Introduction
This has been an informative self challenging course that has helped me see Cancer in such a brighter light. This class has taught me the ends and out of Cancer; from initiation, promotion, transformation, and progression. I've become aware of things that I do interact with that could eventually lead to cancer. I'm extremely cautions of the foods I eat and the chemicals that I may come in contact with. I indeed enjoyed the course from start to finish and can now take this vital information and spread it my friends and family, in order to help them prevent this disease as much as they can.
What are the outcomes?
"The 6 Hallmarks of Cancer"
The 6 Hallmarks of Cancer
Self- sufficiency in growth signals: Cells of the body require hormones and other molecules that act as signals for them to grow and divide. Cancer cells, have the ability to grow without these external signals.
Insensitivity to anti-growth signals: Cancer cells are generally resistant to growth preventing signals from other cells. Cancer cells do not have contact inhibition, and so will continue to grow and divide, regardless of their surroundings.
Tissue Invasion and metastasis: Cancer cells begin to spread to other organs and spread in the tissue and to distant body parts.
Sustained angiogenesis: Cancer cells speads up the process of new blood vessels forming (angiogenesis) ensuring that cells receive a continuous supply of oxygen and nutrients.
Limitless replicative potential: Cancer cells escape the certain number of cell divisions and are able of indefinite growth and division. Some of those cells have damaged chromosomes, which could become cancerous.
Evading apoptosis: Cancer cells are able to bypass this mechanism, leaving behind tons of damaged cells.
Assignment: The goal of this assignment is for us to work in groups to support why our hallmark of cancer is the most important hallmark of all cancer. This included highlighting key features of the particular assigned hallmark and providing examples of its implications in cancer. Above is the power point presentation highlighting our hallmark Evasion of growth Inhibitory signals.
"Gene Mutations"
Deletion: Occurs when part of a DNA molecule is not copied during DNA replication.
Duplication: A type of mutation in which a portion of a genetic material or a chromosome is duplicated or replicated, resulting in multiple copies of that region.
Inversion: Type of genetic mutation that creates changes in a chromosome.
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Paracentric inversion: occurs when there is a break to only one arm of the chromosome, and the inverted segment does not include the centromere, or the area where the arms of the chromosome attaches.
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Pericentric inversion: break occurs between two arms of a chromosome, and the inverted segment does include the centromere.
Insertion: The addition of extra nucleotides in a DNA sequence or chromosome.
Translocation: Chromosome mutations in which chromosome segments, and the genes they contain, change positions.
"Oncogenes and Tumor Suppressor Genes"
Proto-oncogenes are genes that normally help cells grow. When a proto-oncogene mutates or there are too many copies of it, it becomes a bad gene that can become permanently turned on or activated when it is not supposed to be. When this happens, the cell grows out of control, which can lead to cancer. This bad gene created is an Oncogene.
Tumor suppressor genes slows down cell division, repairs DNA, or lets bad cells die when they don't work properly, cells can grow out of control, which can lead to cancer.
Assigment: This was a group assignment where we were assigned a scientific article to read and present. My partners (Alexis Dean and Andrea' Colvin) and I were assigned an artice about Polcyclyic Aromatic Hydrocarbons. I would say this was the hardest assignment I've had to tackle and I'm glad I did. My ability to analyze a scientific article and present the information to my peers was indeed challenging but with the help of my partners we were able to get it done and fully understand what our article was about. Click above to view full presentation!
"The Cell Cycle"
Interphase: Where most cells live and where cells can grow.
G1 Phase:Growth phase where cells prepare for division, and produce extra organelles.
S Phase:DNA replication occurs,chromosomes are duplicated
G2 Phase:Growth and preparation for mitosis
Mitosis:Cell Division occurs
The goal for this assignment was for our class to work in groups on a case study in which we were to research mitosis, forms of cancer and cancer treatments and then decide which were better for three hypothetical patients. This was a very fun creative project incorporating all cancer related topics that we covered. Click above to view the full presentation.
"Steps that lead to Metastasis"
Step 1: Tumor formation
Step 2: Invasion of and infiltration of surrounding normal host cells tissue with penetration of small lymphatic channels.
Step 3: Release of neoplastic cells either in single cells, or small clumps into circulation.
Step 4: Survival of circulation
Step 5: Arrest in the capillary beds of distant organs
Step 6: Penetration of the lymphatic or blood cells followed by growth of dispersed tumor cells.
"How can external or internal stimuli lead to apotosis"
The Extrinsic pathway
Pathway used to tripper apoptosis from the outside of the cell uses a death receptor on the surface of the cell. A signal, known as a death factor binds to the death receptor. When this binding occurs, the receptor changes its shape and comes together with other receptors in an effort to relay the message inside the cell.
The change in shape causes an area known as a death domain located on the receptor to be exposed. Their exposure allows the binding of other proteins necessary for apoptosis to bind. These proteins then send the signal to caspases inside the cell which further carry out the process of apoptosis.
Intrinsic Pathway
Irreparable or too much DNA damage can trigger apoptosis from the inside of the cell. The use of the death receptors and binding proteins that trigger cell death from the outside of the cell are not needed.
"How chronic inflammation and infectious agents can lead to cancer"
In chronic inflammation, the inflammatory process may begin even if there is no injury, and it does not end when it should. Why the inflammation continues is not always known. Chronic inflammation may be caused by infections that don’t go away, abnormal immune reactions to normal tissues, or conditions such as obesity. Over time, chronic inflammation can cause DNA damage and lead to cancer. In general, the longer the inflammation persists, the higher the risk of cancer.
"How cancer cells escape death"
Apoptosis can be seen as an important barrier to developing cancer. Apoptosis, or programmed cell death, evolved as a rapid and irreversible process to efficiently eliminate dysfunctional cells.Cancer cells exhibit many characteristics that would readily trigger apoptosis in healthy cell such as they violate cell cycle checkpoints and can withstand exposure to cytotoxic agents.Because of these characteristics, cancer cells tend to survive.
"Role of diet in cancer development and prevention"
Dietary factors are recognized as having a significant effect on the risk of cancers, with different dietary elements both increasing and reducing risk. Antioxidants are man-made or natural substances that may prevent or delay some types of cell damage. Antioxidants are found in many foods, including fruits and vegetables. They are also available as dietary supplements.
High-dose supplements of antioxidants may be linked to health risks in some cases. For example, high doses of beta-carotene may increase the risk of lung cancer in smokers. High doses of vitamin E may increase risks of prostate cancer and one type of stroke.
References:
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All images are from google images
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All video are from YouTube
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Molecular Biology of Cancer: Mechanisms, Targets and Therapeutics (4th Edition) by Lauren Pecorino. Oxford University Press
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All assignments include their own references inside documents
