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
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.
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.
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.