Professional Documents
Culture Documents
By: Erin Brink, Michaela Peramaki, Raegan Hickok, and Kyra Bussell
Prevalence/Incidence/Etiology
● Etiology
○ Presence of mutated cells (cancer) at the end of the GI tract near the rectum and colon
● Populations, Prevalence, Incidence
○ 1/23 men, 1/25 women
○ More common in older populations, African Americans and Ashkenazi Jews
● Risk Factors
○ Unchangeable: 50+, personal or family history, inherited syndromes, AA, Ashkenazi Jews, type 2
diabetes
○ Changeable: overweight, obese, inactive, certain diets, smoking, alcohol use
● Transmission
○ Not transmitted from person to person
○ Healthy cells in colon develop mutations in their DNA, if metastatic → transmitted throughout
the body
● Genetics
○ Common genetic associations: Lynch syndrome, familial adenomatous polyposis
○ Uncommon genetic associations: Peutz-Jeghers syndrome, MUTYH associated polyposis
○ Higher risk with familial history
● Prevention
○ Cannot be prevented
○ Addressing changeable risk factors can less or lower risk
○ Early detection via: colonoscopy
○ Some studies suggest NSAIDS, HRT for women and certain vitamins, calcium, and magnesium
may lower risk
Pathology
What type of organism (pathogen) is responsible?
● Colorectal cancer is still vastly researched. Many studies
do not clearly state ONE single cause for the cancer.
● Many state environmental factors, bacteria, genetics, etc
● A study named the “Four Horsemen” states that the 4
researched bacteria have an impact:
○ Fusobacterium nucleatum,
○ Escherichia coli,
○ Bacteroides fragilis
○ Salmonella enterica
● Other studies have found that bacteria involved could be
HPV, streptococcus bovis, streptococcus galloliticus
Tissue Damage Location?
● Tissue damage occurs in the colon, intestines and
rectum.
Pathology Continued
Multiple mechanism are being researched on colorectal cancer
● Intestinal dysbiosis- unbalanced bacteria
● Inflammation
● Evasion of tumoral immune response and activation of pro-tumoral signaling
pathways
Cells involved and how they are affected
● Adenoma is formed via some sort of mechanism above
● Epithelial cells become cancerous through multiple gene mutations
● There is a functional lose of APC (adenomatous polyposis coli) and thus lack
of identification and demolition of tumors
● In return, b-catenin is activated in the cells and causes transformation and
division of the tumor cells (promote proliferation)
● This lack of APC tumor suppressor will decrease T-cell production and
decrease mast cells as well
Stages of Colorectal Cancer
Stage I Stage II Stage III Stage IV
● The cancer is ● The cancer has ● The cancer has ● The cancer has
contained in the grown through now spread to spread to many
inner walls of the all the layers of many adjacent adjacent lymph
rectum. the walls of the lymph nodes nodes and now
● In this stage, bowels. ● Not in the has spread to
there is no spread ● Still has not organs. other organs
to surrounding expanded into ● EX- liver, lungs,
lymph nodes + the lymph nodes etc.
organs. + organs.
Pathology Continued
● Secondary complications may include:
○ Blockage of the colon, causing bowel
obstruction
○ Cancer returning in the colon.
○ Cancer spreading to other organs or
tissues (metastasis)
○ Development of a second primary
colorectal cancer
● Latency Period- 5-10 years to develop
Diagnosis
● Individuals are at a higher risk for colorectal cancer if they have familial
history
● PT can occur before and after treatment in order to strengthen the pelvic floor
and help with a better outcome
● Watch for change in bowel movements, blood in the stool, and weight loss
Test Questions
1. b. False
2. c. 50%
3. a. True
Sources
● Antonic V, Stojadinovic A, Kester KE, et al. Significance of infectious agents in colorectal cancer development. J Cancer. 2013;4(3):227-240. doi:10.7150/jca.5835
● Articles. Cedars. https://www.cedars-sinai.org/health-library/diseases-and-conditions/c/colon-and-rectal-cancers.html. Accessed October 15, 2021.
● Brenner H, Kloor M, Pox CP. Colorectal cancer. Lancet. 2014;383(9927):1490-1502. doi:10.1016/S0140-6736(13)61649-9
● Colon cancer treatment, by stage: How to treat colon cancer. American Cancer Society.
https://www.cancer.org/cancer/colon-rectal-cancer/treating/by-stage-colon.html. Published June 29, 2020. Accessed October 16, 2021.
● Colorectal cancer signs and symptoms: Signs of colorectal cancer. American Cancer Society.
https://www.cancer.org/cancer/colon-rectal-cancer/detection-diagnosis-staging/signs-and-symptoms.html. Published June 29, 2020. Accessed October 16, 2021.
● Haggar FA, Boushey RP. Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors. Clin Colon Rectal Surg. 2009;22(4):191-197.
doi:10.1055/s-0029-1242458
● Lee SJ, Yun CC. Colorectal cancer cells - Proliferation, survival and invasion by lysophosphatidic acid. Int J Biochem Cell Biol. 2010;42(12):1907-1910.
doi:10.1016/j.biocel.2010.09.021
● Lee SJ, Yun CC. Colorectal cancer cells - Proliferation, survival and invasion by lysophosphatidic acid. Int J Biochem Cell Biol. 2010;42(12):1907-1910.
doi:10.1016/j.biocel.2010.09.021
● What is colorectal cancer? Centers for Disease Control and Prevention. https://www.cdc.gov/cancer/colorectal/basic_info/what-is-colorectal-cancer.htm. Published
February 8, 2021. Accessed October 15, 2021.
● Living as a Colorectal Cancer Survivor. Cancer.org. Accessed October 18, 2021.
https://www.cancer.org/cancer/colon-rectal-cancer/after-treatment/living.html
● Colon cancer. Mayoclinic.org. Accessed October 18, 2021. https://www.mayoclinic.org/diseases-conditions/colon-cancer/symptoms-causes/syc-20353669
● Colorectal Cancer - Statistics. Cancer.net. Published June 25, 2012. Accessed October 18, 2021.
https://www.cancer.net/cancer-types/colorectal-cancer/statistics
● Mone A. The ERAS Pathway: A Quicker Recovery after Colorectal Surgery | Colorectal Surgeon Jonathan Efron.; 2016.