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Merci Gilbert
Dr. Angela White
ORG-Biology 101
30 November 2017

Outside of the Classroom Organization Paper: Tri-Beta Breast Cancer Walk

This semester I enrolled a Biology 101 course with Dr. Smith-Pearson. One of our
assignments this semester was an outside of the classroom volunteer project. For this project I
was selected to participate in the Tri- Beta Breast Cancer Walk. As a participant, I had to do
several things to prepare for the volunteer event including a learning session. During this
session, I learned exactly what breast cancer is, the different types, and the main causes. I
further learned about breast cancer through a scientific aspect in my biology class when we
covered the cell cycles function and cell mutation. We learned that cancer is when cells are over
actively reproduced, which is caused by a mutation in the cell cycle that suppresses our bodys
ability to function normally and stop this. Also, we learned about some of the different subtypes
of breast cancer like, HER2+ (ER-), Basal-Like (Triple Negative Breast Cancer), Normal-Like,
Luminal A, and Luminal B. HER2+ (ER-) breast cancer is less common, but it is very
aggressive. HER2 is a gene in our bodies that produces receptor proteins, which are responsible
for regulating the growth and repair of breast cells. When these HER2 receptor proteins are
expressed too much, it causes excessive reproduction of breast cells. It is thought that African
Americans have a higher risk for this type (Mandell). Basal-Like, or more commonly called,
Triple Negative Breast Cancer is very aggressive, usually the most aggressive. Basal-like means
that the ways the cells look with this cancer resemble the cells that line the breast ducts (Breast
Cancer Organization). Basal-like cancers are more aggressive, just like triple-negative breast
cancers. According to research most triple-negative breast cancer cells have the basal-like cell
type (Breast Cancer Organization). It mostly occurs in premenopausal African American Women
who are under 40. Normal-Like breast cancer is called normal-like because it looks a lot like
normal breast tissue. The levels of estrogen and progesterone receptors have low expression with
this cancer, and it does not have the epidermal growth receptor (National Breast Cancer
Foundation). Luminal A breast cancer is another cancer that looks a lot like normal breast tissue.
Also, this cancer has low expression of the estrogen and progesterone receptors, and does not
have the epidermal growth receptor. The tumors for Luminal A most times are HER2 receptor
negative. Luminal B breast cancer is very similar to Luminal A. Women with luminal B tumors
are often diagnosed at a younger age than those with Luminal A tumors (Komen, Susan.G).
The tumors for Luminal B are most time much larger and usually are ER+/PR-. Also, in the
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learning session for the Breast Cancer walk, we learned that the top factors that cause breast
cancer are age, environment, and genetics.

After mutations happen in the cell cycle, the cell becomes cancerous. According to
research findings from the Cancer Genome Project, most cancer cells possess 60 or more
mutations (Cancer Genome Project). A lot of research for cancer recently has been to see which
mutations cause certain cancers. There are some chemotherapy drugs that have worked very well
to prevent cell mutations by blocking the growth-signaling protein receptors. We learned in
biology class from the chapter dealing with cell mutations about an example of a breast cancer
drug called Herceptin. Herceptin works to block overactive receptor tyrosine kinases. Another
drug we learned about is Gleevec, it blocks a mutant growth-signaling associated with chronic
myelogenous leukemia. There are other types cancer-related mutations that shut down the genes
that stop the operation of the cell cycle. These specific genes are called tumor suppressor genes.
In class we learned that they normally function like brakes for over excessive reproduction. Both
copies within a cell must be mutated for division to occur at a high rate. For example, many
cancer cells have two mutant copies of the gene that codes for p53, which is a protein that
normally senses DNA damage and acts as a transcription factor for checkpoint control genes
(Khan Academy). When a mutation gives a cancer cell a growth advantage, it can make more
copies of itself than a normal cell can, its clones are able to exceed the function of normal cells,
they do this to better to compete for resources. After this, a second mutation gives the cancer cell
with another reproductive advantage, which adds more of a competitive advantage. Also,
sometimes checkpoints in the cell cycle are missed or repair genes can be damaged, which
causes accumulation of damage accumulation (Khan Academy). If this process is continued,
each new mutation helps the growth of cancerous cells.

Cancer is a disease of uncontrolled cell division. Its growth and progression are usually
connected to mutations in the function of cell cycle regulators. For example, inhibitors of the cell
cycle keep cells from dividing when conditions are irregular, so when the functions of these
inhibitors are suppressed they can promote cancer. Also, normal regulators of cell division can
lead to cancer if they are over active. In most cases, these changes in activity are due to
mutations in the genes that control cell cycle regulator proteins. Mutations in genes can cause
cancer by speeding up the process of cell division rates or stopping the normal functions. When
cancerous cells collect together, it develops into a tumor. Cancer cells can also invade
neighboring tissues and sometimes even break off and travel to other parts of the body, leading
to the formation of new tumors at those sites. I was able to learn a lot dealing with this topic
through my biology class when we covered the operation of the cell cycle and mutated cells. I
also learned a lot about breast cancer through the learning session required for the Tri-Beta
Breast Cancer Walk. Overall, I feel as though the rewarding experience I received from
volunteering at the actual event and interacting directly with the survivors is what made me
interested in learning more about breast cancer.
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References

Academy, K. (2015, September). Cancer and the Cell Cycle. Retrieved November 12, 2017,

from https://www.khanacademy.org/science/biology/cellular-molecular-biology/stem-

cells-and-cancer/a/cancer

How Triple-Negative Breast Cancer Behaves and Looks. (2017, February 20). Retrieved

November 10, 2017, from

http://www.breastcancer.org/symptoms/diagnosis/trip_neg/behavior

Learn About Molecular Subtypes of Breast Cancer at Susan G. Komen. (2017, October 31).

Retrieved November 10, 2017, from

https://ww5.komen.org/BreastCancer/SubtypesofBreastCancer.html

Madell, R. (2017, August 01). HER2-Positive Breast Cancer Survival Rates and Other Statistics.

Retrieved November 10, 2017, from

https://www.healthline.com/health/breast-cancer/her2-positive-survival-rates-

statistics#overview1

Nbcf. (2016). Breast Cancer Types: The National Breast Cancer Foundation. Retrieved

November 30, 2017, from http://www.nationalbreastcancer.org/types-of-breast-cancer

Project, C. G. (2017, May 4). The Cancer Genome Atlas. Retrieved November 12, 2017, from

https://www.genome.gov/17516564/the-cancer-genome-atlas/