Thanks for posting and this is definitely a point of controversy regarding the activation of Telomerase to lengthen telomeres.
My first reaction when I read that article ( written in 2009) is that it was a hit piece.
Either TA-65 is weak or strong at inducing our cells to produce telomerase. You cannot have it both ways.
Aggressive cancers already "know" how to strongly produce telomerase, so TA-65 cannot be a factor in aggressive tumors, even if its effect is strong.
There is a reason cancers occur more frequently later in life. When telomerese are shorter.
From my research to date, cancers are more frequent as we age because telomeres are shorter, and chromosomes then are unable to reproduce perfectly, leading two chromosomes to fuse, etc, These configurations have been observed in one cell creatures, as their telomers shorten, leading to the configurations often seen under the microscope in human cancer cells.
From everything I have seen, having long telomeres will not create cancers or even make the chance of cancers starting increase.
I believe that the best way to prevent cancer is to grow your telomeres or at least stop them from shortening.
It is confusing that cancers make use of telomerase to keep their telomeres long so they can continue to divide without end. But they do this without our help.
When we get to the end of our ropes - unless we can somehow lengthen the rope - its over. And everything I think I know tells me we want to do what Ed Park described in Telomere Timebombs - extend our telomeres to the lengths we had when we were teeagers.