Overview of Colon Cancer
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colon cancer colonoscopy
It is important to recognize the increased risk for cancer in patients with hereditary cancer syndromes, but by far the most common form of colon cancer is sporadic in nature, without an associated strong family history.
Although the cause and pathogenesis of adenocarcinoma are similar throughout the large bowel, colon cancer, significant differences in the use of diagnostic and therapeutic modalities separate colonic from rectal cancers. This distinction is largely due to the confinement of the rectum by the bony pelvis. The limited mobility of the rectum allows MRI to generate better images and increases its sensitivity. In addition, the proximity of the rectum to the anus permits easy access of ultrasound probes for more accurate assessment of the extent of penetration of the bowel wall and the involvement of adjacent lymph nodes. The limited accessibility of the rectum, the proximity to the anal sphincter, and the close association with the autonomic nerves supplying the bladder and genitalia require special and unique consideration when planning treatment for cancer of the rectum. Therefore, colon and rectal adenocarcinomas are discussed separately.
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Posted in Colon cancer, Diagnosis, Prognosis | 
Tags: clinical, colon cancer, colorectal cancer, Diagnosis, large bowel, management, Surgery, Symptoms
Ulcerative Colitis & Crohn’s Disease with Colon Cancer ?
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Cancer that occurs in patients with ulcerative colitis can arise in any portion of the large bowel, and it carries the same prognosis as colon cancer in general. Although the risk of cancer is relatively low in the first decade after the onset of colitis, it increases to approximately 20% each decade thereafter. In addition to duration of disease, the incidence of colon cancer rises with extent of colonic involvement and severity of disease.Because all currently available screening tests (including repetitive biopsies linking dysplasia and bowel mucosa transformation to cancer) are problematic,most patients with this unusually high risk for colon cancer will probably benefit at some point from prophylactic colectomy. The application of molecular markers (e.g., sucrase isomaltase) may more quantitatively define risk for transformation in an individual patient, allowing a more rational recommendation for preemptive surgery.When ileoproctostomy is performed, preserving the distal rectum and anus, a worrisome incidence of carcinoma has still been observed. Proctocolectomy with a Brooke ileostomy or abdominal colectomy, mucosal proctectomy, and ileoanal reconnection with one of the reservoir procedures can be applied to individual patients, which provides complete freedom from subsequent cancer development and the most appropriate bowel function for the patient’s psychological and functional well-being to be chosen.
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Colon Cancer and Polyposis FAP – HNPPC ?
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Certain groups of patients have a predisposition to the development of cancer of the large bowel. These identifiable high-risk cohorts also have a greater possibility for early intervention and cancer prevention and include patients with inherited conditions such as familial adenomatous polyposis (FAP), hereditary nonpolyposis colon cancer (HNPCC), and ulcerative colitis. Patients with FAP (frequency estimated at 1:7,000 to 10,000 live births) have a lifetime risk of the development of colon cancer that approaches 100%. The disease is inherited as an autosomal dominant trait, and affected individuals will transmit this predisposition, with each of their offspring having nearly a 50% chance of developing polyposis coli. The gene that causes FAP (adenomatous polyposis coli [APC] gene) resides on chromosome 5 and has been cloned and sequenced.
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Nature of Colon Cancer – Natural History
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Most colon cancers were reported to arise in the distal bowel. The rubric that rectal examination plus rigid proctosigmoidoscopy finds 75% of all colon cancers is no longer valid . Approximately 25% of all polyps can be reached by the rigid proctoscope and 60% can be reached with the 60-cm flexible sigmoidoscope. Although no satisfactory explanation for the change in the segmental distribution of colon and rectal carcinoma is conclusive, there are numerous possibilities. First, because the more proximal colon is more accessible through the wider application of endoscopic techniques and because there is greater use of double-contrast barium studies, more right-sided or proximal bowel lesions may be diagnosed that were always there but were less frequently diagnosed. Second, there may actually be multiple environmental and genetic risk factors that determine right-sided or proximal bowel lesions that are distinct from the causes of left-sided or distal bowel tumors. Numerous formalized treatment protocols of bowel cancer demonstrate that the natural history of right-sided lesions differs from that of left-sided lesions. The natural history of sigmoid cancers differs from that of more proximal colonic tumor. The natural history of rectal cancer is different from that of colon cancer. These differences are reflected in patterns of recurrence and include responsiveness to multimodality adjuvant therapy.
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Clinical diagnosis – Amsterdam criteria,Besthesda guideline
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| Amsterdam Criteria (1991) |
| 1. Three of more relatives, of whom two are first-degree relative of the third, with documented colorectal cancer |
| 2. Cancer occurring across two or more generations |
| 3. One or more cancers diagnosed before age 50 |
| 4. Familial adenomatous polyposis excluded |
| Bethesda Guidelines (1997) |
| 1. Individuals who meet the Amsterdam criteria |
| 2. Individual with two HNPCC-related cancers (synchronous/metachronous colorectal cancers or extracolonic cancers) |
| 3. Individuals with colorectal cancer and a first-degree relative with |
| a. Colorectal cancer diagnosed before age 45 or |
| b. HNPCC-related extracolonic cancer diagnosed before age 45 or |
| c. Colorectal adenoma diagnosed before age 40 |
| 4. Individuals with colorectal cancer or endometrial cancer diagnosed before age 45 or |
| 5. Individuals with proximal colon cancer of undifferentiated type or histopathology diagnosed before age 45 |
| 6. Individuals with signet ring cell colorectal cancer diagnosed before age 45 |
| 7. Individuals with colorectal adenomas diagnosed before age 40 |
| HNPCC = hereditary nonpolyposis colorectal cancer. |
