Colorectal cancer is a disease with an increasing incidence. Environmental factors and genetic factors are known to increase the likelihood of colorectal cancer. Most colorectal cancer patients are members of families with hereditary colon cancer syndrome. , inflammatory bowel disease with a personal or family history of colorectal cancer or adenomas, and greater abdominal radiation exposure.
What are the risk factors for colorectal cancer?1. Genetic factorsSeveral specific genetic diseases with extremely high risk of colon cancer have been identified. Most of these diseases are autosomal dominant, but only account for about 5% of colorectal cancer cases. Familial adenomatous polyposis is the most common familial colon cancer syndrome, and polyposis and its variants account for less than 1% of colorectal cancers.
In classic polyposis, many colon adenomas develop during childhood. The average age at onset of symptoms is approximately 16 years, and 90% of untreated individuals develop colon cancer before the age of 45. Although attenuating polyposis is associated with a higher risk of colon cancer, it is characterized by fewer adenomas and an older average age at diagnosis.
2. History of related diseasesPersonal or family history of sporadic colorectal cancer or adenomatous polyps. Patients with a personal history of colorectal cancer or colon adenomatous polyps are at risk for future colon cancer. If patients undergo a single colorectal cancer resection, 1.5%-3% of patients will develop metachronous primary cancer within 5 years after surgery. Although genetic susceptibility increases the risk of colorectal cancer most clearly, most colorectal cancers are sporadic rather than familial.
A personal history of macroadenomatous polyps, villous or tubulovillous polyps, or high-grade dysplasia, especially multiple polyps, also increases the risk of colorectal cancer. On the other hand, patients with one or two small tubular adenomas do not appear to have a substantial increased risk of developing metachronous colorectal cancer.
Even beyond syndromes with clear genetic susceptibility, family history remains an important risk factor. If a patient has a first-degree relative with colorectal cancer, the risk of colorectal cancer is approximately twice that of the general population. The risk is further increased if the patient's mother or father has two first-degree relatives with colon cancer or if the proband is diagnosed under the age of 50-60 years.
3. Inflammatory bowel diseaseAn association between chronic ulcerative colitis and colon tumors has been demonstrated, with disease extent, duration, and activity of ulcerative colitis being major determinants. Compared with the expected incidence of colon tumors in the general population, pancolitis increases the risk to 5-15 times, while colitis limited to the left colon has a relative risk of 3 times; in contrast, colitis alone Enteritis or proctosigmoiditis did not appear to significantly increase risk. Evidence that some treatments for inflammatory colitis reduce colorectal cancer risk and that the risk of colorectal cancer is less in quiescent disease than in chronic active disease justifies reduced frequency of surveillance.
The risk of colon cancer begins to increase 8 to 10 years after the initial diagnosis of pancolitis, and for colitis limited to the left colon, the risk begins to increase 15 to 20 years after diagnosis. The likelihood of cancer increases with the duration of the disease and is also increased in patients with active inflammation.
4. Abdominal radiotherapyAdult survivors of childhood malignancies who have received abdominal radiation therapy are at significantly increased risk of developing gastrointestinal tumors, many of which are colorectal cancer. A history of radiation therapy for prostate cancer is associated with an increased risk of rectal cancer, a risk similar to that seen in patients with a family history of colon adenomas. Whether these cancers also evolve from adenomas and whether increased screening of these patients will improve cancer detection rates and outcomes are unknown.
