Home' Nova National : NOVA NATIONAL OCTOBER 12 Contents Epigenetics
While our parents' diet and
lifestyle have moulded
us to some degree,
we, in turn, can largely
control our health and
wellbeing through our own
choices. Peter Dingle PhD
continues his research
into the emerging field of
18 © NOVA OCTOBER 2012
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Various genetic messages are
'turned on' (expressed) or
'turned off ' (silenced) through
epigenetic processes like DNA
methylation. When turned off, it is as if
a protein glove covers the DNA message
so it can no longer be read or acted
upon. Although epigenetic modification
of our genes is a natural part of our
development and wellbeing, these
processes can interact with various
chemicals in our environment and in
foods and drinks we consume, leading to
the development of disease. Conversely,
epigenetic actions of other compounds
in our environment and nutrition are
thought to hold the key to providing
therapies to fight and prevent disease.
If a genetic mutation for a disease
is 'turned off ' by epigenetic markers,
that particular gene, in such an instance,
cannot cause disease. For example, an
individual may have inherited the genes
for a particular disease; if, however, those
genes are not expressed, the disease will
not develop. However, change to the
epigenetic markers (of a mutated gene)
could cause the mutated gene to 'tune
into' and hence develop a specific
Many human diseases have been
associated with epigenetic modifications
due to environmental exposure. These
include cancer, obesity, diabetes, asthma,
multiple sclerosis, mental illness and
behavioural disorders, as well as premat-
ure ageing 1,2,3,4.
Humans are most vulnerable to
epigenetic changes during the develop-
ment of the embryo in the womb,
embryogenesis, where epigenetic disrupt-
ions can be passed down through
multiple generations 5. One study on
diethylstilbestrol (DES), an environmental
oestrogen, found that DES induced a
genetic predisposition to a certain cancer
and congenital birth defects that was
passed down two generations 6. Similarly,
foetal exposures to plasticisers such as
bisphenol A, a chemical found commonly
in plastic, contribute to epigenetic changes,
which lead to immune abnormalities.
Maternal smoking leads to increased
pulmonary disease in adulthood including
asthma; and certain therapeutic drug
exposure leads to vascular defects.
These can all be classified as epigenetic
During the past decade, evidence
has accumulated showing that apart
from genetic alterations (mutations),
epigenetic alterations play a major role in
the initiation and progression of cancer 7.
Human cancers arise from a multi-step
process characterised by tumour initiation
and progression 8, but only 5% of cancers
can be attributed to heredity. Genetics
alone cannot explain all of the properties
of cancer. It is now understood that epi-
genetic abnormalities and the turning off
and on of certain genes play a major role
in tumour genesis -- the development of
and proliferation of tumours 9,10.
Cancer, which is caused by uncontroll-
ed cellular growth, is induced by mutat-
ions in the DNA, which can be initiated
by errors in the DNA or foreign
chemicals called carcinogens. In addition
to uncontrolled cellular growth, a
characteristic of cancer is inhibition of
normal programmed cellular death, called
apoptosis. When the body's DNA makes
mistakes in a cell, the mistakes are either
fixed by additional DNA repair mechan-
isms or the cell is destroyed to prevent
further damage (apoptosis). Unfortunately,
the genes that are responsible for destroy-
ing rogue cells can be silenced (turned
off) through epigenetics and, as a result,
mistakes in the DNA cannot be rectified
before they spread. The genes associated
with cellular pathways that are prone to
cause cancer are called oncogenes. The
silencing of tumour-suppressing genes,
activation of oncogenes, and defects in
DNA can be caused by epigenetic mechan-
isms, which can affect several, if not
many, of the steps in a cancer line 11.
We have literally removed the various
roadblocks to formation of cancer. Many
of the genes that are inactivated by
methylation in carcinogenesis have classic
tumour-suppressor functions or play a
critical role in cell cycle control (repair of
damage to DNA) apoptosis, differentiation,
angiogenesis, metastasis, growth factor
response, drug resistance and detox-
ification 12. An incorrect change in the
methylation of the DNA caused by
epigenetic carcinogens is the most
common activation of cancer cell lines.
Although methylation changes occur to
different genes depending on the type
of cancer, all cancers undergo changes
in methylation, suggesting DNA methy-
lation is a major factor in tumour
development and can be used as a genetic
marker in tumour development 13.
To put this in perspective, methylation
in some areas of the DNA, called CpG
sites, in some tumour suppressor coding
regions contributes to as much as 50% of
all inactivating mutations in some cancers
and 25% of cancers in general.
In contrast to genetic changes in
cancer, epigenetic changes are gradual in
onset and are progressive. Their effects
are dose-dependent and are potentially
reversible which increases the scope for
the development of epigenetic therapies
for disease 14. These observations pre-
sent new opportunities in cancer risk
modification and prevention using dietary
and lifestyle factors, as well as treatment
as you will see below. In this regard,
folate, a water-soluble B vitamin, has been
a focus of intense interest because of an
inverse association between folate levels
and the risk of several malignancies (in
particular, colorectal cancer) and because
'Epigenetic actions... in our
environment and nutrition are
thought to hold the key to
providing therapies to fight and
'Humans are most vulnerable
to epigenetic changes
during the development of
the embryo in the womb,
(Read Part 1 "Beating our Genes" in our September issue 19.7 at
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