Download General ideas and radical concepts in epigenetics and

General ideas
and radical
concepts in
epigenetics
and DNA
methylation
Research Project, K. Randazzo
Jonathan Gutierrez
12/8/2009
Introduction
In order to understand the ideas behind
epigentics, it is important to understand
general concepts behind basic genetics,
and the inherited information received
from a male and female organism during
reproduction.
The standard explanation of genetics
explains that DNA provides the
instruction to make RNA, and that RNA
creates proteins that control all cellular
activity through protein synthesis and
regulation.
In the past, the general belief in biology,
was that you received a very specific
genetic code
(DNA) from each parent, your mother
passing an X-chromosome along with
her genetic information. The father
passing a Y-chromosome or an Xchromosome, which determines the
gender of the offspring as well as
passing his own unique and specific
genetic traits.
After sexual reproduction and
conception, the newly formed organism
is created through the union of two
haploid cells and combination of
gametes from each contributing parent.
From the point of its conception, the
zygote begins to grow, develops, and
divides. Eventually developing into a
new generation of a particular species.
Possessing similar traits of its elder
generation, and many generations past.
Directly after the creation of a zygocyte, the
cell begins to divide and develop
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independently of its parents. Containing a
genetic “blue print” and all the relative
information to develop into a normal healthy
human being in the refection “mom and
dad” and
Once the child began to develop, it is
predetermined to look a specific way, have
very unique traits, hair color eye color, etc.
On the bad side, be predisposed to
developing a wide range of genetic diseases
and disorders, also contained in the DNA
code.
Recent advancements and research in biotechnologies, are starting to suggest that the
information that you received from your
parents is only half the story. The relatively
new scientific field of epigentics is
suggesting that we have the power to
manipulate the very genetic code passed to
us by our parents that, once believe, was the
ultimate determining factor in our
development
In a sense, our inherited destiny of
hereditary disease, bad teeth, being obese or
having too many freckles.
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Many researcher and geneticists around the
world have begun research studies in the
realm of epigentics for a wide range of
reasons. Many using monozygotic twins
(identical twins) who’s DNA is genetically
identical to the other, to study the changes
that occur in their genetic code and gene
expression as they age.
Epigenetics is a relatively new field of
genetics, that studies chemical alterations on
chromosomes, which result in changes in
gene expression by condensing the
chromosome or affecting the binding of
transcription factors. Methylation of CpG
islands is one such alteration. Twin studies
have opened the doors to understanding how
these changes occur: They’re inherited.
Epigentics answers and creates more
questions. As well as challenges the
everyday view that we are just the combined
image of our parents and DNA does not
have the final word.
Gene expression and general epigenetic
theory
Epigentics or Epigenome translates into
“above the Genome” and can be best
described as anything affecting or
manipulating the genome and gene
expression that is not already encode in
DNA itself.
Epigenetics affects many areas of biology.
In animals, one of the most important
changes happens during embryonic
development. Genes use epigenetics to guide
proper development of stem cells into
different cells of the body.[11]
In some cases, different DNA methylation
effects from the mother and father compete
to determine which parent contributes the
trait. For example, when a donkey and horse
mate, the resulting mule is different
depending on which species was mother or
father. This also explains why individuals
with the same genome, such as identical
twins, exhibit different characteristics,
depending on whose epigenetic effects mom's or dad's- won out in each baby[3]
If DNA really is the predetermined map of
our development and eventually create an
adult from an embryo from its specific “blue
print” as received from each parent.
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In the past gene expression patterns and
translation of genetics information was
thought to be contained with in the DNA, a
set of instructions telling embryonic cells or
stem cell to distinguish itself by developing
into a hepatocyte, skin cell or one of
thousands of different cells contained in the
body. Since 10-20% of genes are “active”
in anyone cell, This prevents genes of one
cell type from being expressed in another,
for example, the gene for eye color is
expressed in the eye, and not in the liver or
skin cells[3] but recent research is beginning
to develop a much more interesting picture
Gene expression. The process by which
information from a gene is used in the
synthesis of a functional gene product.
These products are often proteins, but in
non-protein coding genes such as rRNA
genes or tRNA genes, the product is a
functional RNA. The process of gene
expression is used by all known life eukaryotes (including multicellular
organisms), prokaryotes (bacteria and
archaea) and viruses - to generate the
macromolecular machinery for life. Several
steps in the gene expression process may be
modulated, including the transcription, RNA
splicing, translation, and post-translational
modification of a protein.[2] Gene regulation
gives the cell control over structure and
function, and is the basis for cellular
differentiation, morphogenesis and the
versatility and adaptability of any organism.
Gene regulation may also serve as a
substrate for evolutionary change, since
control of the timing, location, and amount
of gene expression can have a profound
effect on the functions (actions) of the gene]
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in a cell or in a multicellular organism.[2][3
Control of gene expression can be handled
in different ways. Sometimes, small
molecules bind to DNA, changing its ability
to give instructions. These molecules
originate as proteins, protein complexes or
small bits of RNA. For example, in times of
drought, the body produces molecules to
modify DNA and turn on or off genes that
help it endure difficult circumstances.[16]
Giving the organism a very specific trait,
blue or brown eyes, brown hair or a
muscular build.
The Epigentic phenomenon is best
represented in the process of cellular
differation in normal development of a
human child.
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Long before the child’s birth, during the first
few weeks of child development. Stem cell
are going through a process of
differentiation being distinguished into
unique cells, some will become liver cells,
other cardiac cells, among countless others.
Genetically, all these cells are the same.
Each containing genes that the other has.
Skin cells have the necessary gene and
genetic information to become lung cell, or
cardiac cell, or blood cell. With all the genes
being genetically identical and contains all
of the human genome, how does a cell know
how to change into its desired cell? How
does it know what to become?
Since you can not tell the genetic difference
from one cell to the next, yet have many
highly specialized and complex cells with
the body, the process in which each cell
become unique and have very different gene
expression, has been termed -Epigentics.
Through Epigenetic mechanisms, genes that
the cell or tissue does not need are
specifically turned off or “Silenced” and
while gene expression that is necessary to
the functionality and specialization of the
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cell are protected from silencing, by the
same epigenetic mechanisms. The Entire
human genome is passed on to daughter
cells, along with epigenetic information that
keeps the same properties of the parent cell.
re: a liver cell divides into another liver cell
and not a lymphatic cell. Turns out that there
are two different modifications that can
affect DNA. One is a Biochemical
modification that attaches directly to the
DNA, silencing a specific area of genetic
information, The other control the physical
shape of the DNA strand itself by effecting
the protein in which DNA is wrapped, again,
effectually expressing or silencing the
specific trait or gene. In sense a second
genome.... The Epigenome,
Gene Expression through methylation
and histone markers in mice
DNA methyltransferase is an enzyme in
cells that recognizes CpG islands, strings of
cytosines and guanines, and attaches a
methyl group to cytosine. This DNA
methylation is absent during embryonic
development due to the high level of
replication and gene expression. The
alteration is thought to condense the
chromatin around histone, closing off access
to the DNA for transcription factors as gene
expression wanes and is shut off. In fact,
altered methylation patterns are thought to
play a role in the development of some
cancers, which result from aberrant cellular
programming.[22,23][1]
Methylation denotes the addition of a
methyl group to a substrate or the
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substitution of an atom or group by a methyl
group. Methylation is a form of alkylation
with specifically a methyl group, rather than
a larger carbon chain, replacing a hydrogen
atom. These terms are commonly used in
chemistry, and biological sciences.
In biological systems, methylation is
catalyzed by enzymes; such methylation can
be involved in modification of heavy metals,
regulation of gene expression, regulation of
protein function, and RNA metabolism.
Methylation of heavy metals can also occur
outside of biological systems. Chemical
methylation of tissue samples is also one
method for reducing certain histological
staining artifacts.[22]
These Methyl groups are very common and
can be found in foods, house hold chemicals
and environmental pollutants. These methyl
groups if acquired and introduced to the
DNA structure can interfere and affect the
way that DNA translates into RNA, and in
turn proteins and cellular function. The
process is referred to as DNA methylation
and in simple terms, turns gene on and off.
Methyl groups attach to a specific point in
the DNA Strand and inhibit its ability to
translate or express, in a way mask it from
sharing its genetic information.[22]
“If the genome were like the hardware of a
computer, the epigenome would be the
software that tells the computer, how to
work and when.” Randall Jirtle PhD., a
professor of radiation oncology at Duke
University.[24]
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Through his work in the field of epigentics
and the epigenome, Randall Jirtle of Duke
has been able to manipulate the epigenome
in genes of the mice that cause obesity and
hair color, through feeding the mice food
with specific nutrients and toxins. He has
been able to change accumulation of adipose
tissue and hair color in mice that are
genetically identical. Through controlling
the variable in which the mice are
introduced to, mainly diet and nutrition, he
has been able to manipulate the agouti gene
or agouti signaling peptide.
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In mice, the agouti gene encodes a paracrine
signaling molecule that causes hair follicle
melanocytes to synthesize pheomelanin, a
yellow pigment, instead of the black or
brown pigment, eumelanin. Pleiotropic
effects of constitutive expression of the
mouse gene include adult-onset obesity,
increased tumor susceptibility, and
premature infertility. This gene is highly
similar to the mouse gene that encodes a
secreted protein that may (1) affect the
quality of hair pigmentation, (2) act as an
inverse agonist of alpha-melanocytestimulating hormone, (3) play a role in
neuroendocrine aspects of melanocortin
action, and (4) have a functional role in
regulating lipid metabolism in adipocytes.[25]
By feeding a group of mice (group A) a diet
high in methyl groups, he was able to
silence the agouti gene, creating mice with
average body weight and mass (approx 34
grams) and who had dark brown hair
pigmentation. The mice were also less prone
to genetic encourage disease such as cancer
and diabetes. The genetic traits were passed
on to further generations, even of the newer
generations that were feed a normal diet.
They retained the gene expression and
methylation characteristics from parent
mice.
In contrast by feeding a group (group B) of
mice a diet rich in toxins that disrupted and
destroyed the methyl groups given to group
(A) mice, he recorded that they were of a
much lighter pigment and skin color,
although of a normal and average weight in
young mice, as they developed into adulthood, almost 100%of mice suffered from
adult-onset obesity. Weighing an average of
70 gram, almost twice the weight of group
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(A). They had much higher occurrence of
diabetes and other diseases related to a
dramatically increased BMI, Secondary
conditions such as reduced cardiovascular
efficiency and increase in cardiac disease.
As well as arthritis, decreased life
expectancy and other diseases associated
with high levels of adipose tissue.
In a interview with NOVA, and PBS
broadcasting company, Dr. Jirtle, stated,
“this research shows that this potentially has
severe repercussions on our health, and
essentially, the old phrase “you are what you
eat” is true, but you are also what your
parents eat and your grandparents and so on
ate”. He goes on to encourage, healthy life
style changes for future generations, not
only through learned and influenced habits
in our children, but what is genetically
passed on.
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Phenotype expression through Histone
Modification
The second way on which Gene expression
occurs is through DNA physical relationship
with the histone. In biology, histones are
strong alkaline proteins found in eukaryotic
cell nuclei, which package and order the
DNA into structural units called
nucleosomes.[1] [2] They are the chief protein
components of chromatin, act as spools
around which DNA winds, and play a role in
gene regulation. Without histones, the
unwound DNA in chromosomes would be
very long.
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For example, each human cell has about 1.8
meters of DNA, but wound on the histones it
has about 90 millimeters of chromatin,
which, when duplicated and condensed
during mitosis, result in about 120
micrometers of chromosomes.[3]Histones act
as spools around which DNA winds. This
enables the compaction necessary to fit the
large genomes of eukaryotes inside cell
nuclei: the compacted molecule is 40,000
times shorter than an unpacked molecule.
Histones undergo posttranslational
modifications which alter their interactin
with DNA and nuclear proteins.
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The H3 and H4 histones have long tails
protruding from the nucleosome which can
be covalently modified at several places.
Modifications of the tail include,
methylation, acetylation, phosphorylation,
ubiquitination, sumoylation, citrullination
and ADP-ribosylation. The core of the
histones H2A and H3 can also be modified.
Combinations of modifications are thought
to constitute a code, the so-called "histone
code."[9][10] Histone modifications act in
diverse biological processes such as gene
regulation, DNA repair and chromosome
condensation (mitosis).
Through the introduction of methyl group
and other proteins, Scientists have been able
to change the structure of the DNA by
changing or “loosening” the histone.
Differing from the Methyl groups and DNA
methylation, which attach directly to the
DNA strand and inhibit the DNAs’ ability to
produce RNA and functional proteins?
Histone formation is controlled by several
proteins that when introduced to the histone,
change the general structure of the histone,
relaxing or Contracting it. Allowing DNA to
unwind and be “loose “against the histone.
When DNA is in this state, the gene are
easily expressed and are turned “on” where
as the lack of these proteins cause the
histone to contract and tighten up, Hiding a
gene from being expressed. In retrospect,
Turning the gene “off” by manipulating the
protein that cause this effect and change the
tension and mechanical properties of the
histone structure we can control gene
expression. Ultimately choosing which
genes we turn “on” and allow to be
expressed. Genes such as obesity, longevity,
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or hair color. Turning gene off that cause the
over production in cholesterol and other
substances which cause harm in excess or
scarcity.
Epigenetic manipulation through
environmental variables
A certain laboratory strain of the fruit
fly Drosophila melanogaster has white eyes.
If the surrounding temperature of the
embryos, which are normally nurtured at 25
degrees Celsius, is briefly raised to 37
degrees Celsius, the flies later hatch with red
eyes. If these flies are again crossed, the
following generations are partly red-eyed –
without further temperature treatment – even
though only white-eyed flies are expected
according to the rules of genetics.
Environment affects inheritance
Researchers in a group led by Renato Paro,
professor for Biosystems at the Department
of Biosystems Science and Engineering (DBSSE), crossed the flies for six generations.
In this experiment, they were able to prove
that the temperature treatment changes the
eye color of this specific strain of fly, and
that the treated individual flies pass on the
change to their offspring over several
generations. However, the DNA sequence
for the gene responsible for eye color was
proven to remain the same for white-eyed
parents and red-eyed offspring.
The concept of epigenetics offers an
explanation for this result. Epigenetics
examines the inheritance of characteristics
that are not set out in the DNA sequence
This change in phenotype and gene
expression is a direct result on the
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environmental stresses placed in the fruit
flies Histone configuration, believing that
the introduction of temperature variations
inhibited the proteins involved with histone
expression and tension.
in their environment, some of which might
alter their appearance and behavior.
If one committed a crime and unwittingly
left samples for forensic analysis, it would
be impossible to determine the baddie from
DNA fingerprint analysis. However, closer
inspection of their molecules may reveal
significant differences. Although the lads
share the same genes, recent evidence
suggests that some genes might be active in
one twin and not the other. They might be
identical genetically but not
epigenetically.[12] Biochemical fine-tuning
of the genome determines which genes get
switched on, so twins are not necessarily
destined to share the same fate.
Monozygotic twins and Epigenome
Theories,
Since the early 1990s, the scientific
literature has seen studies begin to appear
regarding the disproportionate occurrence of
disease in identical twins, something that
was not completely explained by genetics
alone and leads to questions about how
identical monozygotic twins actually are.
Monozygotic twins arise with an incidence
of 1 in every 250 births worldwide. For
reasons yet unknown, a fertilized egg cell
can clone itself and give rise to separate
embryos. Each will begin and end life with
the same genetic make-up, but as they grow
and develop they will experience differences
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Recent research on monozygotic twins has
revealed that their DNA is marked in
different ways by a tiny molecule called
methyl. So it’s not really true to say that
they are identical. What’s more, these
differences were much more pronounced in
older than younger twins.
As in the studies done at Duke University
under Dr. Jirtle, and knowing that all
organisms on the earth reproduce through
the use of DNA. The biology of this has
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implications to that of human health.
Through understanding of how we develop
disease and how environmental factors
affect our bodies and our development.
Since, the human race is genetically
different, each having genetic information
form our parents, we run into difficulties
testing theories in genetics with everyone
being genetically different and complex but
through homozygotic twins, epigentics has
had some interesting results, all of which are
less then Subtle.
Spain. Began a Research study in Identical
twins, ranging from age 3 to age 74. His
research was aimed to discover how similar
the Homozygotic twins really were...or were
not.
After Collecting tissue Samples from over
40 identical twins and Through DNA
amplification and electrophoresis, they were
able to compare the genes of these twins and
analyze differences between a twins sibling
and other identical twins.
DNA electrophoresis is an analytical
technique used to separate DNA
( Identical twins are so alike that, they have
difficulty understanding mirrors and
reflected images until much later in child
development compared to other children)
In the case of iIdentical twins (homozygotic
twins) are siblings that are also genetically
identical; they are the perfect Lab “humans”
in the case of genetics.
In 2005, Dr. Manel Esteller Director of the
Cancer Epigenetics and Biology Program
(PEBC) of the Bellvitge Institute for
Biomedical Research (IDIBELL) in
Barcelona and leader of the Cancer
Epigenetics Group genetic study in Madrid,
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fragments by size. The DNA molecule to be
analyzed is cut up into variously sized
fragments by reacting it with a restriction
enzyme. These fragments are set upon a
viscous medium, the gel, where an electric
field forces the fragments to migrate toward
the positive potential, the anode, due to the
net negative charge of the phosphate
backbone of the DNA chain. The separation
of these fragments is accomplished by
exploiting the mobility with which different
sized molecules are able to traverse the gel.
Longer molecules migrate more slowly
because they experience more drag within
the gel.
Because the size of the molecule affects its
mobility, smaller fragments end up nearer to
the anode than longer ones in a given period.
After some time, the voltage is removed and
the fragmentation gradient is analyzed. The
DNA fragments of different lengths are
visualized using a fluorescent dye specific
for DNA, such as ethidium bromide.
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“The Twin Studies” and genotype
similarities
Dr. Esteller’s Study suggested that as we
age, our epigenome become different and
change on a regular basis due to outside
influences and pressures. As we age we are
exposed to environmental stresses, nutrition
factors, tobacco and alcohol use, even
climate change and emotional stress. All of
which effect our internal bodies and
homeostasis in some minor or even major
ways.
The gel shows bands corresponding to
different DNA molecules populations with
different molecular weight. Fragment size is
usually reported in "nucleotides", "base
pairs" or "kb" (for thousands of base pairs)
depending upon whether single- or doublestranded DNA has been separated. Fragment
size determination is typically done by
comparison to commercially available DNA
ladders containing linear DNA fragments of
known length.
Gels have conventionally been run in a
"slab" format such as that shown in the
figure, but capillary electrophoresis has
become important for applications such as
high-throughput DNA sequencing.
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When DNA was analyzed through
electrophoresis, and particular genes of two
sets of identical twins from various ages
were compared, they showed dramatic
differences in gene expression similarity.
Through the process of electrophereises,
several genes were collected from each
sibling of a monozygotic twin pair and then
over-lapped with the same genes of their
sibling. And then were compared to see
how identical they really were.
The diagram below show several sets of
genes, over-lapped and in comparison to
each sibling. The yellow represents genes
that are identical, resulting in similar
genotypes and phenotype expression. The
alternate colors represent differences in the
genotype of the individual twin.
Not only does this show that identical twins
are not a perfect copy of their sibling, but it
also suggest that as we age and are exposed
to outside influences, our epigenome
changes to adapt. In looking at the two
diagrams, you can see that the similarities in
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the 3 year old homozygotic twins are much
more similar in gene expression and
genotype than homozygotic twins that are 50
years of age.
Through much greater time period and
exposure to stress, injury and repair, cellular
reproduction and division, variants in
nutrition, exposure to pathogens, and life
style differences. They have grown
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remarkably different. The gene expression
has grown different and unique,
resulting in difference in phenotype of the
individual. This concept helps explain why
one sibling of a homozygotic twin pair,
would develop a disease or disorder that has
strong inherited ties. Such as forms of
cancer and diabetes, when the other sibling
will not. Although leaving the unaffected
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twin at a high risk of developing the disease,
the questions still remain, why would one
develop and disease and the other would not.
DNA methylation and concepts in cancer
Epigenetic inactivation of genes that are
crucial for the control of normal cell growth
are a hallmark of cancer cells. These
epigenetic mechanisms include crosstalk
between DNA methylation, histone
modification and other components of
chromatin higher-order structure, and lead to
the regulation of gene transcription. Reexpression of genes epigenetically
inactivated can result in the suppression of
tumour growth or sensitization to other
anticancer therapies. Small molecules that
reverse epigenetic inactivation are now
undergoing clinical trials in cancer patients.
This, together with epigenomic analysis of
chromatin alterations such as DNA
methylation and histone acetylation, opens
up the potential both to define epigenetic
patterns of gene inactivation in tumours and
to use drugs that target epigenetic
silencing.[6]
Epigenomic analysis of chromatin
alterations in tumours opens the potential to
define mechanisms of epigenetic gene
silencing, and to develop drugs that reverse
transcriptional repression of tumour
suppressor genes and genes associated with
resistence to anticancer therapies[6]
Alterations in DNA methylation are
regarded as epigenetic and not genetic
changes, although epigenetic changes affect
the structure of DNA, they do not materially
affect the genetic code. In recent years,
numerous studies have demonstrated that a
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close correlation exists between methylation
and transcriptional inactivation, supporting
the notion that not only genetic changes, but
also epigenetic changes can contribute to
the carcinogenic process (Strathdee et al.,
2002; Yan et al., 2001). The pattern of
methylation observed in cancer generally
shows a dramatic shift compared with that
of normal tissue. The methylation pattern in
tumors consists of a global hypomethylation,
in conjunction with localized
hypermethylation at CpG islands. This
regional hypermethylation at CpG islands is
associated with the transcriptional
inactivation of cancer related genes.
Recent studies have demonstrated that
hypermethylation of CpG islands may
be implicated in tumorigenesis, acting as a
mechanism to inactivate specific gene
expression of a diverse array of genes.
(Baylin et al., 2001). Genes that have been
reported to be regulated by CpG
hypermethylation, include tumor suppressor
genes, cell cycle related genes, DNA
mismatch repair genes, hormone receptors,
and tissue or cell adhesion molecules. For
example, tumor-specific deficiency of
expression of the DNA repair genes MLH1
and MGMT[8] and the tumor suppressors,
p16, CDKN2 and MTS1, has been directly
correlated to hypermethylation.
Increased CpG island methylation can result
in the inactivation of these genes, resulting
in increased levels of genetic damage,
predisposing cells to later genetic instability
which then contributes to tumor
progression.[5]
Hypermethylation is now the most well
characterized epigenetic change to occur in
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tumors, and it is found in virtually every
type of human neoplasm. Promoter
hypermethylation is as common as the
disruption of classic tumor-suppressor genes
in human cancer by mutation and possibly
more so. Approximately 50% of the genes
that cause familial forms of cancer when
mutated in the germ line are also known to
undergo methylation-associated silencing in
various sporadic forms of cancer.[9]
The more recent work concentrated on
isolating the difference between the gene
sequence and the epigenetic pattern, which
would have a wide reaching affect on
inherited forms of disease. Epigenetics is a
complexity not taken into consideration until
recent years, and may complicate
preventative therapy, prognosis, and
treatment.
Conclusion and personal
thoughts
This concept was very interesting to me for
many personal reasons. Being a twin, I have
always been fascinated in our differences,
although we are only fraternal twins, we
have very little in common, from physical
appearance to personal preference.
Also having a work related background in
oncology and a family that have suffered
loss of a sister to ovarian cancer, when she
was a child, gave me a curiosity in the
concept of epigentics and DNA methylation,
and its role in tumor genesis
I currently work in the field of
cardiovascular genetics and on a daily basis
interact with people that either suffer from
strong inherited disease and disorder, or are
leaders in the field of hyperlipidemia
(Breast cancer cells)
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and lipid science, and there genetic
influences on cardiovascular disease.
I found a great deal of interest in DNA
methylation and lipid disorders, stemmed
from my research on this interesting subject
and plan to continue exploring the subject.
The prevalence of aberrant epigenetic
inactivation of genes in tumors makes it an
attractive target for novel anticancer
therapies and a concept which needs more
extensive research. Several small molecules
are now entering early clinical trials, that
give hope to the belief that we may be able
to cure cancer in the future or promote
longevity.
The concepts behind epigentics research are
new frontiers in genetics research, show us
just how complex we are, from a DNA
perspective, and how little we really know.
increase the life expectancy of the average
human, that we would be able to shake the
hand of one’s grandchildren’s’ great
grandchildren.
Do new questions in ethics arise if we gain
the ability to “plan” a child through
Epigenetic influences, giving our offspring a
desired eye color, physical appearance or
gender specific attributes that are desired by
a general view from society. Would
epigentics bring up the moral dilemma of
“playing god” in contrast to the progression
of science?
I am excited to follow the development into
such a interesting field of science and hope
that we can harness this for the many
benefits that this may offer.
In after thought, since writing this paper, I
find myself overly excited to think of all the
implications and profound effects in the
world today with strong evidence that shows
us that our lives and the nutrition and
environments that we expose ourselves to,
are in a way, rewriting our DNA, and the
way we pass that on to our children and
grand children.
In thoughts toward the future, what if the
science community was to learn how to
control the phenotype expression through
DNA methylation and Histone configuration
with increased accuracy? Would we be able
to cure inherited disease, would cancer be
the next history concept similar to smallpox,
only existing in a test tube? Would we be
able to “ turn-on” the longevity gene and
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