STUDY: HARMFUL CHEMICALS MAY REPROGRAM GENE RESPONSE TO ESTROGEN

ILENA ROSE 2005-05-31 15:01:04

Thanks to Carolyn Wolf for forwarding this important study.

I believe it will eventually have to be admitted that chemicals and
other harmful agents in the environment or in the body, implanted or
otherwise ... also trigger many of the autoimmune diseases that we see
in abundance around the chemically poisoned -- silicone implanted
people amongst them ...

I believe that the vast chemical industry cover-up and disinformation
that engulfs the Multiple Chemical Sensitivity issue ... has held
science and treatments back for way too long.

www.BreastImplantAwareness.org

EXCERPT:

The discovery is important because it changes conventional thinking
about the way in which genetic predisposition and things in the
environment interact to increase disease risk. Until now, scientists
thought that exposure to harmful agents in the environment caused
damage to the gene. This study, however, indicates that an
environmental agent can actually change or reprogram the gene so that
it functions differently.

http://www.nih.gov/news/pr/may2005/niehs-31.htm

National Institute of Environmental Health Sciences (NIEHS)

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FOR IMMEDIATE RELEASE
Tuesday, May 31, 2005

Harmful Chemicals May Reprogram Gene Response to Estrogen

New research shows that exposure to harmful chemicals and drugs during
critical developmental periods early in life may actually reprogram
the way certain genes respond to the female hormone estrogen. This
genetic reprogramming may determine whether people with a genetic
predisposition for a disease actually develop the disease.

The new research shows that when rats with a genetic predisposition to
uterine tumors also receive an early-life exposure to
diethylstilbestrol (DES), a synthetic form of estrogen linked to
vaginal cancer, the incidence of uterine tumors rises to almost 100
percent. By comparison, slightly more than half of the unexposed
animals, those having only the genetic defect, developed the uterine
tumors.

DES is a drug that was prescribed for women from 1938 to 1971 to
prevent miscarriages and premature deliveries. Daughters of women who
used DES are at increased risk for reproductive tract abnormalities,
pregnancy complications such as ectopic pregnancies and preterm
deliveries, infertility, and a rare vaginal and cervical cancer called
clear-cell adenocarcinoma. Other research conducted by NIEHS
scientists indicates that women exposed to DES in utero have a higher
risk of uterine fibroids.

The National Institute of Environmental Health Sciences, a component
of the National Institutes of Health, provided funding to researchers
at the University of Texas M.D. Anderson Cancer Center for the
two-year study. The study results will be published in the May 2005
issue of the Proceedings of the National Academy of Sciences.

The discovery is important because it changes conventional thinking
about the way in which genetic predisposition and things in the
environment interact to increase disease risk. Until now, scientists
thought that exposure to harmful agents in the environment caused
damage to the gene. This study, however, indicates that an
environmental agent can actually change or reprogram the gene so that
it functions differently.

This study is telling us that an environmental reprogramming of a
normal response, combined with an inherited gene defect, work together
to promote cancer, said NIEHS Director David Schwartz, M.D. If this
model is correct, it will help doctors to determine which individuals
are more likely to develop cancers of the uterus, breast and
prostate.

The finding should alert doctors to ask more questions about a
patients early-life exposures to chemicals and other harmful agents
in order to better predict that persons cancer risk.

Most people with a family history for a particular disease are
concerned about their recent exposures to harmful agents in the
environment, said Cheryl Walker, Ph.D., professor of molecular
carcinogenesis at the M.D. Anderson Cancer Center and lead author on
the study. We are just beginning to realize that exposures received
decades earlier, during critical developmental stages, may be much
more important in determining who develops cancer as an adult.

The researchers used a special strain of rats with a defect in a gene
called Tsc-2 (tuberous sclerosis complex 2) that made them more
susceptible to uterine leiomyomas, benign tumors that are common in
women over 30 years of age. These rats were then treated with DES
during days 3, 4 and 5 of life, during a critical period of uterine
development.

Once the rats reached adulthood, almost 95 percent had developed the
uterine tumors. Furthermore, the tumors were much larger and more
numerous than those in genetically defective rats not receiving the
DES treatment. These data suggest that environmental exposures during
development of the uterus can interact with a preexisting genetic
susceptibility to increase the risk of disease, said Walker. We are
looking at a new kind of gene-environment interaction that determines
who gets cancer and who doesnt.

According to Walker, the increase in frequency and size of the uterine
tumors is due to DES ability to influence estrogen, a female hormone
that is involved in promoting the growth of tumors by regulating the
activity of key genes involved in cell growth. We found that the DES
treatment somehow reprogrammed how these genes respond to estrogen,
making them much more responsive to estrogen than normal, said
Walker. We realized that the DES exposure enabled estrogen to drive
the tumor development when combined with a genetic predisposition.

While DES exposure can lead to the development of vaginal and cervical
cancers, the fact that most DES-exposed women did not develop the
cancers suggests that genetic predisposition is an important part of
the equation. In most cases, we already have tests that can determine
if a woman has a genetic predisposition for cancer, said Walker.

This is not the first study to suggest that cancer risk is influenced
by both genetic and environmental factors. A 2003 study of Jewish
women born with a defect in BRCA1, the gene that is linked to
inherited forms of breast and ovarian cancer, showed that those women
born before 1940 had a much lower risk of developing breast cancer
than women born after 1940. The researchers believe this discrepancy
is due to differences in diet, exercise, hormonal factors and chemical
exposures.

Walker believes more research needs to be done to test this concept in
people. NIEHS is partnering with the National Academy of Sciences to
fund additional research on early-life exposures and cancer risk in
human populations, she said.