The same team had previously shown that
people with colon cancer and other diseases such as inflammatory bowel
diseases, Crohn's disease and ulcerative colitis have increased numbers of a
sticky type of E. coli
in their colons.
They discovered that the pks genes found in
these E.coli is capable of damaging the DNA of cells lining the gut. These
damaging bacteria are more commonly found in the colons of patients with
inflammatory bowel disease and colon cancer than in those who are healthy. On
an average it was found that two thirds of patients with colon cancer carry
these E. coli
, compared to its presence in one in five
people whose colons were healthy.
Other studies have shown that mice that
suffered from colitis were more likely to develop colon cancer if they harbored
containing pks genes but
were observed not to develop cancer if it carried another strain of identical
E.coli that did not harbor pks genes. The presence of these genes, however, did
not cause increased inflammation of the gut. It was the ability of pks
genes to cause cancer without causing inflammation that prompted studies on its
role in colon cancer.
The increased presence of the E.coli
in the colon of patients with
inflammatory bowel disease, and also in those with colon cancer who do not
suffer from inflammatory bowel disease, suggests that toxins generated by
the pks genes have a deleterious effect
on the DNA and can promote colon cancer.
The research has implicated that E. Coli
has a much deeper involvement in the
development of colon cancer than previously thought and it is important to
understand why these bacteria are present in some types of people and not in
Earlier research by the Liverpool team also
discovered that dietary agents,
particularly plantain and broccoli, could prevent the promotion and transport
of E. coli
through the gut
cells, while fat emulsifiers found in processed foods encouraged the transport
of bacteria through gut cells.