CANCER

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CANCER
BY
SIR. SEMWEZI ENOCK
Cancer affects many people in many different ways. You may be a carrier or a sufferer wanting to know more about how and
why the disease occurs
Cancer results from the uncontrolled proliferation of cells in certain tissues in the human
body.
The onset of cancer can be triggered by:



Long term exposure to certain viral infections
Chemical carcinogens
In a small minority of people, by an inherent mis-wiring in the cells,
All of which can destabilize the delicate balance that controls how a cell



Divides (proliferation),
Changes into new cells (differentiation)
How a cell dies (apoptosis).
NB: Cancer cannot spread from one person to another (like the common cold for example, which is
spread by viruses). Cancers arise from cells within our own bodies.
DID YOU KNOW THAT?
That normal cell are transformed into cancers as a result of changes in these genetic networks at the molecular,
biochemical and cellular level.
Almost all known animal species on the planet can develop cancer.
The only species that we know of, that is highly resistant to developing cancer, is an extraordinary rodent called the
naked mole rat. These tiny rodents (each one weighs less than 35g), also happen to have an exceptionally long life
(about 28 years). They have a special type of sugar called hmm-ha (high molecular mass -hyaluronan).
This glue-like molecule make the naked mole rat cells particularly sticky, preventing cell overcrowding and forming
tumours.
What is cancer?
Cancer is a disease that involves changes or mutations in the cell genome.
These changes (DNA mutations) produce proteins that disrupt the delicate cellular balance between cell
division and quiescence, resulting in cells that keep dividing to form cancers.
Already known causes of cancer include:
cigarette smoking is associated with a high risk of developing lung cancers.( hydrocarbons again in the
tar)
age, almost 60% of all cancers that you see around the world is linked to age. And this is found typically
in people over the age of 65. So this is a very clear cut evidence that the longer you live, there's an
increased risk of getting cancer
obesity, lack of physical activity, high calorie diets, all of which increases the risk of getting certain types
of cancers.
Viruses can be a big role causing cancer;e.g. Cervical cancers. Where the infection with a virus
called as the Human Papilloma Virus has shown to be a causal agent for developing cervical
cancers in women.
The good news is that
It's not simply one single infection with HPV that gives you the cervical cancer. You need a lot
of hosts of contributing factors and that includes things like a long sexual history with the
different partners, diet, life style, smoking, all of which can increase the risk of getting cervical
cancers in women who have been infected with HPV.
GENES
The gene, the genome and you
A gene is a section of DNA that, once transcribed and
then translated, codes for a protein. DNA stands for
DeoxyriboNucleic Acid.
The genome is all of the DNA in a cell that specifies the
form and function of an individual organism. Most cells
contain a complete genome in the form of multiple, linear
DNA molecules, compacted into chromosomes.
A gene is a subset of the genome that is switched on (ie
expressed) by the cell to make mainly proteins, and a cell
can make hundreds of proteins through more than 20,000
genes. Proteins are the building blocks of a cell. A properly
functioning cell is controlled by genes, which produce the
correct subset of proteins, at the correct times, in the correct
amounts, and in the correct places. Some proteins also
act as switches, turning genes on or off, which in turn
can dictate how a cell behaves.
Correct gene expression is essential for
 normal cellular function.
 Cell growth and division is part of normal function.
What is epigenetics and why is it important in cancer?
it is now described as a mechanism through which the
expression of a gene can be controlled without affecting
the sequence of DNA. Rather, epigenetics controls the
packaging of DNA and how it is accessible for gene
expression.
Epigenetics controls the expression of genes. This is done
either by:

turning the gene on or off by simply adding a chemical
tag or mark on DNA (such as a single methyl group to a
cytosine) or

controlling how DNA can be unwrapped to enable
access to key genes. Packaging DNA into structures
called chromatin is important for compressing the
massive human DNA inside a micrometer-sized cell. In
order for a gene buried deep inside this chromatin to be
expressed, DNA needs to unwrap first to allow access
by the synthesis machinery. Specialised proteins
control the wrapping and unwrapping of DNA and
genes.
Epigenetics is key to normal cellular processes, for
example, during development, through the inactivation of
one of the two X-chromosomes in females or ensuring that
the same chemical marks / tags on the DNA are passed on
from the mother or father to the offspring (imprinting) or
during cell division. Exciting recent research also shows that
epigenetic marks can arise from environmental factors
including diet and smoking.
To summarise, the genome contains the DNA sequences
which form genes, whereas the epigenome includes
chemical modifications on the DNA itself and/or histone
proteins, which affect DNA packaging and gene expression.
epigenetics can also alter the expression of genes resulting
in the growth of cancer cells. Epigenetic silencing of cancerrelated genes occur in a number of different ways. Genes
may be silenced by the addition of chemical marks (like
methyl groups) in the promoter region of a tumour
suppressor gene. A promoter is a region of DNA located in
front of any gene and which controls gene expression.
Therefore, if the promoter of a tumour suppressor gene is
switched off by the chemical mark, the protein will not be
made and therefore the brakes on cell division is removed.
Alternatively, the tumour suppressor genes may be
compacted tightly within the chromatin, preventing them
from being expressed.
A potential avenue for cancer therapy would be to enable
access to these tumour suppressor genes, by inhibiting
enzymes that wrap or compress DNA. Some examples of
successful inhibitors of these DNA compaction enzymes
are azacitidine, an inhibitor of DNA methylation,
and eninostat, an inhibitor of histone deacetylation. Used in
combination this treatment prevents DNA methylation from
occurring and also prevents chromatin compaction,
therefore ensuring that genes can be expressed. The
efficacy of this treatment was shown recently in lung
cancers where patients showed a total response following a
one year course with combined epigenetic therapy
of azacitidine with eninostat.
DNA mutations and rogue cells
Cancer is a heterogenous disease, involving an
accumulation of multiple mutations in a multi-step
process. Tumours are not simply a group of cells that
divide uncontrollably, but a complex tissue with
different cell types all of which actively work together.
DNA mutations result in defects in the regulatory circuits of
a cell which disrupt normal cell proliferation behaviour.
However, the complexity of this disease is not as simple at
the cellular and molecular level. Individual cell behaviour is
not autonomous and usually relies on external signals from
surrounding cells in the tissue or microenvironment. There
are more than 100 distinct types of cancers and any specific
organ can contain tumours of more than one subtype. This
provokes several questions.
1. How many of these regulatory circuits need to be
broken to transform a normal cell into a cancerous
one?
2. Is there a common regulatory circuit that is broken
among different types of cancers?
3. Which of these circuits are broken inside a cell and
which of these are linked to external signals from
neighbouring cells in the tissue?
The answers to these questions can be summarised in a
heterotypic model, simplified down to a few fundamental
concepts that alter the internal cell circuit and cell
physiology, that was first proposed by Douglas Hanahan
and Robert Weinberg. These fundamental concepts
or Roads to Cancer will be covered over the next two
weeks. This currently accepted model can be best
described using a traffic light analogy.

Produce ‘Go’ signals:
Normal cells carefully control how and when they
divide. This control is critical to maintain the normal
tissue structure and function. Cancer cells, on the other
hand, disrupt this control by producing and releasing
their own chemical signals (or GO proteins) that keep
the cell division ‘switch’ on for much longer. Examples
of these ‘Go’ proteins are growth factors that will bind to
proteins on the surface called receptors and will allow
continued cell proliferation (covered in more detail
in Step 2.4).

Override ‘Stop’ signals:
Again, cell division in normal cells is usually kept in
check by proteins that put the ‘brakes on’, so called
growth suppressors or Tumour Suppressor Proteins.
Cancer cells cleverly bypass these brakes, or
deactivate these STOP proteins, in order to continue
dividing (Step 2.4).

Defying death:
Cell death is part of life in normal tissues. A normal cell
will be told to kill itself if the cell division conditions are
not ideal, or if the cell has sustained excessive damage
to its DNA (due to exposure to DNA damaging agents)
or simply if there is too much or inappropriate cell
division. Cancer cells however, produce proteins that
sneak past or knock out these death-inducing proteins
and allow them to grow and divide (Step 2.7).

Keeping the supply lines open:
Angiogenesis means stimulating new blood vessel
growth. Cancer cells will not be able to sustain their
own growth without their blood supply (blood vessels
that carry oxygen and nutrients). Therefore, cancer
cells secrete factors that stimulate new blood vessels to
expand alongside their own cell division (Step 3.2).

Spreading out – Metastasis:
This is the final stage in which cancer breaks through
the tissue barrier (stroma) and spread through the
bloodstream and lymphatic system to colonise tissues
in remote sites. A vast majority of death in cancer is
due to metastasis (Step 3.4).

Others:
A host of new concepts have also been implicated in
cancer development and progression. This include the
idea of the cancer stem cell (CSC). This concept posits
that cancer arises due to disruptions in differentiation.
Differentiation is the process in which a stem cell is
instructed to change or differentiate into a specialised
cell such as a heart cell, liver cell, neuron etc. An
increasing number of tumours now show
subpopulations of CSCs, adding weight to the idea that
cancers arise due to disrupted differentiation signals
Cell signalling, oncogenes and
tumour suppressors
Chemical signals and cancer cells
Cell signalling involves the release from one cell of a
chemical signal that is recognised by other cells,
usually because the recipient cell possesses a receptor
that is highly specific for the signal molecule.
Signalling, or cell communication, is required to co-ordinate
cell behaviour and is particularly important in organisms
made up of many tissues and cell types. Multicellular
organisms depend on cell signalling for correct
development, tissue maintenance and homeostasis. Signals
may instruct cells to survive or to die (through programmed
cell death or apoptosis), to differentiate and become a
specialised mature cell type, or to divide (proliferate). These
instructions are part of the normal processes of
development and tissue renewal (eg in skin or gut), and can
each go wrong in cancer.
Signal-receptor interaction starts a chain of molecular
changes within the cell. The molecular relay or intracellular
signalling pathway allows amplification of the signal and
dispersal of the signal to different parts of the cell to bring
about changes in cell behaviour. Tight control is needed
over cell division (proliferation) to maintain tissues of the
correct size and containing the correct cell types to perform
the normal functions of that tissue. Dividing cells are said to
go through the cell division cycle.
To begin, the cell cycle signals are needed that promote the
transition from the resting phase, G1, to begin the synthesis
of DNA in S phase (when each of the chromosomes are
copied in preparation for cell division). In cancers, one or
more of the signalling components becomes activated
inappropriately, usually as a result of gene mutations. The
mutated genes are known as oncogenes, which produce
hyperactive forms of signalling proteins that can promote
cell division in the absence of the correct signal.
Tumour suppressor genes normally function to stop cells
from beginning the cell cycle. They produce cell cycle
regulators that usually function to keep the cell in check until
the correct signals for cell proliferation are received.
Mutations in tumour suppressor genes also occur in cancer
cells, which can then more easily begin the cell cycle
without the proper instructions.
Cancer cells escape the normal controls over cell survival,
proliferation and organisation. Cancers go through a series
of different stages as cancer cells acquire successive
mutations in oncogenes and tumour suppressor genes.
Excess proliferation of cells within their original tissue can
lead to the formation of a benign tumour.
Accumulation of further mutations in key genes can lead to
cells invading surrounding tissues, when the tumour is said
to become malignant. Malignant tumours can cause
damage that may be life-threatening, including spreading to
other parts of the body in a process termed metastasis.
These events occur due to a series of mutations in genes
that normally regulate cell proliferation, survival and
organisation within tissues.
How cancer cells defy death
Death is a part of life, and this is also the case in
tumours.
By the 1960s, we knew that spontaneous loss of tumour
cells was part of the process of growth of tumours. In 1972,
three scientists (Kerr, Wylie and Currie) proposed that
cancer occurs not simply because of excessive cell
proliferation, but also due to reduced cell death.
In the first session this week, we explored some of the roads
to cancer and how normal cells will kill themselves rather
than tolerating irreparable damage to their DNA. We shall
now examine how cancer cells defy death. Before we do
this, I would first like to explain how cells die.
There are two common ways this can happen:
1. Necrosis: This is a really messy way for a cell to die
and typically happens to cells in injured tissues
(untreated wounds, frostbite, chronic infections etc).
The cells swell up and burst, spilling all the contents
outside. This leads to an inflammatory response and
the process is uncontrolled. If left untreated, necrotic
cells can lead to a build up of decomposing tissues, in
turn leading to gangrene.
2. Genetically-controlled Programmed Cell Death
(PCD): Among the most common form of PCD is
apoptosis (from the Greek for falling leaves). This is a
highly-controlled operation, dictated with almost
military-precision by genes. No messy spilling, no
inflammatory response, the cell simply dismantles itself
systematically, like taking down the scaffolding from a
building. The DNA and cellular components are
packaged neatly into little bodies called
‘apoptosomes’. All evidence that a cell ever existed in
that location is removed completely AND (this is
fascinating bit) this is usually done by a neighbouring
cell or by an immune cell called a phagocyte, which
eats up this dying apoptotic cell. Another form of PCD
that is getting a lot of attention is autophagy (literally
eat oneself). This is the typical response of a starving
cell trying to protect itself by degrading some of its
internal proteins by organelles called lysosomes.
So now that we have looked at ways in which cells die, lets
look at how tumours develop due to reduced cell death.
One of main pathways that is disrupted in cancer cells is
apoptosis. Apoptosis is normal. Hundreds of cells in our
body die regularly due to apoptosis, eg during development.
Did you know we were all born as ducks? We all had
webbed fingers early in our development in the womb.
Apoptosis instructs the cells in the webbing of our fingers to
kill themselves, and that is how our fingers are sculpted into
digits!
The same apoptotic process also happens in fine-tuning our
immune system or in getting rid of the unfertilised egg
during the menstrual cycle.
Controlling the process of apoptosis is critical and any
disruption can lead to either:

Too much apoptosis (like when brain neurons die in
Alzheimer’s disease), or

Too little apoptosis, as we find in tumour development
and metastasis or spread.
Apoptosis is hard-wired into every cell, like a ticking time
bomb, only switched on
by gatekeeper or guardian proteins called tumour
suppressor proteins (such as p53 or retinoblastoma, which
we covered in the Step 2.4).
In cancer cells, these tumour suppressor proteins cannot do
their job because of mutations or inhibitors (such as viral
oncoproteins) prevent apoptosis being switched on and the
cells in the tumour will continue to grow.
If you are interested, further information about the specific
genes and proteins and the pathways involved are provided
in the links below.
In the next session, we will look at other ways that tumours
develop and grow.
Angiogenesis: how cancer cells switch on the blood supply
One of the main pathways to cancer development is
angiogenesis.
Angiogenesis can be defined as the formation of new
capillaries from pre-existing blood vessels by migration and
proliferation of specialised cells, called endothelial cells,
which form the inner wall of the blood capillary. It is a key
step in a number of physiological processes such as wound
healing or the female menstrual cycle. In tumours however,
angiogenesis is responsible for the growth of the tumour,
invasion and spread (metastasis).
How do tumours switch on angiogenesis?
Like all normal tissues, tumours are also dependent on
oxygen and nutrients provided by the blood vessels
(capillary microvasculature). However, endothelial cells do
not normally proliferate and therefore, initially, the growth of
the tumour is restricted (usually no more than a few mm3 in
size). In the later stages, with subsequent mutations, tumour
cells release proteins (called angiogenic factors) that
stimulate the proliferation of endothelial cells to create a
new vasculature of their own. This tumour neo-vasculature
triggers a rapid expansion and growth of tumour cells.
In most normal tissues, proliferation of endothelial cells is
tightly regulated through the production of naturally
occurring pro-angiogenic factors (such as VEGF – vascular
endothelial growth factor) and angiogenic inhibitors (such as
endostatin). The levels of angiogenic inhibitors predominate,
thereby keeping blood vessel growth in check.
Consequently, the structure of vasculature in healthy tissues
is regular and fed by straight vessels that branch into
smaller capillaries and microvessels.
Tumours flip this angiogenic switch by releasing angiogenic
factors, which results in the stimulation of angiogenesis.
This neo-vasculature in tumours is disorganised in every
aspect of their structure and function. They are tangled,
irregular, oversized, leaky and with areas that may lack
these microvessels altogether. The blood flow may be brisk
in one part of the tumour but static in another, or flow in
reversible directions. The major consequences of this erratic
vasculature are:

Uneven drug delivery, which results in either the drugs
being ineffective or the tumour cells becoming resistant
to the effectiveness of the drug

It increases the chance of the cancer cells spreading to
other locations (metastasis).
What are the molecular mechanisms underlying angiogenesis in tumours?
Angiogenic factors released by tumours, such as vascular
endothelial growth factor (VEGF), activate endothelial cells.
This results in the secretion and activation of a special class
of enzymes that breaks down the surrounding tissue protein
matrix, called matrix metalloproteinases (MMPs). MMPs
break down the thin outer lining of the blood vessel, called
the basement membrane. The endothelial cells of the blood
vessels are now free to migrate towards the tumour cells
and proliferate into the space created by the action of the
MMPs. Another class of receptors, called integrins, that are
found on the surface of the endothelial cells, act as the
‘velcro’ by pulling the cells towards tumour cells. These
newly formed microvessels secrete further growth factors,
such as platelet-derived growth factor (PDGF), which attract
supporting cells and the eventual expansion of the capillary
network.
Anti-angiogenic targets for treating cancer
Drugs targeted at inhibiting angiogenesis have had some
success in Clinical Trials. Avastin® (bevacizumab), which
neutralises the angiogenic factor VEGF, was shown to be
effective against recurrent glioblastoma (a type of brain
tumour). Sutent® blocks the receptor for VEGF. However,
some cancers have shown to be unresponsive to anti-
angiogenic drugs; Avastin® was ineffective against colon
cancers.
Key concepts

Angiogenesis is the formation of new blood vessels.
This process is activated by cancer cells to enable
tumours to grow in size

In most tissues, angiogenesis is switched off by large
amounts of anti-angiogenic proteins

The vascular network in tumours is irregular, oversized
and leaky, resulting in increased risk of spread and
developing resistance to drugs

Cancer cells release angiogenic factors which stimulate
blood vessels to divide and expand to form vascular
networks

Anti-angiogenic drugs target these factors to stop
expansion of blood vessels.
Metastasis: when cancer cells spread
What is metastasis?
Metastasis is the spread of cancer cells throughout the
body. It is the most common cause of death from
cancer but it still remains one of the most poorly
understood areas of cancer research.
Most solid tumours are either benign or malignant. Benign
tumours can grow and have all the features of cancer we
have highlighted so far butthey are always contained within
the tissue basement membrane, with defined shapes,
whatever their size.
Malignant tumours (cancers), by contrast, break through the
basement membrane barrier and pass into the blood
vessels and metastasise. Cancer invasiveness represents
one of the first stages of metastasis, which is the spread of
cancer cells throughout the body and the colonisation of
distinct, often distant tissues.
The metastatic process
Metastasis is an inefficient process, which can be broadly
divided into the following 6 stages:
1. Localised invasion: This involves the growth of the
primary tumour and breaking out through the basement
membrane.
2. Intravasation: Tumour cells squeeze through the
capillary wall and into the blood and lymph. A vast
majority of tumour cells do not survive this harsh
environment because of their interaction with the blood
components, including lymphocytes of the immune
system.
3. Transport through circulation and arrest in
microvessels of secondary organs: Tumour cells
that do survive now accumulate in areas of sluggish
circulation in the body, such as the microvessels in the
lungs, liver etc. This is also one of the reasons why
heart cancers are rare.
4. Extravasation: Tumour cells squeeze back out of the
blood vessel into the surrounding tissue.
5. Formation of micrometastasis: The process of
growth and proliferation, without the induction of
angiogenesis
6. Formation of macrometastasis: The last stage of
actively growing and angiogenic tumour.
Studies have shown that after extravasation, a subset of
tumour cells may remain either as:

dormant, solitary cells

dormant, pre-angiogenic micrometastasis or

actively growing, angiogenic metastasis.
It is usually the active, angiogenic metastatic tumour that is
clinically detectable with imaging.
The molecular genetics of metastasis
Metastasis is a complex process controlled by molecular
genetic pathways that are either inherent in the tumour cell
or dependent on a more complex interaction between these
tumour cells and cells from the host tissue/organ (tumour–
host interaction). The inherent genetic pathway underlying
metastasis is often due to the abnormal expression of genes
that are not essential, but are usually switched on during
stress conditions. The genes themselves remain typically
unchanged, but the levels of the protein that they express
usually change.
In order for a cancer cell to metastasise, it must have two
essential functions:
1. Invasiveness, which allows tumour cells to break
through the tissue basement membrane of the main
tumour, surviving the harsh environment of the blood
and lymph, reach the capillary bed of the target organ
and form a secondary metastasis at the second site.
The key molecular genetic switch needed for invasion
is EMT (epithelial-mesenchymal transition), wherein
tumour cells switch on the expression of proteins
needed for this role. They reduce proteins that enable
them to stick to the matrix (eg E-cadherin) and
overproduce proteins that enable degradation of the
matrix (MMPs) and motility (integrins). You may recall
these proteins from the earlier session on
angiogenesis.
Intriguingly, this switch is reversed after the cancer cells
have reached the secondary target tissue, called MET
(mesenchymal-epithelial transition). This reversal
enable cancer cells to now colonise the secondary site
and form micro- and macro-metastatic tumours.
2. Anchorage-independent survival enables tumour cells
to survive the harsh environment in the blood and
lymph, without the need of a scaffold to hold on to. This
is in contrast to normal cells, which usually die from a
unique type of cell death called anoikis when they lose
contact with their surrounding matrix.
Genetic programs that confer these properties of
invasiveness and anchorage-independence are absent in
benign tumour cells.
The cancer stem cell and other genetic pathways to cancer
Most human cancers are complex tissues arising from
the clonal selection of subpopulations of cells with
distinctive genetic heterogeneity. As we have seen from
the clonal origins model, most tumours show varying
degrees of differentiation, mutations, vasculature or
metastatic potential.
Recent research suggests an alternative, but not mutually
exclusive, explanation for this tissue heterogeneity, termed
cancer stem cell (CSC) theory. This is based on the
observation that, in some tumours but not all, cells show
abnormal differentiation. The diverse subpopulations of cells
in tumours represent cells at different stages of
differentiation.
Generally, differentiated cells in adult organs have a finite
lifespan, ranging from days (intestine and skin), months (red
blood cells) to decades (neurons and memory-type
lymphocytes). Dead cells are replaced by adult stem cells
which have two essential properties, self-renewal and
differentiation. Remarkably, an adult stem cell can do both
in one go, through asymmetrical cell division. When an adult
stem cell divides to form two daughter cells, one of them
retains all the stem cell properties (self-renewal) while the
other is committed to differentiate into a specialised cell
(such as a liver or heart cell). Adult stem cells tend to divide
very rarely, in stark contrast to differentiated cells which
divide rapidly (called progenitor cells or transit-amplifying
cells).
The rapid division of the progenitor cells is soon exhausted
and the cells become terminally differentiated (ie do not
divide but perform specialist functions, such as a neuron).
CSCs arise due to the oncogenic transformation of normal
adult stem cells in any of these stages. Initially implicated in
metastatic blood cancers, CSCs have now been also
implicated in certain types of breast and colon cancers.
Other genetic pathways
The genetic pathways of cancer development listed below
are based on some of the recent research in the area but
are yet to be fully validated and accepted by the global
research community. Hence, these are categorised as
emerging pathways:
1. Evading the immune system: Almost all cancers
show the presence of cells of the immune system at
varying densities. Their presence suggests an antitumour response by the immune system to eliminate
the aberrant cells. However, there is compelling
evidence which suggests that, paradoxically, the
inflammatory response by the immune system
exacerbates cancer progression, by supplying
molecular mediators (such as growth factors,
angiogenic and invasive factors) which increase
proliferation, growth and spread of tumours.
2. Genetic reprogramming of cellular metabolism: The
uncontrolled cell division that defines cancer also poses
a huge demand for energy resources to fuel this
growth. Otto Warburg was the first to notice that cancer
cells reprogram their glucose metabolism pathway to
sustain the rapid cell proliferation. Glucose is broken
down (glycolysis) even when oxygen levels are low
(aerobic glycolysis). One of the ways cancer cells do
this is by increasing the number of glucose transporters
(Glut1) which import glucose into the cell.
3. Immortality of cell division: Another defining feature
of cancer cells is their ability to divide endlessly, unlike
normal cells, which undergo senescence (stop
dividing). An internal clocking device, the telomeres
(hexameric DNA repeat sequences, which protect the
ends of chromosomes) determines how many times a
cell can divide, but usually gets shorter every time a cell
divides. Telomerase, the enzyme that adds telomeres,
is usually absent in normal cells but is functionally
active in more than 90% of immortal cancer cells.
To summarise, some of the key molecular genetic pathways
to cancer development involve oncogenes that maintain cell
division, dysfunctional tumour suppressor genes, antiapoptotic genes that resist cell death, pro-angiogenic genes,
and genes that activate invasiveness and metastasis.
Emerging pathways include altered energy metabolism,
genome instability and inflammation. A broad understanding
of these key genetic pathways will help further our research
into treating human cancer.
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