Then in 1961 other confirmation came, this time from living animals rather than tissue cultures.
Radioactive tracer s ubs tances were injected into cancerous mice. Then by careful
meas ureme nts of their respiration, it was found that the fermentation rate was markedly above
normal, jus t as Warburg had fores een. Meas ured by the s tandards es tablis hed by Warburg,
most pesticides meet the criteri on of the perfect carcinogen too well for comf ort. As we have
s een in the precedi ng chapter, many of the chl orinate d hy drocarbons , the phenols , and s ome
herbicides interfere with oxidation and energy production within the cell. By thes e means they
may be creating sleeping cancer cells, in which an irreversible malignancy will slumber long and
unde tected until finally—its caus e long forgotten and eve n uns us pected—it flares into the open
as recognizable cancer.
Another path to cancer may be by way of the chromos omes. Many of the mos t dis tinguis hed
research men in this field look with s us picion on any agent that damages the chromos omes ,
interferes with cell division, or caus es mutations. In the view of thes e men any mutation is a
pote ntial caus e of cancer. Although dis cus sions of mutations us ually refer to thos e in the germ
cells, which may then make their effect felt in future generations, there may also be mutations
in the body cells. According to the mutation the ory of the origin of cancer, a cell, perhaps under
the influence of radiation or of a chemical, develops a mutation that allows it to escape the
controls the body normally ass erts over cell divis ion. It is therefore able to multiply in a wild
and unregulated manne r. The new cells res ulting from thes e divis ions have the s ame ability to
es cape control, and in time enough s uch cells have accumulated to cons titute a cancer. Other
inves tigators point to the fact that the chromos omes in cancer tis s ue are uns table; they tend to
be broken or damaged, the number may be erratic, there may even be double sets.
The first investigators to trace chromosome abnormalities all the way to actual malignancy
were Albert Levan and John J. Biesele, working at the Sloan-Ketteri ng Ins titute in New York. As
to which came firs t, the malignancy or the dis turbance of the chromosomes, these workers say
without hesitation that ‘the chromosomal irregularities precede the malignancy.’ Perhaps , they
speculate, after the initial chromosome damage and the resulting instability there is a long
period of trial and error through many cell generations (the long latent period of malignancy)
during which a collection of mutations is finally accumulated which allow the cells to escape
from control and embark on the unregulated multiplication that is cancer.
Ojvind Winge, one of the early proponents of the theory of chromos ome ins tability, felt that
chromos ome doublings were es pecially s ignificant. Is it coincidence, then, that benzene
hexachloride and its relative, lindane, are known through repeate d obs ervations to double the
chro mos o mes i n experi mental plants —and that these same chemicals have been implicated in
many well-docume nte d cas es of fatal anemias? And what of the many othe r pes ticides that
interfere with cell division, break chromosomes, cause mutations? It is eas y to s ee why
leukemia s hould be one of the mos t common dis eas es to res ult from expos ure to radiation or
to chemicals that imitate radiation. The principal targets of physical or chemical mutagenic
agents are cells that are undergoing es pecially active divis ion. This includes various tiss ues but
mos t importantly thos e engaged in the production of blood. The bone marrow is the chief
produce r of red blood cells throughout life, s ending s ome 10 million new cells per s econd into
the bloods tream of ma n. White corpus cles are formed in the lymph glands and in s ome of the
marrow cells at a variable, but still prodigious, rate.
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