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World J Gastroenterol ; Dietary patterns, food groups, and rectal cancer risk in Whites and African-Americans. Cancer Epidemiol Biomarkers Prev ; Association between consumption of fruits and vegetables and risk of colorectal adenoma: a PRISMA-compliant meta-analysis of observational studies.

Med ; J Hum Nutr Diet ; Dietary patterns and colorectal cancer risk in a Korean population: a case-control study. Polyphenols in colorectal cancer: Current state of knowledge including clinical trials and molecular mechanism of action. Biomed Res Int ; PLoS One ;e Mechanisms linking dietary fiber, gut microbiota and colon cancer prevention.

World J Gastrointest Oncol ; Omega-3 polyunsaturated fatty acids for the treatment and prevention of colorectal cancer. Gut ; Dietary patterns and risk of colorectal cancer: a factor analysis in Uruguay. Asian Pac J Cancer Prev ; Associations of colorectal cancer incidence with nutrient and food group intakes in Korean adults: a case-control study.

Clin nutr ; Dietary patterns and risk of colon cancer and adenoma in a cohort of men United States. Diet and cancer prevention: the roles of observation and experimentation. Nat Rev Cancer ; Popkin BM. Understanding global nutrition dynamics as a step towards controlling cancer incidence. PloS one ;8:e Meats, milk and fat consumption in colorectal cancer. Secondary bile acids: an underrecognized cause of colon cancer. World J Surg Oncol ; Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies.

PloS One ;6:e Red and processed meat consumption and colorectal cancer risk: a systematic review and meta-analysis. Oncotarget ; Dissecting the mechanisms and molecules underlying the potential carcinogenicity of red and processed meat in colorectal cancer CRC : an overview on the current state of knowledge. Infect Agent Cancer ; Cancer Prev Res ; Colorectal cancer biomarkers: To be or not to be?

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Cautionary tales from a road well travelled. World J Gastroenterol; DNA methylation biomarkers as diagnostic and prognostic tools in colorectal cancer. J Mol Med ; Epigenomic analysis of aberrantly methylated genes in colorectal cancer identifies genes commonly affected by epigenetic alterations.

Ann Surg Oncol Levin B. Molecular screening testing for colorectal cancer. Clin Cancer Res ; Clinical applications of DNA methylation biomarkers in colorectal cancer. Epigenomics ; Journal Management System. Designed by sinaweb. DOI: Aga Syed Sameer 1 ; Saniya Nissar 2. Colorectal cancer CRC is a third most common epithelial carcinoma. Colorectal cancer ; Epigenetics ; Hypermethylation ; Biomarkers. Measurement of fecal pyruvate kinase type M2 tumor M2-PK concentrations in patients with gastric cancer, colorectal cancer, colorectal adenomas and controls.

Anticancer Res ; Total levels of tissue inhibitor of metalloproteinases 1 in plasma yield high diagnostic sensitivity and specificity in patients with colon cancer. Detection of methylated SEPT9 in plasma is a reliable screening method for both left- and right-sided colon cancers. PLoS One ;7:e Septin 9 methylated DNA is a sensitive and specific blood test for colorectal cancer. BMC Med ; The stool DNA test is more accurate than the plasma septin 9 test in detecting colorectal neoplasia. Clin Gastroenterol Hepatol ; Prospective evaluation of methylated SEPT9 in plasma for detection of asymptomatic colorectal cancer.

BMC Cancer ; N-Myc downstream-regulated gene 4 NDRG4 : a candidate tumor suppressor gene and potential biomarker for colorectal cancer. J Natl Cancer Inst ; Cancer Res ; Methylation of TFPI2 gene is frequently detected in advanced well differentiated colorectal cancer.

Detection of TFPI2 methylation in the serum of colorectal cancer patients. Cancer Lett ; DNA methylation as an epigenetic biomarker in colorectal cancer. Oncol Lett ; Evaluation of markers for CpG island methylator phenotype CIMP in colorectal cancer by a large population-based sample. J Mol Diagn ; Methylation of serum DNA is an independent prognostic marker in colorectal cancer. Clin Cancer Res ; Prognostic role of methylated free circulating DNA in colorectal cancer. Int J Cancer ; PLoS One ;5:e DNA methylation biomarkers for blood-based colorectal cancer screening. Clin Chem ; The recently suggested intestinal cancer stem cell marker DCLK1 is an epigenetic biomarker for colorectal cancer.

Epigenetics ; A panel of genes methylated with high frequency in colorectal cancer. Cancer ; Colectomy, removal of the colon, may not suffice as a preventative measure because of the high risk of rectal cancer if the rectum remains. 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 MACC1 , has 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.

Colorectal Cancer

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. The mutations can be inherited or acquired , and most probably occur in the intestinal crypt stem cell.

These genes are normally important for stem cell renewal and differentiation, but when inappropriately expressed at high levels, they can cause cancer. 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. 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. For example, genes encoding the proteins KRAS , RAF , and PI3K , which normally stimulate the cell to divide in response to growth factors, can acquire mutations that result in over-activation of cell proliferation.

Colon Cancer: Risk, Prevention, and Screening - Fola May, MD, PhD, MPhil

The chronological order of mutations is sometimes important. If a previous APC mutation occurred, a primary KRAS mutation often progresses to cancer rather than a self-limiting hyperplastic or borderline lesion. Comprehensive, genome-scale analysis has revealed that colorectal carcinomas can be categorized into hypermutated and non-hypermutated tumor types.

Mismatch repair MMR deficient tumours are characterized by a relatively high amount of poly-nucleotide tandem repeats. Lynch syndrome. The polyp to cancer progression sequence is the classical model of colorectal cancer pathogenesis. The term "field cancerization" was first used in to describe an area or "field" of epithelium that has been preconditioned by what were largely unknown processes at the time to predispose it towards development of cancer.

Field defects are important in progression to colon cancer. However, in most cancer research, as pointed out by Rubin [55] "The vast majority of studies in cancer research has been done on well-defined tumors in vivo , or on discrete neoplastic foci in vitro. Likewise, epigenetic alterations present in tumors may have occurred in pre-neoplastic field defects. 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.

Epigenetic alterations are much more frequent in colon cancer than genetic mutational alterations. As described by Vogelstein et al. The oncogenes and tumor suppressor genes are well studied and are described above under Pathogenesis. 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.

Epigenetic reductions of DNA repair enzyme expression may likely lead to the genomic and epigenomic instability characteristic of cancer. Epigenetic alterations involved in the development of colorectal cancer may affect a person's response to chemotherapy. 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.

Presence of metastases is determined by a CT scan of the chest, abdomen and pelvis. As with most other forms of cancer, tumor staging is based on the TNM system which considers how much the initial tumor has spread and the presence of metastases in lymph nodes and more distant organs. 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.

The most common form of colon cancer is adenocarcinoma. Other, rarer types include lymphoma , adenosquamous and squamous cell carcinoma. Some subtypes have been found to be more aggressive. Cancers on the right side of the large intestine ascending colon and cecum tend to be exophytic, that is, the tumor grows outwards from one location in the bowel wall. This very rarely causes obstruction of feces , and presents with symptoms such as anemia.

Colorectal cancer

Left-sided tumors tend to be circumferential, and can obstruct the bowel lumen, much like a napkin ring, and results in thinner caliber stools. 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. Tumor cells describe irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma "back to back" aspect.

Sometimes, tumor cells are discohesive and secrete mucus, which invades the interstitium producing large pools of mucus. This occurs in mucinous adenocarcinoma, in which cells are poorly differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery, this occurs in " signet-ring cell. In cases where a metastasis from colorectal cancer is suspected, immunohistochemistry is used to ascertain correct diagnosis. Certain markers isolated from the tumor can indicate specific cancer types or susceptibility to different treatments.

Appearance of the inside of the colon showing one invasive colorectal carcinoma the crater-like, reddish, irregularly shaped tumor. Gross appearance of a colectomy specimen containing two adenomatous polyps the brownish oval tumors above the labels, attached to the normal beige lining by a stalk and one invasive colorectal carcinoma the crater-like, reddish, irregularly shaped tumor located above the label.

Endoscopic image of colon cancer identified in sigmoid colon on screening colonoscopy in the setting of Crohn's disease. Besides the primary tumor a lot of lesions can be seen. On cursor position: lung nodule. Cancer — Invasive adenocarcinoma the most common type of colorectal cancer. The cancerous cells are seen in the center and at the bottom right of the image blue. Near normal colon-lining cells are seen at the top right of the image. Precancer — Tubular adenoma left of image , a type of colonic polyp and a precursor of colorectal cancer.

Normal colorectal mucosa is seen on the right. Precancer — Colorectal villous adenoma. The Astler-Coller classification and the Dukes classification are now less used. T stands for tumor stage and ranges from 0, no evidence of primary tumor, to T4 when the tumor penetrates the surface of the peritoneum or directly invades other organs or structures.

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The N stage reflects the number of metastatic lymph nodes and ranges from 0 no lymph node metastasis to 2 four or more lymph node metastasis , and the M stage gives information about distant metastasis M0 stands for no distant metastasis, and M1 for the presence of distant metastasis. 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 postulated to represent an epithelial—mesenchymal transition EMT.


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Unfortunately, its universal acceptance as a reportable factor has been held back by a lack of definitional uniformity with respect to both qualitative and quantitative aspects of tumor budding. 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. Lifestyle risk factors with strong evidence include lack of exercise, cigarette smoking, alcohol, and obesity. Starting in the s, dietary recommendations to prevent colorectal cancer often included increasing the consumption of whole grains, fruits and vegetables, and reducing the intake of red meat and processed meats.

This was based on animal studies and retrospective observational studies. However, large scale prospective studies have failed to demonstrate a significant protective effect, and due to the multiple causes of cancer and the complexity of studying correlations between diet and health, it is uncertain whether any specific dietary interventions outside of eating a healthy diet will have significant protective effects. With regard to dietary fiber, the World Health Organization cancer report noted that it has been hypothesized that fiber might help prevent colorectal cancer, but most studies have not borne this out, and status of the science remained unclear as of Higher physical activity is recommended.

The risk is not negated by regular exercise, though it is lowered. Aspirin and celecoxib appear to decrease the risk of colorectal cancer in those at high risk. There is tentative evidence for calcium supplementation, but it is not sufficient to make a recommendation.

How does colorectal cancer start?

The three main screening tests are colonoscopy , fecal occult blood testing, and flexible sigmoidoscopy. Fecal occult blood testing FOBT of the stool is typically recommended every two years and can be either guaiac-based or immunochemical. Virtual colonoscopy via a CT scan appears as good as standard colonoscopy for detecting cancers and large adenomas but is expensive, associated with radiation exposure, and cannot remove any detected abnormal growths like standard colonoscopy can.

A positive result should be followed by colonoscopy. For those at high risk, screenings usually begin at around In Canada, among those 50 to 75 years old at normal risk, fecal immunochemical testing or FOBT is recommended every two years or sigmoidoscopy every 10 years.

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Some countries have national colorectal screening programs which offer FOBT screening for all adults within a certain age group, typically starting between ages 50 to Examples of countries with organised screening include the United Kingdom, [] Australia, [] and the Netherlands.

The treatment of colorectal cancer can be aimed at cure or palliation. The decision on which aim to adopt depends on various factors, including the person's health and preferences, as well as the stage of the tumor. However, when it is detected at later stages for which metastases are present , this is less likely and treatment is often directed at palliation, to relieve symptoms caused by the tumour and keep the person as comfortable as possible.

If the cancer is found at a very early stage, it may be removed during a colonoscopy. This can either be done by an open laparotomy or sometimes laparoscopically. If there are only a few metastases in the liver or lungs they may also be removed. Sometimes chemotherapy is used before surgery to shrink the cancer before attempting to remove it. The two most common sites of recurrence of colorectal cancer are the liver and lungs.

In both cancer of the colon and rectum , chemotherapy may be used in addition to surgery in certain cases. The decision to add chemotherapy in management of colon and rectal cancer depends on the stage of the disease. In Stage I colon cancer, no chemotherapy is offered, and surgery is the definitive treatment. The role of chemotherapy in Stage II colon cancer is debatable, and is usually not offered unless risk factors such as T4 tumor, undifferentiated tumor, vascular and perineural invasion or inadequate lymph node sampling is identified.

If cancer has spread to the lymph nodes or distant organs, which is the case with stage III and stage IV colon cancer respectively, adding chemotherapy agents fluorouracil , capecitabine or oxaliplatin increases life expectancy. If the lymph nodes do not contain cancer, the benefits of chemotherapy are controversial.

If the cancer is widely metastatic or unresectable, treatment is then palliative. Typically in this setting, a number of different chemotherapy medications may be used. Another class of drugs used in the second line setting are epidermal growth factor receptor inhibitors, of which the two FDA approved ones are cetuximab and panitumumab.

The primary difference in the approach to low stage rectal cancer is the incorporation of radiation therapy. Often, it is used in conjunction with chemotherapy in a neoadjuvant fashion to enable surgical resection, so that ultimately as colostomy is not required. However, it may not be possible in low lying tumors, in which case, a permanent colostomy may be required.

Stage IV rectal cancer is treated similar to stage IV colon cancer. While a combination of radiation and chemotherapy may be useful for rectal cancer , [19] its use in colon cancer is not routine due to the sensitivity of the bowels to radiation. For locally advanced rectal cancer, neoadjuvant chemoradiotherapy has become the standard treatment. Immunotherapy with immune checkpoint inhibitors has been found to be useful for a type of colorectal cancer with mismatch repair deficiency and microsatellite instability.

Palliative care is recommended for any person who has advanced colon cancer or who has significant symptoms.