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Naturally Occurring Polymers—Animals 371

but the telomers shorten more rapidly so that at least cell aging involves not only the length of
telomers, but also the rate at which they become shorter. Recently, it was found that certain genes
on chromosome 6 appear with differing versions for long-lived males, and other versions for long-
lived females.
In the laboratory, the immortal cell lines are those derived from cancer. The most famous is
the HeLa cancer cells that many of us use as one of the cell lines tested against various anticancer
agents. The HeLa cells are derived from Henrietta Lacks, a black woman, who died from cervical
cancer. They are so strong, that they are know to invade other cell lines, both healthy and other can-
cer cell lines giving contaminated or mutated cell lines. HeLa cells have good telomerase levels. If
antisense RNA is added to HeLa cells so that the RNA contains the opposite message to the ordi-
nary RNA in the telomerase, the effect is to block the telomerase and the HeLa cells are no longer
immortal and die after about 25 replications.
It is estimated that about 700 genes are probably involved in the overall aging process and TEPI
is only one of these.
It can be argued as to whether all cancers occur as a direct result of our genes, but the relation-
ship between cancer and genes is present. We are aware that many chemical agents and high-energy
radiation that result in cancer do so through damaging DNA. Oncoviruses are also known to cause
cancer and these oncoviruses are not viruses but are really genes. In general, cancer genes are genes
that cause growth. Fortunately we have other genes that detect excessive growth and whose job it
is to stop the growth. These genes are called tumor-suppressor genes as opposed to the oncogenes.
The misfunctioning of either can result in cancer. If the oncogenes are not switched off then cancer
occurs or if the tumor-suppressor genes are not permitted to work, then cancer occurs.
On the short arm of chromosome 17 is a gene called TP . This gene is a tumor-suppressor gene
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and it codes for the production of a protein called p53 that is being tested as an anticancer drug.
TP is found to be broken in more than 50% of tested human cancers and is found broken in 95%
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of those with lung cancer. The most resistant cancers such as melanoma, lung, colorectal, and blad-
der cancers are ones where mutated TP are found. Further, where a patent initially responds to
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treatment, but then develops so-called resistant cells, again it is often found that the TP genes have
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mutated. (Thus, it should be possible to look at this gene to see if it has been mutated to see if addi-
tional chemo may be useful in the treatment of a particular cancer.) Those born with one of the two
TP genes broken have a 95% chance of developing cancer, and generally early in their lives. We
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can look at the progress of colorectal cancer. Here, cancer begins with a mutation of the tumor-sup-
pressor gene APC. If the developing polyp then undergoes a second mutation causing an oncogene
to operate without restraint, the polyp becomes an adenoma. If the adenoma then undergoes a third
mutation of a tumor-suppressor gene, then it continues to grow. If a fourth mutation occurs, now
in the TP gene, it becomes a full blown carcinoma. Many other cancers follow a similar scenario
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often with TP as the final mutated tumor-suppressor gene. Thus, this gene appears to be important

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in the production of cancer and in the fight against it.

TP is about 1,179 base-pairs long and it encodes for the production of the protein p53. This
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protein is normally rapidly degraded by other enzymes with a half-life of only about 20 min-
utes. But when a certain signal occurs, protein production greatly increases and its degradation
becomes less rapid. The signal appears to be caused by selective damage to DNA with the dam-
aged parts calling for production of excess p53. The p53 protein then “takes over” the cell acti-
vating, essentially causing the cell, to either stop making DNA until repair is made, or signals to
the cell to commit suicide. Another indicator for p53 is a shortage of cellular oxygen. Cancerous
cells often outgrow their oxygen availability so that they send out new arteries to capture more
oxygen for themselves. Some of the drugs being developed are aimed at preventing such adven-
turous artery formation.
Opposing forces operate in our bodies, often guided by our genes. These opposing forces or
activities are both important but become dangerous when not held in check. Thus, oncogenes
cause cell growth necessary for injury repair and cell replacement. They are held in check by

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