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COLORECTAL CANCER
OBJECTIVES
When the student has finished this module, she/he will be able to:
1. Identify three possible risk factors for the development of colorectal cancer.
2. Identify an ethnic risk factor that increases the risk of developing colorectal cancer.
3. Identify two medical conditions that increase the risk for developing colorectal cancer.
4. Identify the genetic mechanisms thought to be responsible for colorectal cancer.
5. Identify the type gene that is thought to be responsible or most colorectal cancers.
6. Identify the type of neoplasm that is the most common cause of colorectal cancer.
7. Identify three possible signs and symptoms of colorectal cancer
8. Identify the possible role of diet in the development of colorectal cancer.
9. Identify a test that uses stool to check for the presence of colorectal cancer.
10. Identify a blood test that can be used to check for the presence of colorectal cancer.
11. Identify two invasive procedures used to check for the presence of colorectal cancer.
12. Identify the three parameters used to stage colorectal cancer.
13. Identify three possible complications of colorectal cancer.
14. Identify the four basic treatments used for colorectal cancer.
15. Identify three risk factors that would indicate the need for more frequent screening.
EPIDEMIOLOGY
Colorectal cancer is the third most common cancer in the United States, and it the third
most common cause of cancer mortality in the United States.1 Colorectal cancer appears
to affect men and women equally.2 The disease is more common in African Americans
than in whites and people of Hispanic background have the lowest incidence of the
disease.3,4 The incidence of colorectal cancer and deaths from the disease have been
declining in the United States in the past 20 years.5 However, given the fact that
colorectal cancer is preventable and treatable, it is clear that more screening and more
available treatment are needed.6
RISK FACTORS FOR COLORECTAL CANCER
Colorectal cancer is a complex disease. There are genetic factors, environmental
factors, and lifestyle factors that combine to cause the disease.

Diet: The effect of diet as a causative/contributing factor for the development of
colorectal cancer has been studied extensively. Diets high in fat and red meat and
low in fiber have been implicated as increasing risk, and conversely, diets low in
fat and red meat and high in fiber have been thought to have a protective effect.
However, the evidence for or against specific dietary components (e.g., fat, fiber,
folate, red meat, alcohol, calcium, and other dietary components) causing or
preventing colorectal cancer is inconclusive.7,8

Race: African Americans have a higher incidence of colorectal cancer then
whites. In addition, when they are diagnosed, the cancers tend to more advanced
and their prognosis is worse. After diagnosis, African Americans are
approximately 38% - 43% more likely to die of the disease than whites.9 It
appears that most of this disparity can be explained by socioeconomic status
(which affects treatment, surveillance rates, etc), and there is little evidence that
suggests a genetic basis for these differences.10

Metabolic syndrome/Obesity: Metabolic syndrome is a complex disorder of
multiple cardiac and metabolic abnormalities. It is characterized by high fasting
serum glucose, an elevated blood pressure, elevated serum triglycerides, low
serum high-density lipoprotein (HDL) cholesterol, and a waist circumference
significantly above normal. There is a substantial evidence that has linked the
metabolic syndrome and colon cancer.11 The presence of the metabolic syndrome
can increase the risk of developing colorectal cancer by 75%; the higher the body
mass index (BMI) and the greater number of risk factors associated with the
metabolic syndrome present, the greater the risk becomes.12 It is possible that
some of the pathological processes that occur in the metabolic syndrome (e.g.,
insulin resistance, chronic/low-level inflammation, increased adipose cell
proliferation, etc.) are among the possible causes of the cancer. 13

Sedentary lifestyle: A sedentary lifestyle has been associated with an increased
risk for developing colorectal cancer.14

Smoking: Cigarette smoking is considered to be a risk factor for developing
colorectal cancer.15

Alcohol use: Excessive alcohol use may increase the risk of developing colorectal
cancer, but the evidence is not conclusive, and lower levels of alcohol intake do
not appear to increase the risk.16,17

Age: Age is risk factor for colorectal cancer. The peak incidence of the disease
occurs at age 65.18

Inflammatory bowel disease: People with long-standing ulcerative colitis or
Chrohn’s disease have a significantly higher risk of developing colorectal cancer
than the general population of the same age.19 The greater the duration of the
inflammatory bowel disease and the greater the extent of the gut that is involved,
the greater the risk of developing colorectal cancer.20

Family history: Family history of colorectal cancer is a risk factor for developing
the disease. If someone’s first-degree relative (parent, sibling, children) has
colorectal cancer, that person’s risk of developing a colorectal cancer is increased
twofold to threefold.21 If more than one first-degree relative has colorectal cancer,
or the relative’s cancer was diagnosed before the age of 45, the risk is even
greater.22

Genetics: The genetic basis of colorectal cancer is complex. Colorectal tumors
have been found to have an average of 90 mutant genes, and each tumor has its
own distinct mixture of mutant genes.23 It appears that colorectal tumors are,
basically, caused by activation of oncogenes and inactivation of tumor
suppressor genes. This leads to a progressive alteration and instability of the
genetic material of the epithelial cells of the colon.24 This genetic instability and
alteration takes two basic forms: chromosomal instability (CIN) and microsatellite
instability MSI).25 Chromosomal instability occurs when there is chromosomal
loss and changes in chromosome numbers. These losses and changes in numbers
of chromosomes affect specific genes; the most important of these genes is the
APC (adenomatous polyposis coli gene). The APC gene is a tumor suppressor
gene. It encodes the production of an intracellular protein that determines how
often a cell divides and makes sure that when cells divide, they have the correct
number of chromosomes. When there is a mutation of the APC gene, cells
become unstable and prone to the development of neoplasms. Microsatellite
instability causes colorectal cancer by affecting the cell’s ability to sense and
repair mismatches in DNA, repairing DNA synthesis errors, and repairing certain
DNA breaks. Microsatellite instability is also caused by a mutation in the APC
gene. When there is a mutation of the APC gene, the DNA mismatches are not
repaired and unproliferated cell growth – colorectal cancer – can occur.25
Learning Break: There are two well known forms of hereditary colon cancer. Familial
adenomatous polyposis (FAP) is caused by a defect in the APC gene. Lynch syndrome is
caused by a mutation in DNA mismatch repair genes. However, these forms of colorectal
cancer are caused by what are called single or major genes; mutations of these genes are
sufficient in and of themselves to cause cancer. However, single/major gene causes of
cancer are the exception. Most cancers – such as colorectal cancers – are caused by a
subtle interplay of circumstances, environmental and/or lifestyle exposure and the
presence of susceptibility genes. Susceptibility genes increase the risk of developing a
particular disease and they can be inherited. But as mentioned before, there are many,
many genes that may be involved in causing colorectal cancer.26,27
PATHOPHYSIOLOGY
The great majority (approximately 95%) of colorectal tumors are carcinomas (tumors
that arise from epithelial cells) and approximately 95% of those tumors are
adenocarcinomas (a cancer that is derived from glandular tissue, also called an
adenoma).28
The majority of colorectal cancers occur when an adenomatous polyp progresses
to a malignancy.29 An adenomatous polyp is a benign tumor, but it can become
cancerous. The risk of a malignancy developing increases with increasing size of the
polyp, the degree of dysplasia within the adenoma, and what is called villous pathology
(this means that the adenoma has the appearance of having many villi).30 It takes time for
an adenomatous polyp to become cancerous: a minimum of four years and an average of
10 years.31
Adenomas are quite common. They are found in approximately 30% - 40% of people
aged 60 years and older.32 The risk of developing colorectal cancer from an adenoma is
15% - 25%; as mentioned earlier, the risk is higher with certain characteristics of the
tumor.33 The risk also increases with. Five years after diagnosis, the risk of an adenoma
becoming cancerous is approximately 4% but at 20 years after diagnosis the risk is
approximately 37%.34
SIGNS AND SYMPTOMS OF COLORECTAL CANCER
The great majority of patients who have colorectal polyps and/or colorectal cancer
have no signs and symptoms of the disease. If the polyp is > 1 cm, it is more likely to
produce signs and symptoms. Diarrhea, abdominal cramping, overt or occult bleeding,
weakness, fatigue, anemia, cramping, and constipation may be noted.35
DIAGNOSING COLORECTAL CANCER
If it is suspected that the patient has colorectal cancer, a fecal occult blood test (FOBT)
should be performed. The FOBT has been shown to be an effective screening test that can
significantly reduce mortality from colorectal cancer. The preferred test is the highsensitivity guaiac FOBT or the fecal immunochemical test (also called the FIT, this
screening procedure uses a test strip that has a monoclonal antibody that detects
hemoglobin). However, these tests cannot be considered 100% diagnostic as there can be
other reasons for blood in the stool. Exfoliated DNA in the stool can also be checked.
This test detects DNA mutations that are commonly seen in colorectal cancers.
Laboratory test should include a complete blood count to check for anemia, a
chemistry profile, liver function studies, and serum carcinoembryonic antigen (CEA) test.
Learning Break: The carcinoembryonic antigen is a glycoprotein that is involved in fetal
development. It is not present in the serum of normal adults, but elevated levels of CEA
can be found in people with colorectal cancer and other cancers.
There are four procedures that can be used to make the diagnosis of an adenomatous
polyp and/or colorectal cancer: colonoscopy, sigmoidoscopy, double contrast barium
enema, or a computed tomography (CT) colonography.

CT colonography: This procedure is also called virtual colonoscopy. The
preparation is essentially the same as for a colonoscopy. A bowel prep is used to
clean the coon and the patient must be NPO for a period of time prior to the
procedure. A small flexible tube is inserted into the rectum and air is instilled in
order to distend the colon and make visualization easy and accurate. Once the air
is instilled, CT is performed and the images are obtained; the procedure takes
about 15 minutes. Patients may experience abdominal bloating and cramping, but
these are usually short-lived and minimal in intensity. CT colonography has
several advantages: accuracy, sensitivity, full visualization of the colon, safety
(perforation rate from 0.06% to 0.08%), patient comfort, and a clear advantage
over the barium enema as a screening and diagnostic procedure.36 The patient is
subjected to ionizing radiation, but the risk appears to be minimal. If cancers or
polyps are detected during the test, they cannot be removed and the patient will
need to have a sigmoidoscope or colonoscopy.

Double-contrast barium enema: The double-contrast barium enema has been used
as a screening test to detect and diagnose colorectal cancer. Radio-opaque barium
is instilled into the colon, and then air is instilled to distend the colon and allow
for greater visualization. The radiation doses are higher than what is delivered
during CT colonography, the test has a lower sensitivity and specificity than CT
colonography, and it is not as sensitive as colonoscopy.37,38,39 Also, if cancers or
polyps are detected during the test, they cannot be removed and the patient will
need to have a sigmoidoscope or colonoscopy.

Colonoscopy: The colonoscopy has become the most popular diagnostic tool for
detecting colorectal cancers and polyps. The patient must take a bowel prep to
clean the colon and must be NPO for a period of time before the test. The
procedure is done under sedation and takes approximately 45 minutes. A flexible
scope is inserted and the entire length of the colon is visualized. Any cancers or
polyps that are visualized can be removed during the procedure. Perforation and
bleeding are possible, but very uncommon. Most patients experience some mild
abdominal cramping and diarrhea later in the day after the procedure. Although
the colonoscopy has become the most commonly performed diagnostic and
screening procedure, there is little evidence that it significantly reduces mortality
or that it is superior to flexible sigmoidoscope.40,41 There are no randomized
controlled trials comparing the effectiveness of colonoscopy and other
screening/diagnostic tests.42

Flexible sigmoidoscope: The flexible sigmoidoscope is among the tests
recommended by the American Cancer Society.43 It does not visualize the full
extent of the colon, cancers/polyps in the right colon may be missed, and small
polyps may be missed. However, it has been shown to be an effective screening
and diagnostic tool.44 The preparation, side effects and risks are virtually identical
to colonoscopy, but most patients will not need sedation.
Learning Break: At this time, there is no specific recommendation for one of these four
tests as preferable to another. Which one that is used will depend on several factors.
STAGING THE DISEASE
When colorectal cancer has been discovered, the next step is to stage the disease. The
TNM staging system is the staging system that is the international standard. The TNM
staging system – T for primary tumor, N for lymph node, and M for metastases – will
help the treating physician make a prognosis and determine the best course of treatment.45
There are nine Stages in the TNM staging system: 0, I, II, IIA, IIB, IIIA, IIIB, IIIC, IV. .
For example, a case of colorectal cancer would be Stage O if it I limited to the lining of
the colon or rectum. A case of colorectal cancer will be Stage IV (the most serious) when
the tumor has invaded not only the submucosa, but nearby organs and structures, when
there are many lymph nodes involved, and when there is metastases to the liver, lungs, or
elsewhere.46,47
COMPLICATIONS, MORBIDITY, AND MORTALITY
Colorectal cancer can cause bleeding, obstruction, plus a wide range of physical signs
and symptoms. Most patients with colorectal cancer do not succumb to the primary
disease, but die because of metastases.48 Serious complications of colorectal cancer are
metastases to the liver, lungs, lymph nodes, peritoneum, and the brain (the last two are
uncommon).

Liver metastasis: Metastasis of colorectal cancer to the liver is common. As many
as 25% of patients with colorectal cancer will have liver involvement at the time
of the diagnosis, and approximately 25% -30% will develop liver metastases in
the two to three years after that.49 If a patient with colorectal cancer and liver
metastases is not treated, life expectancy is less than a year.50

Lung metastasis: Approximately 10% - 15% of all patients with colorectal cancer
will develop metastases to the lungs.51 Lung masses usually occur after liver
masses. Isolated lung metastases are possible, but uncommon.52

Lymph node metastasis: Lymph node involvement is considered to be the most
important prognostic sign in colorectal cancer.53 Knowing the extent of lymph
node involvement is vital for determining an accurate prognosis and planning
treatment.54
The National Cancer Institute estimates that 142,570 Americans will develop
colorectal cancer in 2010, and approximately 51,370 people will die from the disease.55
Most of the people diagnosed with colorectal cancer will be 70 years of age or older. For
people of all ages, the lifetime risk of developing colorectal cancer is approximately
5.12%.56 Survival after the disease has been detected depends, in large part, on how far
the disease has spread. If the disease is local, the five-year survival rate is estimated to be
90.4%. If the disease has spread to the lymph nodes, the five-year survival rate is
estimated to be 69.5%. And if there are metastases, the five-year survival rate is
estimated to be 11.6%.57
Learning Break: Unfortunately, many people with colorectal cancer are not diagnosed
until the disease has advanced significantly and for these people the five-year survival
rate is approximately 10%.58
TREATING COLORECTAL CANCER
There are four treatment modalities that can be used to try and cure colorectal cancer.
Quite often these therapies are combined. It would not be possible to summarize all the
therapeutic approaches that can be used to treat colorectal cancer, because treatments are
individualized based on age, prognosis, sage of the disease, metastases, etc.

Radiation therapy: Radiation therapy is the primary treatment for patients with
rectal cancer, but it has only limited use for treating patients with colon cancer.59
Chemoradiation is also the treatment of choice before surgery for patients with
advanced rectal cancer.60

Biologic agents: Monoclonal antibodies have significantly improved the outcomes
in patients with metastatic colorectal cancer.61 Bevacizumab (Avastin®) is a
monoclonal antibody that works against vascular endothelial growth factor and
limits tumor size and growth by inhibiting angiogenesis. When it is combined
with leucovorin and fluoruoacil or other chemotherapeutic drugs, the progressionfree survival rate and the response of tumors to therapy are improved.62,63
Cetuximab (Erbitux®) is a monoclonal antibody immunoglobulin that is an
epidermal growth factor receptor inhibitor. When cetuximab has been combined
with irinotecan (Camptosar®), the tumor response rate has been doubled.64
Learning Break: One of the most important steps in tumor metastasis is angiogenesis,
the growth of new blood vessels. The process of angiogenesis is normally controlled by
inhibitors and activators. Tumors promote angiogenesis – and thus their own growth and
spread – by producing proteins such as vascular endothelial growth factor that are
angiogenesis activators.
Learning Break: Tumor response rate refers to the amount a tumor decreases in
response to therapy.

Chemotherapy: Chemotherapy can be used as a stand-alone therapy or as adjuvant
therapy to surgery. The drugs used and the protocols will depend on prognosis,
disease stage, etc. Irinotecan and oxilaplatin (Eloxitan®) can be combined with
the drugs that have been traditionally used, 5-fluorouacil (5-FU) and leucovorin
(LV). The irinotecan, 5-FU, and LV combination is called FOLFIRI; the
oxiaplatin, 5-FU, and LV combination is called FOLFOX. These regimens have
increased the tumor response rate from less than 25% to 40% - 50%, and they
have allowed surgeons to more successfully resect tumors.65

Surgery: Surgery is the only treatment that offers a potential cure or colorectal
cancer and colorectal cancer with metastases.66,67 The surgeon will attempt to
resect the colonic tumor and resect metastatic lesions if this is needed: patients
with metastatic disease will require adjuvant chemotherapy. Depending on the
location and size of the primary lesion (s), local tumor destruction and/or removal
can be done, as can variations of colectomies, e.g., partial colectomy,
hemicolcetomy, and total colectomy. Laparoscopic surgery as a treatment option
for colorectal cancer has been shown to be as effective as the open approach.68
Learning Break: Surgery provides a cure in approximately 50% of patients with
localized colorectal cancer. Unfortunately, recurrences are common.69
SCREENING FOR COLON CANCER
Although there are still some questions as to exactly how effective screening can be,
there is good evidence that screening reduces mortality from colorectal cancer and is
cost-effective.70 According to guidelines published by the American Cancer Society in
2010, people with an average risk of colorectal cancer should be screened for the disease
using one of the following:71

Annual fecal occult blood testing or the fecal immunochemical test (FIT)

Exfoliated DNA in the stool. This test detects DNA mutations that are commonly
seen in colorectal cancers. The optimal timing interval for this test has not been
determined.

Flexible sigmoidoscopy every five years.

Colonoscopy every 10 years.

Double-contrast barium enema (DCBE) every 10 years.

Computerized tomography colonography (aka, virtual colonoscopy) every five
years.
The screening guidelines differ for people who are considered to be at high risk for
developing colorectal cancer. This would include people who a) have had an
adenomatous polyp, b) who have a first-degree relative who has had colorectal cancer or
an adenomatous polyp, c) have inflammatory bowel disease, d) have a hereditary
syndrome that increases susceptibility to the disease, and d) have had resection of the
colon to cure colorectal cancer. People who are in one of those categories should receive
more frequent screening.72
PREVENTION OF COLORECTAL CANCER
Modifying risk factors, polyp removal, and the use of certain medications have been
investigated as possible ways to prevent colorectal cancer.

Non-steroidal anti-inflammatory drugs, aspirin: There is some evidence that in
certain patients, non-steroidal anti-inflammatory (NSAID) drugs and aspirin can
reduce the incidence of adenomas and adenomatous polyps.73 However, the
evidence is inconclusive and at this time, the routine use of these drugs for the
prevention of colorectal cancer is not recommended.74

COX-2 inhibitors: Prostaglandins are thought to play a role in carcinogenesis, and
some clinical trials have shown that using the OX-2 inhibitors (e.g., ) could
possibly stop the development and progression of colorectal cancers.75,76

Diet and exercise: A recent large-sale study in Europe found that decreasing body
mass index (BMI) and increasing the level of physical activity could reduce the
incidence of colorectal cancer in males and females.77 Folic acid supplements,
vitamin D supplements, and calcium supplements have also been investigated as
prophylactic treatments to prevent colorectal cancer, but the evidence for their
efficacy is inconclusive.78,79

Polyp removal: There is strong and consistent evidence that removing
adenomatous polyps has a positive effect on mortality rates of colorectal cancer.80

Post-menopausal hormone use: Using estrogen and progesterone in postmenopausal women can decrease the incidence of colorectal cancer, but the risks
– increased incidence of thromboembolic events, coronary heart disease, and
breast cancer – are significant.81,82
NURSING CARE
There are many issues involving nursing care of the patient with colorectal cancer.
Specific medical issues would include obstruction, hemorrhage, and anemia. Nursing
diagnoses related to caring for a patient with colorectal cancer would include:83

Imbalanced nutrition: Patients may be NPO, may be on enteral or parenteral
feedings, or may suffer from various gastrointestinal complaints such as anorexia
or bloating that make it difficult for them to maintain good nutrition.

Constipation/diarrhea: Constipation or diarrhea can be significant problems for
the patient with colorectal cancer in the later stages of the disease.

Chronic pain: managing the chronic pain of colorectal cancer can be difficult.
Opioid analgesics are very helpful, but have side effects and dependency issues
that can, at times, make them difficult to use

Fatigue: Both thee disease itself, the complications it causes, and the treatments
used can produce profound fatigue. The patient will need support and help in
planning his/her activities of daily living.

Fear: Colorectal cancer is a frightening disease. Patients diagnosed with colorectal
cancer will need emotional and psychological support.
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