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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. This is then followed by medical imaging to determine if the disease has spread. Treatments used for colorectal cancer may include some combination of surgery, radiation therapy, chemotherapy and targeted therapy. A number of genetic syndromes are also associated with higher rates of colorectal cancer.
Most deaths due to colon cancer are associated with metastatic disease. It is a transcriptional factor that influences the expression of hepatocyte growth factor. 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 tract, most frequently as a result of mutations in the Wnt signaling pathway that increase signaling activity. Beyond the defects in the Wnt signaling pathway, other mutations must occur for the cell to become cancerous. The p53 protein, produced by the TP53 gene, normally monitors cell division and kills cells if they have Wnt pathway defects. TGF-β has a deactivating mutation in at least half of colorectal cancers. Some genes are oncogenes: they are overexpressed in colorectal cancer.
Comprehensive, genome-scale analysis has revealed that colorectal carcinomas can be categorized into hypermutated and non-hypermutated tumor types. Longitudinally opened freshly resected colon segment showing a cancer and four polyps. The diagram indicates sub-clones and sub-sub-clones that were precursors to the tumors. Field defects are important in progression to colon cancer. However, in most cancer research, as pointed out by Rubin “The vast majority of studies in cancer research has been done on well-defined tumors in vivo, or on discrete neoplastic foci in vitro. An expanded view of field effect has been termed “etiologic field effect”, which encompasses not only molecular and pathologic changes in pre-neoplastic cells but also influences of exogenous environmental factors and molecular changes in the local microenvironment on neoplastic evolution from tumor initiation to death. As described by Vogelstein et al. However, by comparison, epigenetic alterations in colon cancers are frequent and affect hundreds of genes.
For instance, there are types of small RNAs called microRNAs that are about 22 nucleotides long. Expression of these miRNAs can be epigenetically altered. Changes in the level of miR-137 expression result in changed mRNA expression of the target genes by 2 to 20-fold and corresponding, though often smaller, changes in expression of the protein products of the genes. Other microRNAs, with likely comparable numbers of target genes, are even more frequently epigenetically altered in colonic field defects and in the colon cancers that arise from them. In addition to epigenetic alteration of expression of miRNAs, other common types of epigenetic alterations in cancers that change gene expression levels include direct hypermethylation or hypomethylation of CpG islands of protein-encoding genes and alterations in histones and chromosomal architecture that influence gene expression. Recent evidence indicates that early epigenetic reductions of DNA repair enzyme expression likely lead to the genomic and epigenomic instability characteristic of cancer. As summarized in the articles Carcinogenesis and Neoplasm, for sporadic cancers in general, a deficiency in DNA repair is occasionally due to a mutation in a DNA repair gene, but is much more frequently due to epigenetic alterations that reduce or silence expression of DNA repair genes. Colorectal cancer diagnosis is performed by sampling of areas of the colon suspicious for possible tumor development, typically during colonoscopy or sigmoidoscopy, depending on the location of the lesion. It is confirmed by microscopical examination of a tissue sample.
Disease extent is usually determined by a CT scan of the chest, abdomen and pelvis. Colon cancer staging is done next and is based on radiology and pathology. As for all other forms of cancer, tumor staging is based on the TNM system which considers how much the initial tumor has spread, if and where there are lymph node metastasis and if there are metastases in more distant organs, usually liver. The microscopic cellular characteristics of the tumor are reported from the analysis of tissue taken from a biopsy or surgery. A pathology report contains a description of the microscopical characteristics of the tumor tissue, including both tumor cells and how the tumor invades into healthy tissues and finally if the tumor appears to be completely removed. This very rarely causes obstruction of feces, and presents with symptoms such as anemia. Adenocarcinoma is a malignant epithelial tumor, originating from superficial glandular epithelial cells lining the colon and rectum.
It invades the wall, infiltrating the muscularis mucosae layer, the submucosa, and then the muscularis propria. In cases where a metastasis from colorectal cancer is suspected, immunohistochemistry is used to ascertain correct diagnosis. Proteins that are more specifically expressed in colorectal cancer and can be used as diagnostic markers are cytokeratin 20, CDX2, SATB2 and CDH17. CT of a staging exam of colon carcinoma. Besides the primary tumor a lot of lesions can be seen. Near normal colon-lining cells are seen at the top right of the image. Normal colorectal mucosa is seen on the right. Staging is typically made according to the TNM staging system from the WHO organization, the UICC and the AJCC. The T stages of bowel cancer.
The most common metastasis sites for colorectal cancer are the liver, the lung and the peritoneum. Tumor budding in colorectal cancer is loosely defined by the presence of individual cells and small clusters of tumor cells at the invasive front of carcinomas. It has been estimated that about half of colorectal cancer cases are due to lifestyle factors, and about a quarter of all cases are preventable. Increasing surveillance, engaging in physical activity, consuming a diet high in fiber, and reducing smoking and alcohol consumption decrease the risk. Current dietary recommendations to prevent colorectal cancer include increasing the consumption of whole grains, fruits and vegetables, and reducing the intake of red meat and processed meats. Aspirin and celecoxib appear to decrease the risk of colorectal cancer in those at high risk.
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