Generally Treating Locally Advanced Rectal Cancer Includes
Colorectal cancer CRCalso known as bowel cancercolon canceror rectal canceris the development of cancer from the colon or rectum parts of the large intestine.
Most colorectal cancers are due to old age and lifestyle factors, with only a small number of cases due to underlying genetic disorders. Bowel cancer may be diagnosed by obtaining a sample of the colon during a sigmoidoscopy or colonoscopy.
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Aspirin and other non-steroidal anti-inflammatory drugs decrease the risk. Treatments used for colorectal cancer may include some combination of surgery, radiation therapychemotherapy and targeted therapy. The signs and symptoms of colorectal cancer depend on the location of the tumor in the boweland whether it has spread elsewhere in the body metastasis. Geneally classic warning signs include: worsening constipationblood in the stool, decrease in stool caliber thicknessloss of appetite, loss of weight, and nausea or vomiting in someone over 50 years old.
Rectal bleeding or anemia are high-risk symptoms in people over the age of People with inflammatory bowel disease ulcerative colitis and Crohn's disease are at increased risk of colon cancer. A number of genetic syndromes are also associated with higher rates of colorectal cancer.
Colectomy, removal of the colon, may not suffice as a preventative measure Tfeating of the high risk of rectal cancer if the rectum remains.
Progress in Treating GI Cancers Through Molecular Testing: The 2021 Advance of the Year
Most deaths due to colon cancer are associated with metastatic disease. A gene that appears to contribute to the potential for metastatic disease, metastasis associated in colon cancer 1 MACC1has been isolated. This gene is associated with the proliferation, invasion and scattering of colon cancer cells in cell culture, and tumor growth and metastasis in mice. MACC1 may be a potential target for cancer intervention, but this possibility needs to be confirmed with clinical studies.
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Epigenetic factors, such as abnormal DNA methylation of tumor suppressor promoters, play a role in the development of colorectal cancer. Colorectal cancer is a disease originating from the epithelial cells lining the colon or rectum of the gastrointestinal tractmost frequently as a result of mutations in the Wnt signaling pathway that increase signaling activity. The mutations can be inherited or acquiredand most probably occur in the intestinal crypt stem cell. These genes are normally important for stem cell Generaally and differentiation, but when inappropriately expressed link high levels, they can cause cancer.
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Beyond the defects in the Wnt signaling pathwayother mutations must occur for the cell to become cancerous. The p53 protein, produced by the TP53 gene, normally monitors cell division and induces their programmed death if they have Wnt pathway defects. Eventually, a cell line acquires a mutation in the TP53 gene and transforms the tissue from a benign epithelial tumor into an invasive epithelial cell cancer.
Sometimes the gene encoding p53 is not mutated, but another protective protein named BAX is mutated instead.]
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