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Lecture Notes Nutrition and Cancer, HNH37806, wur
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Lecture notes of all (guest lectures included) lectures given in the course Nutrition and Cancer in the Bachelor of Nutrition and Health.
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Nutrition and cancer lecturenotes
General introduction
Cancer is one of the most frequent and lethal diseases in the world (1 out of 3 persons in Western
countries is diagnosed with cancer). 19.3 million new patients are diagnosed with cancer each year.
Incidence: new diagnoses/new patients. These data are based on cancer registries, there is almost no
registry in regions with emerging economics. For many cancers, there is still no cure. Therefore, 9.6
million cancer-related deaths occur per year.
Mortality: death rate per year.
50.6 million people alive had cancer diagnosed in the previous 5 years. Prevalence: how common
cancer is (over a time of 5 years), indicates the number of people diagnosed with cancer.
Genes play a role in cancer development, but only 5-
10% of all cancers is ‘hereditary’. The risk of
developing cancer increases due to certain
environmental factors. One of these factors can be
nutrition and physical activity. We need evidence-
based dietary guidelines to prevent cancer.
In the image, guidelines for
cancer prevention can be
seen on a population level, published by the world cancer research institute.
Lecture 1 – Hallmarks of cancer
Metastasis: spread of the tumour across the body. Cancer is a multistep
process, starting with a single cell. Multiple cell types are involved. Cancer
cells are responsive to regulatory circuits of cellular proliferation and cell
deaths.
All cancer types have some characteristics in common:
1. Sustaining proliferative signalling: synthesis of growth factors by tumour cells, synthesis of
growth factors by neighbouring cells. The receptor of the growth factor can also be affected,
for example making it always active, even when no growth factor has bound. The number of
receptors can also change or the downstream pathway can be changed. The signal EGFR is
responsible for growth.
2. Evading growth suppressors: in a healthy cell, there a stop signals
that will stop the cell from growing. Cancer cells (tumour
suppressor cells) can prevent this stop signals, so that the cell will
keep growing. For an example of this, see the image on the right.
3. Resisting cell death: if there is a problem with a cell, there is often
cell death (to remove the faulty cell). There are three ways of
removing a cell, of which apoptosis
(programmed cell death) is the most
common. Necrosis is non-programmed cell
death. The protein p53 is also a damage
, sensor (can recognize for example DNA damage). P53 can induce apoptosis, cell cycle arrest,
DNA repair, differentiation or senescence. Sometimes, with cancer, p53 does not work
anymore and cell death is thus supressed.
4. Enabling replicative immortality: normally, the ends of chromosomes are protected by
telomeres. These telomeres protect the chromosomes from damage. With each division,
these telomeres becomes shorter. When the telomeres are too short, a cell goes into
senescence: the cell is alive, but not active anymore. After senescence, a crisis occurs, where
cell death is induced. Cancer cells can extend the telomeres with the use of the enzyme
telomerase.
5. Inducing angiogenesis: angiogenesis is the production of new blood vessels. Angiogenesis
starts in an early stage of cancer, because the blood vessels are necessary for growth.
Angiogenesis is also useful for the spread of the tumour, metagenesis. Angiogenesis is a
target for therapy. The signal VEGF is responsible for angiogenesis and tumour cells can
express this signal.
6. Activating invasion and metastasis: the spread of
cancer cells via blood or lymphatic vessels to distant
organs. This is a multistep process and each tumour
has its own preference for metastasis. For metastasis,
a tumour has to become invasive, where it grows into
neighbouring cells. Intravasation is when the tumour
cells enter the vessel and extravasation is when they
exit the vessels. This can occur due to the EMT
pathway (epithelial-to-mesenchymal transition).
Most cancers originate from epithelial cells (normally
a very organised structure, facilitated by cell
adhesion molecules) and during EMT these organised cells transform to mesenchymal cells.
These mesenchymal cells are not organised and not attached to each other, they can thus
easily migrate. This transition is possible when the cell is losing the
adhesion molecules.
Stages of the cell cycle: proliferation, differentiation (specialisation of the cells)
and replication.
Growth factor: a phosphate group binds to it, so that it can bind to a receptor.
Emerging hallmark: a characteristic of cancer that seems to be important, but
there is not enough proof yet. An example is deregulating cellular energetics,
where cancer cells use and produce their energy in a different way. Another
example was that cancer cells can avoid the immune destruction.
Immunotherapy is based on this characteristic.
Enabling characteristic: can support the hallmarks but are not specific for tumour cells. An example
of this genome instability and mutation. Mutations can alter the function of proteins, for example
with p53 during cancer.
Tumour suppressor genes: genes that inhibit cell growth (can be mutated in cancer).
Oncogenes: genes that are responsible for cell growth.
Passenger mutations: don’t have an active role in cell growth or inhibiting cell death. The passenger
mutations increase with age.
Driver gene mutation: a mutation conferring a selective growth advantage for a cell. It impacts the
ratio of cell death.
, Tumour-promoting inflammation: can infiltrate immune cells and supply bioactive molecules to the
microenvironment. Inflammation is responsible for tumour inhibition as well as proliferation.
Colon cancer: colons consist of crypts (the holes in the image) with stem
cells at the bottom. The Ki67 protein is a marker for cell proliferation and
is expressed during the active phases of the cell cycle. Detection of this
protein can occur using immunohistochemistry. A low fibre diet can
change this at molecular level, which can result in colon cancer.
For research about cancer, most of the time, blood/urine/faeces/saliva is
investigated because it is easy to investigate and to take (kept in the
refrigerator). However, sometimes, fresh tissue needs to be investigated.
Tissues can be frozen as small samples and kept for a long time. For the
collection of fresh tissue, usually 12 biopsies are performed. The hospital
also has tumour blocks stored.
Struggles and considerations cancer research: clinical procedure and
logistics (where to store), ethical consequences, patient
(pain/anxiety/complications) and data analysis.
Lecture 2 - Cancer screening
CRC: colorectal cancer, a disease that occurs later in life. In case of familial or inherited cancer, there
is no screening but endoscopic surveillance.
Before, around 40% of the people first diagnosed with CRC already had metastasis. Metastasis
significantly lowers the survival chance. Therefore, a screening program (=bevolkingsonderzoek) has
been made for people between 55 and 75.
Screening: a good test for detection of an early stage CRC. The test is a faecal immunochemical
testing, where blood in the stool is identified. This test is called the FIT test.
Problems: hemoglobin in faeces disintegrates, so the longer you store it, the less hemoglobin is
measured. Other colon diseases can also give a positive test and a large part of the population will
not participate. There are also too many people between 55 and 75 to be screened, so the test is
now performed every 2 years.
For screening, the mechanism and course of a disease line must be well known. There also must be a
detectable phase in which treatment can
be more effective than in the later phase.
A polyp is an early phase of CRC. It may
take between 5 and 15 years for a polyp
to evaluate cancer.
With screening, the benefits must
outweigh the physical and psychological risks. The costs must be weighed against the benefits.
Endoscopic treatment: to determine if it is still a polyp or a form of
cancer. A benefit of this treatment is that no operation is needed at
the end. With advanced tumours (when it grows through the
muscular layer), operation is needed, because this cannot be
removed with a needle anymore. If there is metastasis, first
chemotherapy is used to get rid of the metastasis. Metastasis with
CRC is often in the lymphnode or the liver. If the metastasis is very
advanced, it can also be in the lung. During surgery, also parts of
lymphnodes and blood vessels, as well as the tissues of the
metastasis are removed to investigate.
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