When developed, obstruction and perforation of large bowel may occur.
Adenocarcinoma is a cancer of glandular epithelial cells in several parts of the body including colons, rectum, breasts, esophagus, lungs, pancreas, and prostates. Colorectal cancer is a cancer of the large bowel caused by multiple genetic lesions that occur in sequence over time. As the disease advances, not only the tissue structure, but cellular genotype change.
credit: large bowel ASCRS
In the early stage of the disease, mutations occur in either the APC gene, which is a human cancer suppressive gene, or a mismatch repair gene. The APC gene regulates cell growth and apoptosis. Mutations in the APC gene may result in colorectal cancer. Mutations of the mismatch repair gene fail to repair DNA transcription errors and the accumulation of the mutations.
Germline mutations in the APC gene result in familial adenomatous polyposis, whereas those of the mismatch repair gene result in hereditary nonpolyposis colon cancer. When mutations accumulate, genetic instability and loss of heterozygosity occur. As a result, because of the loss of individual chromosomes during mitosis, cells have only one allele of a gene. If DNA methylation changes, tumor suppressor genes such as p14 and p16 do not properly work. Other genetic and epigenetic alterations result in metastasis.
Common symptoms of colorectal cancer include rectal bleeding, abdominal pain, and change in bowel function. Systemic symptoms of colorectal cancer may be weight loss, jaundice, and ascites (ascites occur with peritoneal metastases). Symptoms depend on whether the cancer has developed: when it has not developed, bleeding and associated symptoms occur; when it has developed, obstruction and perforation are likely to occur. With rectal cancers, tenesmus and changes in stool size can occur. Rectal cancers affect sacral nerve plexi, resulting in neuropathic pain.