Before reading any of the following, please read Stephen Jay Gould's The Median Isn't the Message, which helps put into perspective some things about statistics.

And remember - somebody has to be in that survival percentage! Why not you?!

More detailed information is available by following the "source" links for each entry.

>>> My list of colon cancer resources. <<<

[ incidence ] [ screening ] [ risk factors ] [ symptoms ] [ staging ] [ treatment ]

links/info last checked/updated 13 Dec 2007


Incidence of colorectal cancer [ top ]

Colorectal cancer is the third most common malignant neoplasm worldwide, and the second leading cause of cancer deaths in the United States. It is estimated that there will be 153,760 new cases diagnosed in the United States in 2007 and 52,180 deaths due to this disease. Between 1973 and 1995, mortality from colorectal cancer declined by 20.5% and incidence declined by 7.4% in the United States. The incidence is higher in men than in women. It ranges from 48.3 per 100,000 per year in Hispanic men to 72.5 in African American men. In women it ranges from 32.3 in Hispanics to 56.0 in African Americans per 100,000 per year. The age-adjusted mortality rates for men and women are 24.8 in men and 17.4 in women. About 6% of Americans are expected to develop the disease within their lifetime. Age-specific incidence and mortality rates show that most cases are diagnosed after 50 years of age.

Genetic, experimental, and epidemiologic studies suggest that colorectal cancer results from complex interactions between inherited susceptibility and environmental or lifestyle factors. Efforts to identify causes and to develop effective preventive measures have led to the hypothesis that adenomatous polyps (adenomas) are precursors for the vast majority of colorectal cancers. In effect, measures which reduce the incidence and prevalence of adenomas may result in a subsequent decrease in the risk of colorectal cancer. In addition, the formation and spontaneous regression of adenomas may also be a dynamic process.

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Screening for colon cancer [ top ]

There are several tests to detect colorectal cancer. Some of these are still under investigation. [more detailed information]

(source)


Factors associated with an increased risk of developing colorectal cancer [ top ]

There are groups which have a high incidence of colorectal cancer. They include those with hereditary conditions, such as:

familial adenomatous polyposis
hereditary nonpolyposis colorectal cancer (inherited in an autosomal dominant manner)

Together these account for no more than 6% of colorectal cancers.


More common conditions associated with an increased risk include:

a personal history of colorectal cancer or adenomas
a first degree relative with colorectal cancer
a first degree relative with adenomas diagnosed before 60 years of age
a personal history of ovarian, endometrial, or breast cancer
a personal history of longstanding chronic ulcerative colitis or Crohn's colitis

These high-risk groups account for about a quarter of all colorectal cancers. Limiting screening or early cancer detection to only these high-risk groups would miss the majority of colorectal cancers.

(source)


More facts and figures.


Colon cancer rates are high in populations with high total fat intakes and are lower in those consuming less fat. On average, fat comprises 40% to 45% of total caloric intake in high-incidence Western countries; in low-risk populations fat accounts for only 10% of dietary calories. In laboratory studies a high fat intake increases the incidence of induced colon tumors in experimental animals. Several  case-control studies have explored the association of colon cancer risk with meat or fat consumption as well as protein and energy intake. Although positive associations with meat consumption or with fat intake have been found frequently, the results have not always achieved statistical significance.

Explanations for the conflicting results regarding whether dietary fat or meat intake affects risk of colorectal cancer include, (a) validity of dietary questionnaires used; (b) differences in the average age of the population studied; (c) variations in methods of meat preparation (in some instances, mutagenic and carcinogenic heterocyclic amines could have been released at high temperatures) and (d) variability in the consumption of other foods, such as vegetables. In addition, some epidemiological studies have reported lower incidence rates of colon cancer in populations with high intakes of both fat and fiber, compared with populations with high levels of fat but low levels of fiber consumption. Although far from clear cut, the available evidence suggests colorectal cancer risk is possibly associated with some interaction of dietary fat and protein and caloric intake.

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More information regarding diet and other possible means of prevention can be found at this NCI link or at this MSKCC link.


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Symptoms of colon cancer [ top ]

Colorectal cancer sometimes arises without any symptoms. For this reason, screening tests (such as colonoscopy and a test for blood in the stool) are recommended to detect the cancer early, when it is more curable.

When symptoms do occur, however, they may include the following:

rectal bleeding or blood in the stool
a change in bowel habits (such as diarrhea, constipation, and narrowing of the stool) that lasts for more than a few days
abdominal pain
a continuous feeling that you need to have a bowel movement, which does not resolve after passing stool
weakness

Some of these symptoms may be caused by other conditions, but you should see your doctor if they persist. Any incidence of rectal bleeding or blood in the stool should be brought to your doctor's attention.

(source)


Some information on screening. (the links are in the box with the heading "screening and early detection")


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Staging of colon cancer [ top ]

Detailed information on current methods of dealing with colorectal cancer can be found at this link to the physicians' version, or at this link to the patients' version (which is written in less technical language).

The TNM classification system is the newer system of tumor classification, made by the American Joint Committee on Cancer (AJCC). Dukes' and Modified Astler-Coller (MAC) are older systems, but you will still run across references to them. Below are an explanation of the TNM classification system; the most recent AJCC staging; equivalencies of the current staging system and the older staging systems; and the Dukes'/MAC versions of the classification system.

TNM classification explanation
[ staging ] [ TNM explanation ][ AJCC staging ] [ old/new equivalents ] [ Dukes'/MAC staging ] [ top ]

T assesses the primary tumor

TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
Tis: Carcinoma in situ: intraepithelial or invasion of the lamina propria (Includes cancer cells confined within the glandular basement membrane (intraepithelial) or lamina propria (intramucosal) with no extension through the muscularis mucosae into the submucosa.)
T1: Tumor invades submucosa
T2: Tumor invades muscularis propria
T3: Tumor invades through the muscularis propria into the subserosa, or into nonperitonealized pericolic or perirectal tissues
T4: Tumor directly invades other organs or structures, and/or perforates visceral peritoneum (Direct invasion includes invasion of other segments of the colorectum by way of the serosa; for example, invasion of the sigmoid colon by a carcinoma of the cecum. Tumor that is adherent macroscopically to other organs or structures is classified T4. If no tumor is present in the adhesion microscopically, however, the classification should be pT3. The V and L substaging should be used to identify the presence or absence of vascular or lymphatic invasion.)


N assesses the regional lymph nodes

NX: Regional nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis in 1 to 3 regional lymph nodes
N2: Metastasis in 4 or more regional lymph nodes

A tumor nodule in the pericolorectal adipose tissue of a primary carcinoma without histologic evidence of residual lymph node in the nodule is classified in the pN category as a regional lymph node metastasis if the nodule has the form and smooth contour of a lymph node. If the nodule has an irregular contour, it should be classified in the T category and also coded as V1 (microscopic venous invasion) or as V2 (if it was grossly evident), because there is a strong likelihood that it represents venous invasion.


M assesses distant metastasis

MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis

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AJCC staging
[ staging ] [ TNM explanation ][ AJCC staging ] [ old/new equivalents ] [ Dukes'/MAC staging ] [ top ]
Stage 0 Tis N0 M0
Stage I T1 N0 M0
T2 N0 M0
Stage IIA T3 N0 M0
Stage IIB T4 N0 M0
Stage IIIA T1 N1 M0
T2 N1 M0
Stage IIIB T3 N1 M0
T4 N1 M0
Stage IIIC any T N2 M0
Stage IV any T any N M1

(source)


AJCC/Dukes'/MAC equivalencies
[ staging ] [ TNM explanation ][ AJCC staging ] [ old/new equivalents ] [ Dukes'/MAC staging ] [ top ]
current: AJCC
old: Dukes
old: MAC
Stage 0 Tis N0 M0
Stage I T1 N0 M0 Dukes A Modified Astler-Coller A and B1
T2 N0 M0
Stage II T3 N0 M0 Dukes B Modified Astler-Coller B2 and B3
T4 N0 M0
Stage III any T N1 M0 Dukes C Modified Astler-Coller C1-C3
any T N2 M0
Stage IV
and recurrent colon cancer
any T any N M1 Dukes D Modified Astler-Coller D

(source pages now broken down by stage: [ stage 0 ] [ stage I ] [ stage II ] [ stage III ] [ stage IV/recurrent ] )


Histopathologic Grade
is also defined by the pathologist and is a measurement of how well differentiated - how well specialized - the cells in the tumor are. A normal cell is very well differentiated. Cancer cells are always less differentiated. The less differentiated they are, the faster they usually grow and the more prone they are to metastasize.

GX: Grade cannot be assessed
G1: Well differentiated
G2: Moderately well differentiated
G3: Poorly differentiated
G4: Undifferentiated.

(source)


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Older tumor classification systems
[ staging ] [ TNM explanation ][ AJCC staging ] [ old/new equivalents ] [ Dukes'/MAC staging ] [ top ]

Dukes'

A: Tumor does not grow beyond muscularis propria
B: Tumor grows beyond muscularis propria
C: Lymph node metastasis/es with the tumor
D: Distant metastasis/es

Astler-Coller

A: Tumor limited to mucosa; carcinoma in situ
B1: Tumor grows through muscularis mucosae but not through muscularis propria
B2: Tumor grows beyond muscularis propria
C1: Stage B1 with regional lymph node metastases
C2: Stage B2 with regional lymph node metastases
D: Distant metastases.

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Treatment of colon cancer [ top ]

Detailed information on current methods of dealing with colorectal cancer can be found at this link to the physicians' version or at this link to the patients' version (which is written in less technical language).


STAGE 0 COLON CANCER

Stage 0 colon cancer is the most superficial of all the lesions and is limited to the mucosa without invasion of the lamina propria. Because of its superficial nature, the surgical procedure may be limited.

Treatment options:
Local excision or simple polypectomy with clear margins.
Colon resection for larger lesions not amenable to local excision.

(source)


STAGE I COLON CANCER (old staging: Dukes' A or Modified Astler-Coller A and B1)

Because of its localized nature, stage I has a high cure rate.

Treatment options:
Wide surgical resection and anastomosis.
The role of laparoscopic techniques in the treatment of colon cancer is under evaluation in a multicenter prospective randomized trial comparing laparoscopic-assisted colectomy (LAC) to open colectomy. The quality-of-life component of this trial has been published and minimal short-term quality-of-life benefits with LAC were reported.
(source)


STAGE II COLON CANCER (old staging: Dukes' B or Modified Astler-Coller B2 and B3)

Treatment options:  [ more information ]
Wide surgical resection and anastomosis.
The role of laparoscopic techniques in the treatment of colon cancer is under evaluation in a multicenter prospective randomized trial comparing laparoscopic-assisted colectomy (LAC) to open colectomy. The quality-of-life component of this trial has been published and minimal short-term quality-of-life benefits with LAC were reported.
Following surgery, patients should be considered for entry into carefully controlled clinical trials evaluating the use of systemic or regional chemotherapy, radiation therapy, or biologic therapy. Adjuvant therapy is not indicated for most patients unless they are entered into a clinical trial. Information about ongoing clinical trials is available from the NCI cancer.gov website

(source)


STAGE III COLON CANCER (old staging: Dukes' C or Modified Astler-Coller C1-C3)

Treatment options:  [ more information ]
Wide surgical resection and anastomosis. For patients who are not candidates for clinical trials, postoperative chemotherapy with fluorouracil (5-FU)-leucovorin for 6 months is an option. Based on preliminary results from the MOSAIC trial presented at the American Society of Clinical Oncology meeting in 2003, adjuvant FOLFOX4 (oxaliplatin, leucovorin, 5-FU) demonstrated prolonged 3-year survival but has not yet demonstrated an overall survival advantage.
The role of laparoscopic techniques in the treatment of colon cancer is under evaluation in a multicenter prospective randomized trial comparing laparoscopic-assisted colectomy (LAC) to open colectomy. The quality-of-life component of this trial has been published and reported minimal short-term quality-of-life benefits with LAC.
Eligible patients should be considered for entry into carefully-controlled clinical trials comparing various postoperative chemotherapy regimens that are now also including oxaliplatin-based and irinotecan-based chemotherapy with new targeted agents or biological therapy, alone or in combination. Information about ongoing clinical trials is available from the NCI cancer.gov website.

(source)


STAGE IV  AND RECURRENT COLON CANCER

Treatment options:  [ more information ]
Surgical resection of locally recurrent cancer.
Surgical resection/anastomosis or bypass of obstructing or bleeding primary lesions in selected metastatic cases.
Resection of liver metastases in selected metastatic patients (5-year cure rate for resection of solitary or combination metastases exceeds 20%) or ablation in selected patients.
Resection of isolated pulmonary or ovarian metastases in selected patients.
Palliative radiation therapy.
Palliative chemotherapy.
Clinical trials evaluating new drugs and biological therapy.
Clinical trials comparing various chemotherapy regimens or biological therapy, alone or in combination.
 

The page linked to from "more information" and "source" contains information on:
Liver Metastasis
Treatment of Patients With Stage IV Disease
First-line Multiagent Chemotherapy
The Addition of Bevacizumab to Multiagent Chemotherapy
Second-line and Third-line Chemotherapy

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