cells". Then they continue with "Although mean telomere length did not increase, there was a significant reduction in the percent short (<4 kbp) telomeres ( p=0.037)". Please note that they say percentage which would suggest that the total number of T-cells and NK-cells remained the same, which they didn't. Also note that they they have been doing very nice baseline tests with the concentration and ratios of the different types of cells measured before the study. They have even sent the samples to two different labs to make sure there are no mistakes. But they do not present the the same detailed tables with concentration or ratio values from the test subjects after the study was completed.

What they do say is that the test subjects had about 15% less Natural Killer cells and about 15-20% less T-cells after they had completed the protocol (picture 4A and 4C). If they are correct in their assumption that the number of NK-cells dropped because the remaining NK's are more active/working more efficient - and the bodies of the test subjects could now make do with 15% less NK's than before, this might be positive (see the text before reference 39) and they have indeed managed to perform a "positive remodeling of the immune system". On the other hand - if the number of NK's dropped because they managed to kill a lot of white blood cells (preferably those with short telomere length to begin with) and the NK's have not turned more active/efficient, this might be seen as quite bad. Because, as they mention, they didn't measure the activity of the NK's - I don't think it's possible to tell which of these two scenarios actually occurred.

It's also interesting to see that they don't comment on the even larger decrease of T-cells and if there's a similar mechanism with "reduction in numbers dues to compensation for increased efficiency" or not.


Where did all the test subjects and the increased telomere lengths go?
From the beginning the study contained n=114 test subjects, where 88 where CMV-positive. When they present the changes in telomere lengths for this population they are happy to announce that two independent tests using two different techniques "showed no consistent change with time on PattonProtocol-1 (data not shown)". Then they present a graph (3A) with the mean telomere lengths of thirteen (13) of the original test subjects. As a reader we have no way of knowing if these 13 test subjects are representative for the whole population of 114 test subjects or not. Or if these where the only 13 test subjects which actually completed the whole protocol. The graph don't even say which kind of blood cells it shows the telomere lengths for or if it's some kind of summary for all kinds included in the test.

At page 10 the study also states that the average telomere length for all the test subjects (114?) declined with an unspecified but nonsignificant length, but that 40% (45.6?) of the test subjects showed an unspecified increase in mean telomere length. This is explained by "cell dynamics" (not defined) and that "telomerase preferentially lengths the shortest telomeres" (which I don't see this study proved happened). It might just be me, but I think this explanation sound a bit vague.

Among the conclusions are that "the protocol lengthens critically short telomeres", but I don't see they have presented conclusive data supporting this statement.


Interesting side notes on TA65
As a side note, an interesting thing which I didn't really notice last time I read this report is that they refer to the protocol used by the test subjects as "PattonProtocol-1", with a counter at the end - indicating there have been changes to this protocol since this study was done. This makes be wanna return to the earlier discussion about what TA65 really is, because this would support the theory that that "PattonProtocol-1" might have been Astragaloside IV and that they have switched to Cycloastragenol in later versions of the protocol (shown in a lab report by Anthony). Another new argument for this is that the test subjects took as much as 10–50mg of the substance. Had this been Cycloastragenol I think they might have ran into the "memory problem", which some people have reported (me included). There have been no reports of such problems for people taking large doses of AIV (I've myself been taking 100mg with no such effects). As earlier have been mentioned, they also say that the molecule used in the first version of the Patton Protocol is related to TAT2 (which we know is Cycloastragenol).

Edited by GreenPower, 20 March 2011 - 10:02 AM.

[GreenPower]

A couple of good introductory lectures by Elisabeth Blackburn which I don't think have been posted before;

Telomeres and Telomerase: Their Implications in Human Health and Disease
Part 1: The Roles of Telomeres and Telomerase
http://www.ibiosemin...lackburn1.shtml

Part 2: Telomeres and Telomerase in Human Stem Cells and in Cancer
http://www.ibiosemin...lackburn2.shtml

Part 3: Stress, Telomeres and Telomerase in Humans
http://www.ibiosemin...lackburn3.shtml

[Anthony_Loera]

A couple of good introductory lectures by Elisabeth Blackburn which I don't think have been posted before;

Telomeres and Telomerase: Their Implications in Human Health and Disease
Part 1: The Roles of Telomeres and Telomerase
http://www.ibiosemin...lackburn1.shtml

Part 2: Telomeres and Telomerase in Human Stem Cells and in Cancer
http://www.ibiosemin...lackburn2.shtml

Part 3: Stress, Telomeres and Telomerase in Humans
http://www.ibiosemin...lackburn3.shtml

GreenPower,

Excellent links, thanks for sharing. hope folks read up on the subject.

A

[Gerald W. Gaston]

Ok, to revisit: a revival of some type of distributed computing with the TE system is definitely on the cards.


Who will be leading this team?

Are we sure we don't want to shift to some other distributed computing project collectively?
We could resume talks with these guys.
Or should we do more than one team?

I put this team in my line up so I now lead it by default. Ill be sending out a memo to the team at least once each month, bumping the recruit topic, and submitting the list of current actives for points. Chrono or another can apply for the position by meeting with me about it if they want and Ill also be looking for somebody/may be getting a hold of Chrono myself.

Lets keep moving with this team, and if somebody wants to start up Rosetta and start getting all of our f@h participants to switch over then we can do that. We can consider phasing f@h out at the right time then.

In the monthly contributions tally list they are all listed in order of how many units they folded for f@h. So the top 3 people that are registered in our registration topic or that we could find in the member search are at the top.

Here are the old prize values in dollars:
75
50
25
15
15
15
15
15
15
15
15
15
and then there were bonuses like the lef coupons

I suggest point values roughly equivalent to those, except "15" given for all of the rest of the folders too.

This is an interesting article on 'botanical immune enhancers'. As for astragalus root extracts, below they find only a 95% ethanol extract of astragalus had adjuvant activity in their specific model:

PMCID: PMC2565601 - Evaluation of Widely Consumed Botanicals as Immunological Adjuvants

Background

Many widely used botanical medicines are claimed to be immune enhancers. Clear evidence of augmentation of immune responses in vivo is lacking in most cases. To select botanicals for further study based on immune enhancing activity, we study them here mixed with antigen and injected subcutaneously (s.c.). Globo H and GD3 are cell surface carbohydrates expressed on glycolipids or glycoproteins on the cell surface of many cancers. When conjugated to keyhole limpet hemocyanin (KLH), mixed with an immunological adjuvant and administered s.c. the magnitude of the antibody responses against globo H, GD3 and KLH depend largely on the potency of the adjuvant. We describe here the results obtained using this s.c. immunization model with 7 botanicals purported to have immune stimulant effects.

Methods

Groups of 5–10 mice were immunized with globo H–KLH or GD3-KLH mixed with botanical, saline or positive control immunological adjuvant, s.c. 3 times at 1 week intervals. Antibody responses were measured 1 and 2 weeks after the 3^rd immunization. The following seven botanicals and fractions were tested: (1) H-48 (Honso USA Co.), (2) Coriolus vesicolor raw water extract, purified polysaccharide-K (PSK) or purified polysaccharide-peptide (PSP) (Institute of Chinese Medicine (ICM)), (3) Maitake extract (Yukiguni Maitake Co Ltd. and Tradeworks Group), (4) Echinacea lipophilic, neutral and acidic extracts (Gaia Herbs), (5) Astragalus water, 50% or 95% ethanol extracts (ICM), (6) Turmeric supercritical (SC) or hydro-ethanolic (HE) extracts (New Chapter) or 60% ethanol extract (ICM) and (7) yeast β-glucan (Biotec Pharmacon). Purified saponin extract QS-21 (Antigenics) and semi-synthetic saponin GPI-0100 (Advanced BioTherapies) were used as positive control adjuvants. Sera were analyzed by ELISA against synthetic globo H ceramide or GD3 and KLH.

Results

Consistent significant adjuvant activity was observed after s.c vaccination with the Coriolus extracts (especially PSK), a 95% ethanol extract of astragalus and yeast β-glucan, and (to a lesser extent) Maitake. Antibodies against KLH in all cases and against globo H in most cases were induced by these botanicals. Little or no adjuvant activity was demonstrated with H48 or Echinacea extracts or the astragalus water extract. Experiments with GD3-KLH as immunogen confirmed the adjuvant activity of the Coriolus, yeast β-glucan and Astragalus extracts. While extraction with ethanol concentrated the active ingredients in astragalus, it had no impact on coriolus where the 90% ethanol precipitate and solute were equally active.

Conclusions

Some, but not all, botanicals purported to be immune stimulants had adjuvant activity in our model. PSK and astragalus were surprisingly active and are being further fractionated to identify the most active adjuvant components.

Edited by frankbuzin, 20 March 2011 - 04:02 PM.

[niteinnyc]

Anthony, I recall reading sometime last year that you had obtained a telomere score for yourself, to serve as a baseline prior to beginning supplementation of your Astral Fruit product. Have you done any follow-up testing, and if so are the results posted somewhere? Also, are you aware if any telomere score data has been published anywhere showing changes in telomere lengths of TA-65 users? Since all those enrolled in the TA-65 program are baseline and follow-up tested, it would be curious if none of that info was available anywhere, especially since if positive results were shown to be the result, it would certainly serve to generate more interest and sales.

Edited by niteinnyc, 21 March 2011 - 05:23 AM.

[Anthony_Loera]

Hi nite,

nope I don't have them.

I understand your inquiry, and believe that only certain cells in those tests will have had a positive results. It certainly will be interesting when I do take time to do these tests, but my schedule simply does not let me. At this time, I rarely spend more than a week in the USA... before leaving for a meeting outside of the country. I have begun to consider my schedule as pretty abnormal compared to others.

I am considering asking for local volunteers to take Astral Fruit for 6 months, taking a few tests to check telomere lengths.

Cheers
A

[niteinnyc]

I am considering asking for local volunteers to take Astral Fruit for 6 months, taking a few tests to check telomere lengths.

Cheers
A

Since I have been considering doing this already, I would certainly be interested in a project like this. It would be even more interesting to have several people involved doing it simultaneously.

I am very curious about data from those enrolled in the TA program and why it doesn't seem to be published anywhere that I can see. If any positive results were there to be shown, even in only certain cells, it would serve their marketing well.

[Zaion]

How it is possible that after so many years there are
not so many controlled studies and it is still not possible to understand clearly if those
supplements can slow down or reverse aging or on the other side stimulate cancer growth ?
Maybe the patents are hindering the research ?

[GreenPower]

How it is possible that after so many years there are
not so many controlled studies and it is still not possible to understand clearly if those
supplements can slow down or reverse aging or on the other side stimulate cancer growth ?
Maybe the patents are hindering the research ?

I think the problem has rather been the opposite. Because it's not possible (at least not in Europe) to take a patent on extracts from a medicinal plant which has been used in traditional medicine for thousands of years, the big pharmaceutical companies are not inclined to spend millions of euros on developing and testing the effects in large clinical studies.

That said, TA Sciences did sponsor the study "A Natural Product Telomerase Activator As Part of a Health Maintenance Program" which you find in post #881 in this thread. As you might have noticed on my comments in post #1215 I'm a bit skeptical to the conclusions they draw of the few bits of results they made public, though.

If Geron's new (likely artificial) substance GRN510 (formerly known as TAT153, and also as TA-1) shows good results, I would expect them to present the kind of test data you're looking for. Here you can find (buy) some more information about their preclinical mouse tests: http://www.biocentur...m/products/ta-1 . I would expect it to be quite expensive if it's actually brought to the market, though.

This leaves us with limited funds to try out the non-patentable substances, many of which are covered in this thread. You can contribute to the results made available to the public by testing yourself before and after a test period on such a substance and then publish the results.

[biochemie]

Hi Max,

The only thing I have against whole astragalus root, is the fact that you have to take about 30 grams a day for it's equivalence to whats found in capsules such as Astral Fruit or TA.

Smith's argument also seems a bit fatalistic in nature, as that kind of thinking would have folks consider a heart operation not necessary because an increase in lifespan would give the person a higher chance to get run over by a bus...



Sorry, it's the first thing that came to mind when I read it. I know it is more complex than that, but it still reminds me of it...

Cheers
A

To be honest, that's quite a bit disappointing of a remark for a perfectly valid point and does nothing for your scientific merit. While telomerase isn't an oncogene in itself the point brought up is perfectly valid of what we know of cancerogenesis. The fact that telomerase is induced in the majority of cancers supports this as well.

You may be correct that avoiding a heart attack and increasing your lifespan puts you at higher risk for cancer or getting rundown by a bus but treating an illness and avoiding death isn't the same as extending the natural lifespan and replicating ability of a cell. Regardless, using something that has so little data available regarding its safety is not something to be promoted without proper warnings IMO. In a world where genetic damage is perfectly corrected and environmental toxins are always properly dealt with it wouldn't pose as big a risk as one where our genome's integrity is constantly challenged.

Edited by biochemie, 22 March 2011 - 09:26 PM.

[Anthony_Loera]

While telomerase isn't an oncogene in itself the point brought up is perfectly valid of what we know of cancerogenesis. The fact that telomerase is induced in the majority of cancers supports this as well.

You are correct, it is induced by cancer (not the other way around), just like cancer also tricks your body into believing it is a wound so that it can divert blood supply and arteries to feed themselves...

It is only after a cell is cancerous does this happen.
You don't see wounds becoming cancerous, so why believe that transient telomerase has such an effect, even after being told it is not an oncogene?

A

[niner]

While telomerase isn't an oncogene in itself the point brought up is perfectly valid of what we know of cancerogenesis. The fact that telomerase is induced in the majority of cancers supports this as well.

You are correct, it is induced by cancer (not the other way around), just like cancer also tricks your body into believing it is a wound so that it can divert blood supply and arteries to feed themselves...

It is only after a cell is cancerous does this happen.

In the majority of cancers, telomerase is constitutively active. Essentially it is permanently stuck in the "on" position. This is distinctly different than the transient (and mild, I suspect) activation that is provided by cycloastragenol. When the cycloastragenol is withdrawn, the telomerase should revert to its native state. Incidentally, the constitutive activation of telomerase would have to happen before a cell could form a cancer. Otherwise, the cell line would be arrested due to telomere attrition, unless the DS break sensing apparatus was defective. That might account for the ten percent of cancers that have normal telomerase.

[hamishm00]

Check this out:

Aging Cell. 2011 Mar 22. doi: 10.1111/j.1474-9726.2011.00700.x. [Epub ahead of
print]
The telomerase activator TA-65 elongates short telomeres and increases health
span of adult/old mice without increasing cancer incidence.
de Jesus BB, Schneeberger K, Vera E, Tejera A, Harley CB, Blasco MA.
Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National
Cancer Centre (CNIO), Melchor Fernández Almagro 3, Madrid, E-28029, Spain Life
Length, Agustín de Betancourt 21, Madrid, E-28003, Spain Telome Health, Menlo
Park, CA, 94025, USA.

Here, we show that a small-molecule activator of telomerase (TA-65) purified from
the root of Astragalus membranaceus is capable of increasing average telomere
length and decreasing the percentage of critically short telomeres and of DNA
damage in haploinsuficient mouse embryonic fibroblasts (MEFs) that harbor
critically short telomeres and a single copy of the telomerase RNA Terc gene (G3
Terc(+/-) MEFs). Importantly, TA-65 does not cause telomere elongation or rescues
DNA damage in similarly treated telomerase-deficient G3 Terc(-/-) littermate
MEFs. These results indicate that TA-65 treatment results in telomerase-dependent
elongation of short telomeres and rescue of associated DNA damage, thus
demonstrating that TA-65 mechanism of action is through the telomerase pathway.
In addition, we demonstrate that TA-65 is capable of increasing mTERT levels in
some mouse tissues and elongating critically short telomeres when supplemented as
part of a standard diet in mice. Finally, TA-65 dietary supplementation in female
mice leads to an improvement of certain health-span indicators including glucose
tolerance, osteoporosis and skin fitness, without significantly increasing global
cancer incidence.


PMID: 21426483

Edited by hamishm00, 30 March 2011 - 09:38 AM.

[beachbum]

Is there some reason why my posts disappeared?

[boylan]

Is there some reason why my posts disappeared?

They're in another thread?

[maxwatt]

Is there some reason why my posts disappeared?

They're in another thread?

Here

[AgeVivo]

The telomerase activator TA-65 elongates short telomeres and increases health
span of adult/old mice without increasing cancer incidence.
PMID: 21426483

what about lifespan?