by Sylvain Comeau
No one lives forever,
and while the thought of their eventual demise does not thrill many people,
much DNA and cancer research suggests that the limits on our life span
is a defensive mechanism, according to Chantal Autexier, a Science College
graduate who returned to Concordia for a recent lecture on The Ends
of DNA: Links to Cancer and Aging.
The ends of DNA (or chromosomes), are called telomeres, and were first
identified in the late 1980s. Telomeres prevent chromosones from coming
into contact with one another and interfering with each others normal
functioning. Most cancer cells have short telomeres, so that genetic mutations
result from chromosomes coming into contact with each other.
Telomere length acts as a kind of cell division clock, said
Autexier, who teaches medicine at McGill and heads a research team at
the Jewish General Hospital. Human cells have a finite life span;
they can only keep doubling so long before they die.
The clock starts to spin into infinity in the case of cancer cells. Cells
can start to double infinitely when there are genetic alterations. In
fact, a cancer cell is in a sense an immortal cell. That is one of the
definitions of cancer.
Ironically, that is one of the reasons we can probably never aspire to
immortality, or even anything close to it. Researchers have theorized
that the limits on human cell division are defensive. It is a tumour-suppressing
mechanism. Otherwise, cancer would be inevitable, Autexier pointed
out in an interview following her lecture for the Science College on September
28.
More irony: Advances in cancer research have failed to outpace the increase
in tumours that are an eventual result of aging.
There will always be limits to how far we can stretch the human
life span. Seventy years ago, people didnt die of cancer as often
as they do now because they died much earlier, before they could develop
tumours. Now people live longer, because we have eradicated some deadly
diseases, and because of better hygiene and medical treatment. But as
people age, genetic mutations at the DNA level - and therefore cancer
- becomes increasingly likely.
This only makes Autexiers work on telomeres more important. She
conducts fundamental research, but she says that future gene therapy applications
could, for example, focus on allowing the telomeres in cancer cells to
disappear.
Even though the telomeres in cancer cells are shorter, they are
somehow maintained indefinitely. Thats probably the key point. If
telomeres are eroded completely, the cancer cell will die. It will no
longer be immortal.
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