Got this from the BBNS wire service:
Some significant misinformation regarding CYGS technology has found it
>way onto the web. We are trying to track it back to its origin in order
>to correct the misconceptions. We don't attribute any malevolent motives
>to Aaron, the apparent author, however he is simply misinformed on
>certain points. Please get this response into his hands of possible. We
>would welcome a call from him if he is interested in correcting these
>errors. our number is 713-780-1399. ---thanks --- Dell Gibson, CYGS
>---------------------------
>From Mike Skillern:
>
>I was asked to respond to an e-mail from a purported Ph.D. in telomere
>genetics which, in the author's opinion, points out flaws in our
>science. The author makes the statement that we intend to "get the cell
>to turn on telomerase by introducing telomere fragments into a cell's
>nucleus". This is patently untrue. Telomere single strands, when
>introduced into the cells, have been shown to seed to the telomere by
>independent means. We have never made any claims to activating
>telomerase through this mechanism, nor do we wish to activate
>telomerase.
>
>The author attributes this blatantly incorrect statement to us, "that
>the shrinkage of a cell's chromosomes without telomerase leads to cell
>shrinkage and that this is the cause of height loss in the elderly".
>CYGS has NEVER made this claim or statement. We agree with the author
>that this statement is clearly untrue. Depletion of cell populations is
>the result of cell lineage senescence, which is believed to be the
>result of telomere shortening (the "telomere hypothesis" related to the
>Hayflick limit), and is a cause of shrinking organ size with age.
>Physical height has nothing to do with this phenomenon. Moreover, the
>literature supports our belief that changing patterns of genetic
>expression (resulting from TRF-1 binding proteins) and telomere
>shortening is a more fundamental cause of an aged phenotype. We simply
>never made the statement which was attributed to us by the unidentified
>author.
>
>The author also erroneously credits CYGS with taking the position that
>if one turns on telomerase in a cell in an otherwise normal cell, that
>the cell can begin to divide and replenish itself, thus reversing aging.
>Again, we do not believe we can, nor do we wish to activate telomerase.
>
>Our claim is that seeding telomere single strands to chromosomal
>telomeres lengthens the telomeres which in turn increases replicative
>capacity. We have made no claims or implications regarding inducing
>mitosis (cellular division). In fact, We agree that inducing mitosis
>would likely heighten the risk of cancer. Moreover, for this very
>reason, and based on existing literature, we believe up-regulating
>telomerase will increase the risk of cancer if not induce it.
>
>Current studies in the field strongly link telomerase expression and
>dedifferentiation levels (carcinogenic grade). We believe this may imply
>that telomerase expression induces a loss in phenotypic expression
>associated with cancer. Of course, telomerase is present at low levels
>in stem cells and germ cells whose phenotypic expression is also at low
>levels (no, we don't believe this is coincidental either).
>
>The author again erroneously claims that CYGS wishes to introduce a
>"mutant" or "poisoned" telomere strand into cancers as a therapy. This
>is again patently untrue. The single strand sequence used in the studies
>we quoted on our press release was TTAGGG, which is the NORMAL telomere
>sequence. This was specified on the press release which is available on
>Business Wire. Claims that we plan to use another sequence or were
>speaking of another sequence is simply wrong.
>
>The author makes an elegant explanation of the problems of chemotherapy.
>He points out that compounds that kill cancer cells also can kill normal
>cells. He is right. However, the fact is that telomere single strands
>have now been shown to be good for normal cells (by increasing
>replicative capacity and re-establishing genetic expression patterns)
>but toxic to cancer cells. This means that vector therapy would not
>involve the same problems as chemotherapy. This also means that the
>therapy need not be targeted to the cancer cell, only to the tissue
>type. The author's allusions to developmental abnormalities by inducing
>cell division in the "wrong" cells is, again,
>an artifact of his misconception about telomerase in general and our
>work in particular.
>
>The author proclaims that CYGS will simply not be able to target cancer
>"as we have claimed". WE HAVE NEVER CLAIMED THIS!
>
>We have claimed that targeting tissue / cell type can be done with the
>vector. This does not mean we can or even wish to target cancer cells
>specifically. Again, targeting the tissue is sufficient because the
>telomere single strands seed to the telomere, thus increase replicative
>capacity, and re-establish genetic expression patterns in normal cells.
>As the new references found in our press release stipulate, the telomere
>single strands kill cancer cells. Incidentally, telomere single strands
>introduced into stem cell populations have been shown to increase their
>numbers and increase their replicative capacity (in the mortal
>lineages). Exactly why telomere single strands produce such different
>effects in cells expressing low levels of telomerase (like stem cells),
>versus high levels of telomerase (like cancer cells, particularly high
>grade cancer cells) remains unclear in the field.
>
>The author's claim that the single strands will "shut down the cells
>from dividing and accelerate aging" is not supportable in the
>literature, any reasonable telomere model, or his own arguments.
>
>The author makes the statement that retroviruses are tissue specific not
>tumor specific. Fact is we agree. However, we never said we were using a
>retrovirus (we may prefer an adenovirus) and we have only spoken of
>targeting tissue and cell type, not targeting specific tumors .
>
>We are familiar with the literature the author references about
>telomerase negative mice and telomerase negative cancer. We have only
>claimed that 90%+ of all cancers express the enzyme, and telomere single
>strands will likely be useful for these types. We would point out, as
>does the author, that the mice are genetically engineered, not naturally
>occurring. Nonetheless, 90%+ of cancers express telomerase and are
>therefore likely candidates for telomere single strand therapy.
>
>The author made the statement, "...it probably won't work as they say it
>will" regarding telomere single strands and cancer. The author is basing
>this on a single, genetically engineered mouse study, for telomerase
>negative cancer which is less than 10% of known cancer types, despite
>the fact Mount Sinai and University of Nebraska and other have shown it
>will. One is left to wonder about the basis of the author's assessment,
>particularly since CYGS has made no claims to how it will work.
>
>The author states flatly, "you can't cure cancer and aging with the same
>therapy, as they are opposite in nature". That may be his opinion, but
>is neither fact nor concensus.
>
> As for the author's opinions on evolutionary pressures, definitions to
>life, and germ line dynamics.....they are precisely that... opinions.
>The purpose of this response it is to correct mistatements and
>misconceptions.
>
>Sincerely,
>
>Mike Skillern
>VP - Technology Development |
