1. Diagnostic Testing
1.1. Initial testing
1.1.1. CBC - check for amenia
1.1.2. Liver function - CRC may spread to the liver
1.1.3. Colonoscopy
1.1.4. CT colography - if colonoscopy is incomplete
1.2. Diagnostic procedures
1.2.1. Biopsy - performed during colonoscopy
1.2.2. CT needle guided biopsy - to evaluate suspected tumors or metastasis.
2. Risk Factors
2.1. Age: >90% of those diagnosed are over the age of 50.
2.2. Personal history of colorectal polyps. Risk increases as number of polyps increase.
2.3. History of inflammatory bowel disease.
2.4. Personal history of cancer. CRC has a high rate of reoccurrence (20-30%).
2.5. Family history of CRC. Having a 1st-degree relative with a history of CRC increase ones risk 1.7 fold.
2.6. Race ans ethnicity. African Americans have the highest incidence and mortality rate in the United States. Gene mutation has been linked to occurrences in Ashkenazi Jews.
2.7. Miscellaneous factors that increase risk: obesity, diabetes, acromegaly, smoking, and alcohol use.
2.8. Inherited syndromes: Lynch syndrome (lifetime risk 52-69%), Familial adenomatous polyposis (affected persons deveopl hundreds to thousands of polyps in the colon and rectum; accounts of <1% of all CRC), Peutz-Jeghers syndrome (people with freckles on hands, feet and mouth ans develop large polyps in GI tract.
3. Genetics
3.1. There does not seem to be a single genetic pathway to CRC.
3.2. <10 % of CRC cases are linked to an inherited gene
3.2.1. APC, a tumor suppression gene altered in familial adenomatous polyposis.
3.2.2. Genes encoding DAN mismatch repair enzymes are implicated in hereditary nonpolyposis colon cancer.
3.2.3. STK11, a tumor supression gene, is altered in Peutz-Jeghers syndrome
3.3. Sporadic cases of CRC have been linked to oncogenes: kras, c-myc, src, HER2/neu, and others.
4. Pathology
4.1. Progression from 1st abnormal cell to CRC happens over a 10-15 year period.
4.2. High-risk polyp findings include multiple polyps, villous polyps, and larger polyps; hyperplastic polyps are less likely to develop int CRC.
4.3. Multiple geenetic and environmental factors have been linked to the development of CRC.
5. Information
5.1. CRC is a neoplasm that develops in the colon or rectum.
5.2. CRC is the 2nd leading cause of cancer related deaths and the 3rd most common cancer in men and women in the US.
5.3. The life time risk of developing CRC, in the US, is about 1 in 21 (4.8%)
5.4. In 2014, in the US, there were 96,830 new cases of colon cancer; 40,000 new cases of rectal cancer; and 50,310 deaths from colon and rectal cancer combined.
5.5. Diets high in fruits and vegetables have been linked with decreased risk; those high in red and processed meats may increase CRC risk.
6. Treatment
6.1. Primary Treatment: Surgical resection
6.1.1. Other surgical options include: hemicolectomy, or colectomy, withnode resection depending on size and invasion.
6.1.2. Surgery for rectal cancer may include local transanal, low anterior, or abdominoperianal resection or pelvic exenteration.
6.1.3. Radiation therapy is most often used for peritoneal or rectal cancers; it is also used to relieve symptoms.
6.2. 1st Line medication: Combination Chemotherapy which may include - oxaliplatin, irinotecan, fluorouracil, leucovorin, and capectabine.
6.3. 2nd line medication: May use along with 1st line medications or alone if 1st line medications do not work.
6.3.1. Bevacizumab (Avastin)- a monoclonal antibody that targets vascular endothelial growth factor; inhibits angiogensis.
6.3.2. Cetuximab (Erbitux) and panitumumab (Vectibix) - monoclonal antobodies that target epidermal growth factor receptors.
6.3.3. Aflibercept and regorafenib are newer agents with actions on vascular endothelial growth factor.