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The CancerWeb Report, What's New In Cancer
Carcinogenesis: November 1995
Last modified on:
Tuesday, April 20, 1999 13:03:10
Copyright © 1994-2008, Information Ventures, Inc.
Chronic Inflammation and Cancer - Chronic inflammation has long been regarded as a predisposing
factor for cancer development. This connection has been
underscored by epidemiological studies. In the case of the
urinary tract, a well known example of this is Bilharzia due to
Schistosoma infection, in which the bladder parasites cause
steady bleeding and inflammation that eventually leads to bladder
cancer. How does it happen? A study reported by a group from
Northwestern University Medical School in the October 15, 1995
issue of Cancer Research, suggests that release of a natural
product of inflammation, interleukin-6, is responsible. They
looked at normal cells from rat bladder that had been exposed
previously to the carcinogen N-methyl-N-nitrosourea, and tested
the effects of a range of products of inflammation. Of those
tested, only interleukin-6 significantly increased the growth
rate of the cells, and enhanced their ability to grow without a
surface on which to anchor, a special feature of cancer cells.
This was a permanent growth advantage and behavioral change. In
this experiment, interleukin-6 may have promoted the completion
of the carcinogenesis process that was initiated by nitrosourea.
Telomerase - Cancer cells are generally said to be immortal, since they can
continue to divide and multiply indefinitely. In contrast,
normal cells divide only a limited number of times and then
finally die off. A possible explanation for this is that there
are surplus sections at the end of each DNA strand that protect
the DNA strand with its vital genetic information, in a similar
manner to the way tabs at the ends of shoe laces protect the lace
from fraying and unravelling and enable it to be thread through
the hole. Each time the DNA strand is copied, bits get lost from
the end until at last the protective section is no longer able to
protect the informational section and enable chromosomes to
function properly. The cell's genetic information cannot be
copied accurately and the cell dies. There is an enzyme called
telomerase that is able to repair the damaged end segments, so
that DNA can be replicated indefinitely without losing the ends.
This enzyme is not found in most normal adult tissues.
Telomerase, and its critical role in making a cell "immortal" in
carcinogenesis was the theme of a session at the American
Association for Cancer Research meeting earlier this year, and
reports on this topic continue at a rapid pace. A paper in the
November, 1995 issue of Clinical Cancer Research by a Japanese group
reported that telomerase was found in 85% of gastric cancer and
95% of colorectal cancer samples as initially collected, and in
all the cells that were grown from these samples. Telomerase was
also found in 100% of colorectal adenomas, 50% of gastric
adenomas, and 23% of stomach metaplasias. Metaplasias and
adenomas are considered to be precancerous conditions. No enzyme
was found in normal mucosa tissue. It appears that telomerase
activity develops as a very early step in carcinogenesis in the
stomach and intestinal tract.
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