A Critique of Pure (Genetic) Information

136 Chapter 4
different place. In either case, cell B would differ from cell A, which remains
unchanged (Temin 1971).
Somatic mutation, in Temin’s view, is not in itself an aberrant occurrence
but rather a basic and unavoidable feature of cellular differentiation.
Viruses emerge from such processes strictly by chance. They result when
a reverse-transcribed stretch of DNA happens to become integrated
into a genome such as to result in a new string of nucleic acids (genes)
that are capable of quasi-independent replication. In the vast majority
of cases, the formation of the reverse-transcribed DNA (a protovirus)
does not result in a virus but only in a properly differentiated somatic
cell. Cancer, according to the Temin theory, is a product of the limited
fidelity of normal somatic-cell differentiation. Cancer, for Temin, is once
again the result of somatic-cell mutation, although only of the odd case
of it.
The usual process leading to cancer could be a variation in the normal physiological
evolution of the protovirus DNA, so that variants which contain information
for the cancer appeared either by mutation of the base sequence or by
integration in incorrect places or both (Temin 1971).
Temin’s idea of differentiation by somatic mutation, with the notable
exception of the immune system, has largely not been borne out. Interesting
as it was, Temin’s hypothesis of cancer causation could not be
redeemed if directed somatic mutation is not found to be operative in
processes of cellular differentiation (other than in the immune system
where just such a process is well established).
The kinetics of RSV-induced tumor formation had long been recognized
as highly variable. Cloning and nucleic acid sequencing studies of
the retroviral genome during the 1970s revealed that there were two
classes of retroviruses, one which was acutely transforming—capable of
rapidly inducing tumor formation in animals—and the other which was
only weakly transforming, that is, capable of inducing tumors but only
after a long latency period. It was soon recognized that these were structurally
different in only one respect. The acutely transforming viruses
were larger than the weakly transforming viruses by one stretch of
nucleic acid, that is, by one gene (Cooper 1990). This gene, whatever it
happened to be, constituted the difference between acutely transforming
and only weakly transforming viruses. Owing to its apparent significance