To acquire an understanding of the fundamental concepts of genomics and biotechnology, and their implications for human biology, evolution, medicine, social policy and individual life path choices in the 21st century.
Treating Cancer
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Del curso dictado por University of Maryland, College Park
Genes and the Human Condition (From Behavior to Biotechnology)
449 calificaciones
University of Maryland, College Park
449 calificaciones
De la lección
An Introduction to Genetic Engineering and Learning the Lingo
Module Five introduces the world of genetic engineering concepts and biotechnology.
Conoce a los instructores
Raymond J. St. LegerProfessor
Department of Entomology
Tammatha O'BrienLecturer
Department of Entomology
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>> Hi and welcome back.
Today we're going to discuss treatments and prevention of cancer.
Early detection is still key.
Basically, catching cancer before it metastasizes or spreads
throughout your body increases your chances of successful remission.
This detection can be done through physical exams to detect tumors.
Other techniques include biopsy, imaging technology such as mammograms,
blood tests, or DNA tests to search for mutated alleles.
And traditional
treatments of cancer, chemotherapy, radiation, and surgery.
All of those have problems.
For instance, the problem with chemotherapy is that it effects
all the cells in your body that are actively dividing.
That includes your skin cells, digestive track cells and cells of hair folicles.
This is not a selective treatment.
When cancer patients are undergoing chemotherapy
they'll lose their hair, they also
tend to lose their appetite and their skins cells aren't allowed to divide.
So all these healthy
cells are adversely effected.
Radiation therapy uses localized radiation to kill cancer cells.
And this tends to be used in conjunction
with chemotherapy or surgery to remove a tumor.
While radiation technology has gotten better to
be more localized; radiation will kill cells and
that means it can kill normal cells or it can damage and mutate normal cells.
And cause them in turn to become cancerous leading to secondary tumours which
is sometimes seen in children.
There's a newer therapy and it uses oncolytic viruses.
Onco again referring to cancer and lytic means to lyse or burst.
And these oncolytic viruses will specificly attack cancer cells.
Oncolytic viruses exploit special cells of your immune
system called macrophages To transport these oncolytic viruses.
And the virus will only become active once the macrophages encounter the
cancer's tumor.
Oncolytic viruses have been used to destroy prostate cancers in mice.
And what we found was that as soon as the cancer
was detected viruses began to attack and destroy the cancer's prostate cells.
Obviously the challenge with this approach is to ensure
that all your immune cells don't attack the oncolytic virus.
And that your immune cells properly deliver
the virus to the appropriate cancer target.
You wouldn't want healthy cells being destroyed by
this oncolytic virus.
So remember how we discussed in a previous lecture
that steroid hormones such as estrogen can increase gene expression.
Well estrogen's been linked to certain types of breast cancer.
When estrogen binds to its receptor these hor, this hormone receptor
complex causes the expression of genes involved in cell growth and proliferation.
Remember the definition of cancer.
We talked about that, uncontrolled cell growth.
Well, by blocking estrogen's functions certain
types of breast cancer can be slowed.
We can use certain drugs that specifically interfere with estrogen binding to
the estrogen receptor to slow the progression of that type of cancer.
The FDA in the United States has approved certain
drugs for treatment of estrogen receptor positive breast cancer.
These drugs are called Selective Estrogen Receptor Modulators, and they destroy
that estrogen receptor complex.
These new approaches focus mainly on treating cancer cells.
A new class of drugs work by blocking growth
factors or repairing broken tumor suppressor genes in cancer cells.
To do this properly we have to compare healthy cells
to cancer cells and compare the genes that are mutated.
Remember that genome approach that I talked about earlier?
Comparing a cancer cell genome to your healthy cell genome.
Well, if we know which specific genes are broken, we
can use a partialized approach of treatment by classifying the cancer.
Not based on where it originated,
like we do now, but based on specific
genes that are mutated that led to that cancer.
This approach uses the genetics of the
specific cancer and specific genes that are
broken as the Achilles' heel for determining
which medications to use to treat that cancer.
So in the future when someone gets cancer, the genome of the cancer
can be sequenced, and a personalized
treatment can be designed that's patient specific.
Doctors can then identify
all the broken genes that lead to the
disruptive signal transduction pathway, and then a doctor can
look up in a database and identify the
specific drugs that can block the mutated gene products.
And using the specific pathways, the doc, that the cancer's addicted
to to survive, you can stop the cancer dead in its tracks.
Gleevac is an example of how the future will work.
The future treatments use drugs that are specific for the broken genes, and
to interfere with these pathways.
Of course, cancer cells can mutate to negate even the effect of Gleevac.
So you'll need to use other drugs in conjunction
with this based on the new mutations that develop.
So the idea here is to target specific genes that are broken, and.
Just target the cancer cells.
So you want to use very specific drugs as
opposed to the current approach of blocking all cell divisions.
It might take years for this treatment to be mainstream.
Mainly because the big issue is sequencing these cancer genomes can be very costly.
Now I'm going to review some terminology we talked about last time.
One was proto-oncogenes, and again, you have proto-oncogenes,
they're normal genes that regulate the cell cycle.
One example of a proto-oncogene is the RAS gene, and
a mutation of the RAS gene, or any other proto-oncogene,
results in an oncogene which will increase cell growth and cell division.
The trick to treatment is to find which specific proto-oncogenes are mutated
or broken so we can fix them when trying to treat cancer.
We can also try to fix broken
tumor suppressor genes like p53 when treating cancer.
Another challenge of treatment is to locate the cancer cells
in a body full of trillions of normal healthy cells.
A cancer is a needle in a haystack, if you would.
There are factors that increase cancer risk, such as viral infections.
How can a virus cause cancer?
Well, remember the helix cells I discussed earlier?
Miss Lacks, she'd been infected with HPV, Human Papillomavirus.
And that's linked to cancer because viruses been within strong promoters.
And remember strong promoters increase gene transcription.
That can increase the rate of the cell cycle if the
virus causes more growth factors to be synthesized in your cells.
You could have inherited cancer genes, but
again, that's not the cause of most cancer.
A poor lifestyle is the big risk factor.
The single biggest preventable cause of cancer is smoking.
Smoking directly leads to DNA mutations.
Smoking or using nicotine products can mutate our DNA.
And anything that can mutate the DNA and increase your chance.
Or risk of developing cancer is called a carcinogen.
And smoking is also
linked to cancers of the oral cavity, larynx, esophagus and lungs.
Having a high animal fat or red meat diet can increase
your risk of colon cancer and that's because animal fat, contains fat
soluble toxins that are carcinogenic, and they can build up when
you eat that animal fat and you expose that toxin to yourselves.
UV can also be a potential mutagen. Exposure to UV
can increase your chances of developing a type of skin cancer called melanoma.
So I listed some factors that can increase your chances of getting cancer.
But it's probably more important that I discuss
ways you can decrease your chances of developing cancer.
Well exercise is high on that list.
Do you remember why?
Exer, exercise increases the activity of your DNA repair mechanisms.
And that's one big reason amongst the many
for you to exercise more.
Also, a diet high in fruits and vegetables that are
rich in antioxidants, as these antioxidants can help with DNA repair.
Avoiding tobacco products like we just mentioned.
Cigarette smoke, second hand smoke, since those contribute to mutations of the DNA.
Also avoiding UV radiation by using a high
spf sunscreen, you should also avoid excessive X-rays which
can damage DNA.
Lastly, vaccinations for viruses, such as the one for HPV.
If you prevent your chances of getting that viral infection,
you reduce your chances of getting cancers associated with that virus.
While there are inherited cancers, lifestyle choices
can really help reduce your risk of cancer.
We can't control the genes we inherit, but we sure can control how we live our lives.
Lifestyle is interestingly important when looking at cancer.
For instance type II diabetes mellitus has
a strong correlation with obesity and abdominal fat.
Abdominal fat can act as a hormone secreting endocrine gland.
And by maintaining a healthy weight and lifestyle
even if you have a genetic predispostion to
this disease, you can reduce and possibly eliminate
your chances of ever having an onset of diabetes.
The role lifestyle plays on the
onset of disease is a pretty tricky one to examine.
Consider multiple sclerosis or MS, an
autoimmune disease that affects your nervous system.
We don't understand why in some people
their immune system begins to attack itself.
But we do know in the case of MS, there's a higher incident of MS.
The farther you grow up. Away from the equator.
It may be a link to the synthesis of vitamin
D, which is an important steroid hormone that regulates calcium levels.
What I want you to take home from today's lecture is
the importance that lifestyle decisions have on cancer and other diseases.
And that genes don't soley determine your destiny.
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