More About Cancer and Telomerase


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Cancer and Telomerase
    This is an attempt to synopsize the paper "Reserve-capacity hypothesis (Weinstein & Ciszek 2002)" discussed here Friday in Telomerase and Cancer, Take 2 .What follows is my attempt to recap the authors' theses.
    The reason that the somatic cells of multi-cellular organisms lack telomerase and are condemned to grow old is because the aging of cells is a back-up mechanism for curbing cells that have entered the first--runaway growth--stage of cancer. Lacking telomerase, these cells replicate until they approach their Hayflick Limit, and then quit reproducing. The resulting tumor stops growing, and hangs around until its senescent cells die of old age. A few particularly-wild cells make it to the next stage where they begin producing their own telomerase, and become the seeds of full-blown cancers. Unfortunately, as a majority of somatic cells approach their Hayflick Limit, they become more and more erratic, as unrepaired damage accumulates, leading to exponentially rising cancer rates.(Part of this damage may be attributable to shortening of the telomeres.) Consequently, what began as an effort to lower cancer rates during the early years of life leads to ever-rising cancer rates later on in life. But by then, the reproductive years have passed, and it's no longer as important to keep the organism cancer-free as it was during the early years.
    This is an ancipital choice that robs Peter to pay Paul.
    If we were to flood a senior citizen with telomerase, this would give a large number of small, occult, benign tumors a new lease on life, allowing them to grow to uncomfortable sizes. Since "prototumor" cell count is a risk factor for cancer, this would increase the chances of creating cells that would manufacture their own telomerase, and thus, become malignant. Also, because prototumor cells would renew replication at a stage of cellular life at which they had already sustained considerable damage, this additional factor would further elevate the chances of cancer, already high among the elderly, to a near certainty.
    The authors argue that evolution optimized the tradeoffs between telomere length and cancer susceptibility tissue by tissue, in order to arrive at an optimum tradeoff between, on the one hand, low early rates of cancer, and on the other hand, a long enough survival period to maximize the reproduction of the species.
    A few tissues that have to produce new tissue continuously, manufacture telomerase: notably the skin, and the bone marrow. However, the authors observe that in the case of the skin, wayward cells would soon be exfoliated from the epidermis. In the case of red blood cells, there are no nuclei, and there is no ability to reproduce. 
    The authors observe that some (optimistic) gerontologists think that nature has selected for the reproductive phase of life, but that selection is inoperative once the individual gets past the reproductive years. leaving us free "to pursue a technological solution to fill in where selection leaves off". But the authors' thesis is that nature has optimally selected senescence as the lesser of two evils, selecting in the senescent phase of life as well as in the reproductive phase, tuning animals to minimum chances of cancer early on at the expense of senescence and exponentially rising cancer rates in the post-reproductive years. 
    There's quite a bit more to say, but it will have to be deferred until tomorrow night.

To Be Continued.