Download Carcinogenesis Powerpoint!.

Mary Fairbanks
Jadaede Charles
Hembly Rivas
Amy Worth
 Carcinogenesis
is the development of tumors
due to alterations in the cells structure. Most
alterations can develop due to facts we face
day by day. In our environment we can be
exposed to harmful substances that can
affect us in the cellular level through food,
water, sun exposure, or our neighborhood,
pollutions and so on. Everything from your
diet to prescribed medications can have
cancerous effects on your body.
 We
chose this question in order to shed light
on the sources that have actually been
observed as having direct correlations to
cancer development. This quashes the
complacent belief that, “Everything causes
cancer.”
 Due to our research, we have realized that
though many aspects of life expose us to
environmental carcinogens, how much
exposure, and the malignancy of the
carcinogen affect the likeliness that an
individual will develop cancer.
 Industrial
Waste
 Medical
Treatments
 Natural
Sources
 Diet
 Industrial
waste can be products or
chemicals introduced to the environment
that originally were not there. If chemicals
are dumped in a river the long terms affect
can alter the river's food chain structure,
animal's DNA structure by impairing or
changing production of proteins, and or
eventually lead to contamination in nearby
oceans.
 Radiation
is one of the many treatments of
environmental carcinogenesis. It mutates
cells as well as sterilizes them. No cancer
can arise from cells that have received high
doses of radiation.
 Hydantoin (glycolylurea) modifies the
immune response by reducing the humoral
response leaving the cellular response
practically intact. This treatment has an
inhibitory effect on tumor growth.

UV! (Or Ultraviolet Radiation)
The cause of the most common type of cancer,
Nonmelanoma skin cancer, is the solar ultraviolet radiation
emitted from the sun naturally to all of us. UV in sunlight
can cause 3 different types of skin cancer and can be a
tumor promoter as well as initiator.
The UV induced DNA damage is attributed to the formation
of pyrimidine dimmers in between the adjacent pyrimidine
bases of DNA. If the damage due to the dimmers is not
immediately repaired, the growth regulatory gene, p53,
may mutate and contribute to tumor development. UVB
has been known to cause Considerable damage to the DNA
in skin but its UVA that has been shown to induce the
pyrimidine dimmers and oxygen and nitrogen reactive
species which damage DNA.

Radon!
Radon is a cancer causing radioactive gas that is
naturally formed from the breakdown of uranium in
soil and rocks. It is the leading cause of lung cancer
for non smokers and second leading for smokers.
Radon affects so many lives because it seeps into
homes through cracks in the basements, foundations
and floor drains.
The alpha particles emitted by radon bombards a
cell, producing chemical radicals that enter the cell
and cause DNA damage. The cells are usually killed or
sterilized but can sometimes survive as damaged
cells. The damaged cell can then reproduce in a
cancerous manner.

Nitric oxide!
Nitric oxide is a pollutant as well as a natural molecule. It
can be produced by combustion of substances in air such as a
car’s engine. It can also be created by more natural
processes for example lightning’s high temperature can
catalyze molecules of oxygen and nitrogen to form it and the
human body can also produce it. Because of the different
ways it can form, nitric oxide is a natural source of
carcinogenesis but not always a source of environmental
carcinogenesis. The human body produces it from L-arginine
by the catalyst
NO syntheses. Nitric oxide is a signaling molecule, that is, it
transmits information between cells by interacting with the
receptors thus triggering responses.
Some sources environmental carcinogenesis in relation
to diet includes eating cooked meats, and alcohol
consumption. Though the protein and nutrients we can
often only find in adequate consumption of meat are
highly beneficial for our bodies, studies have shown that
eating char-broiled foods, or meats, are a major
contributor to adduct in the blood, which lead to
carcinogenesis of healthy cells into cancerous ones.
 The well-done cooking of meats and fish provides
increased exposure to heterocyclic amines, compounds
formed from the pyrolysis of creatines and amino acids,
suspected colon and breast cancer carcinogens.
(Pyrolysis is the anaerobic process of thermochemical
decomposition of organic material at increased
temperatures, it’s a process involved in charring.)


Polycyclic Aromatic Hydrocarbons (PAHs): They’re atmospheric
pollutants that consist of fused aromatic rings, not containing
heteroatoms or carrying substituents. (Heteroatoms are any atoms
that do not contain carbon or hydrogen. Carrying substituents
refers to an atom or group of atoms substituted in place of a
hydrogen atom on the parent chain of a hydrocarbon.)

PAHs occur in oil, coal, and tar deposits, and are produced as
byproducts of fuel burning (whether fossil fuel or biomass), while
also being found in food products and diet. While PAHs are found in
vegetables and cooked meats, the larger intake comes from
cereals, oils, and fats. They’re especially dangerous due to the
fact they’re carcinogenic, mutagenic, and teratogenic. (Mutagenic
means that they change genetic material and increase the
frequency of mutations while teratogenic refers to the interference
of the development of a fetus, they cause birth defects.)
 Will
there ever be a total cure for cancer?
Since there are carcinogenic elements in many,
if not all, facets of everyday life, is there
any way to avoid the developing the
expensive condition of cancer? We can
lessen our exposure, but we have no way to
totally protect ourselves. (That we’ve
discovered so far anyway…)
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http://www.ncbi.nlm.nih.gov/pubmed/11902565
http://cancerres.aacrjournals.org/content/60/14/37
38.full
http://content.karger.com/ProdukteDB/produkte.asp
?doi=10.1159/000106407
http://ohsonline.com/articles/2008/01/epa-radonmay-be-most-potent-carcinogen-in-us-homes.aspx
http://carcin.oxfordjournals.org/content/15/10/226
3.abstract
http://jn.nutrition.org/cgi/content/full/129/2/552S
#SEC4
http://www.springerlink.com/content/m27369m337v
282w8