EMBARGOED FOR RELEASE UNTIL
APRIL 29, 2007
APS Contact
Donna Krupa
Office: (301) 634-7209
Cell: (703) 967-2751
dkrupa@the-aps.org
Newsroom Opens at 12:00 p.m.
Saturday April 28
APS Newsroom
East Registration Area
Washington Convention Center
APS Press Room: (202) 249-4174
New Animal Study May
Explain Why Alcohol Consumption Increases Breast Cancer Risk
WASHINGTON For the first time, scientists have
used a laboratory mouse model to mimic the development of human
alcohol-induced breast cancer. The results are part of a new study,
Chronic Alcohol Consumption Increases Tumor Growth and Amgiogenesis of
Breast Cancer in Female Mice, conducted by Brandi Busby, Wei Tan, Jordan
Covington, Emily Young, and Jian-Wei Gu, all of the University of
Mississippi Medical Center, Department of Physiology and Biophysics,
University of Mississippi Medical Center, Jackson, MS. Dr. Gu will present
the teams findings in detail during the American Physiological Society (APS;
www.the-APS.org) annual meeting, which is being held as part of the
Experimental Biology (EB 07) meeting. More than 12,000 scientists are
attending the conference, being held April 28-May2, 2007 at the Washington,
DC Convention Center.
Background
Alcohol (EtOH) consumption even moderate is a
well-established risk factor for breast cancer in women. A recent study
showed that 60 percent of female breast cancers worldwide were attributable
to alcohol consumption. Nevertheless, the mechanisms of alcohol-induced
breast cancer are poorly understood.
The definitive biological effects and molecular
mechanisms of EtOH on progression and malignancy of breast cancer have not
been investigated using a mammalian breast cancer model that mimics the
human disease. Scientists have suggested that the possible mechanisms
involved include the agitation of estrogen metabolism and response; cell
mutation by the EtOH metabolite acetaldehyde; oxidative damage; and
one-carbon metabolism pathways through reduced folic acid.
Methodology
To date, there has not been an animal model that
faithfully mimics the human disease with respect to characteristics of
breast cancer, immunocompetence, and physiologically relevant EtOH intake.
The researchers addressed and overcame the obstacles and developed a novel
mouse breast cancer model. The model mimics human breast cancer disease in
which the estrogen receptor-positive breast adenocarcinoma cells were
subcutaneously injected near the pad of the fourth mammary gland of female
immunocompetant mice (C57BL/6). The six-week-old female mice were fed with
moderate EtOH (one percent in drinking water) for four weeks, the equivalent
of two drinks per day in humans. The control mice received regular drinking
water only.
In the second week of the
experiment, mouse breast cancer cells (5x105 E0771) were injected
at cite referenced above. At the end of the experiment, the tumors were
isolated to measure tumor size, examine intratumoral microvessel (IM)
density via CD 31 immunohistochemistry staining, and assessing VEGF protein
levels via ELISA. These steps were taken to determine the effects of EtOH
intake in physiologically relevant doses on tumor growth and angiogenesis in
mouse breast cancer.
Results
The researchers found:
-
that moderate alcohol consumption significantly increased
the tumor size of breast cancer in mice, which was a 1.96-fold increase
in tumor weight vs. control mice;
-
that alcohol intake caused a 1.28-fold increase in tumor
microvessel density vs. the control group;
-
a significant increase in tissue protein levels of VEGF
were found in the tumors of the mice treated with EtOH vs. control
group;
-
EtOH intake did not cause significant changes in the body
weight of the mice.
Conclusions
This study presents the first animal model to confirm
that alcohol consumption stimulates tumor growth and malignancy of breast
cancer, and reveals some of the mechanisms of alcohol-induced breast cancer.
The findings demonstrate that even moderate alcohol consumption
significantly stimulates tumor growth of breast cancer and that induction of
tumor angiogenesis and VEGF expressions are mechanisms which are associated
with the progression of this deadly disease.
***
The
American Physiological Society (APS) has been an integral part of the
scientific discovery process since it was established in 1887.
Physiology is the study of how molecules, cells, tissues and organs function
to create health or disease.
# # #
NOTE TO EDITORS: The APS annual meeting is part of the
Experimental Biology 2007 (EB 07) gathering and will be held April 28-May
2, 2007 at the Washington, DC Convention Center. To schedule an interview
with Dr. Gu, please contact Donna Krupa in the newsroom at
202.249.4174, 301.634.7209 (direct dial), 703.967.2751 (cell) or
DKrupa@the-APS.org.
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