| Colorectal cancer |
| Classification and external resources |
Diagram of the lower gastrointestinal tract |
| ICD-10 |
C18-C20/C21 |
| ICD-9 |
153.0-154.1 |
| ICD-O: |
M8140/3 (95% of cases) |
| OMIM |
114500 |
| DiseasesDB |
2975 |
| MedlinePlus |
000262 |
| eMedicine |
med/413 med/1994 ped/3037 |
Colorectal cancer, commonly known as colon cancer or bowel cancer, is a cancer from uncontrolled cell growth in the colon or rectum (parts of the large intestine), or in the appendix. Genetic analysis shows that essentially colon and rectal tumours are genetically the same cancer.[1] Symptoms of colorectal cancer typically include rectal bleeding and anemia which are sometimes associated with weight loss and changes in bowel habits.
Most colorectal cancer occurs due to lifestyle and increasing age with only a minority of cases associated with underlying genetic disorders. It typically starts in the lining of the bowel and if left untreated, can grow into the muscle layers underneath, and then through the bowel wall. Screening is effective at decreasing the chance of dying from colorectal cancer and is recommended starting at the age of 50 and continuing until a person is 75 years old. Localized bowel cancer is usually diagnosed through sigmoidoscopy or colonoscopy.
Cancers that are confined within the wall of the colon are often curable with surgery while cancer that has spread widely around the body is usually not curable and management then focuses on extending the person's life via chemotherapy and improving quality of life. Colorectal cancer is the third most commonly diagnosed cancer in the world, but it is more common in developed countries. Around 60% of cases were diagnosed in the developed world. It is estimated that worldwide, in 2008, 1.23 million new cases of colorectal cancer were clinically diagnosed, and that it killed 608,000 people.[2]
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Contents
- 1 Signs and symptoms
- 2 Cause
- 2.1 Inflammatory bowel disease
- 2.2 Genetics
- 3 Pathogenesis
- 4 Diagnosis
- 5 Prevention
- 5.1 Lifestyle
- 5.2 Medication
- 5.3 Screening
- 6 Management
- 6.1 Surgery
- 6.2 Chemotherapy
- 6.3 Radiation
- 6.4 Palliative care
- 7 Prognosis
- 8 Epidemiology
- 9 Society and culture
- 10 Research
- 11 References
- 12 External links
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Signs and symptoms[edit]
The symptoms and signs of colorectal cancer depend on the location of tumor in the bowel, and whether it has spread elsewhere in the body (metastasis). The classic warning signs include: worsening constipation, blood in the stool, weight loss, fever, loss of appetite, and nausea or vomiting in someone over 50 years old.[3] While rectal bleeding or anemia are high-risk features in those over the age of 50,[4] other commonly-described symptoms including weight loss and change in bowel habit are typically only concerning if associated with bleeding.[4][5]
Cause[edit]
Greater than 75-95% of colon cancer occurs in people with little or no genetic risk.[6][7] Other risk factors include older age, male gender,[7] high intake of fat, alcohol or red meat, obesity, smoking and a lack of physical exercise.[6] Approximately 10% of cases are linked to insufficient activity.[8] The risk for alcohol appears to increase at greater than one drink per day.[9]
Inflammatory bowel disease[edit]
People with inflammatory bowel disease (ulcerative colitis and Crohn's disease) are at increased risk of colon cancer.[10] The risk is greater the longer a person has had the disease,[11] and the worse the severity of inflammation.[12] In these high risk groups both prevention with aspirin and regular colonoscopies are recommended.[11] People with inflammatory bowel disease account for less than 2% of colon cancer cases yearly.[12] In those with Crohn's disease 2% get colorectal cancer after 10 years, 8% after 20 years, and 18% after 30 years.[12] In those with ulcerative colitis approximately 16% develop either a cancer precursor or cancer of the colon over 30 years.[12]
Genetics[edit]
Those with a family history in two or more first-degree relatives have a two to threefold greater risk of disease and this group accounts for about 20% of all cases. A number of genetic syndromes are also associated with higher rates of colorectal cancer. The most common of these is hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome) which is present in about 3% of people with colorectal cancer.[7] Other syndromes that are strongly associated include: Gardner syndrome,[13] and familial adenomatous polyposis (FAP) in which cancer nearly always occurs and is the cause of 1% of cases.[14]
Pathogenesis[edit]
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 artificially increase signaling activity. The mutations can be inherited or are acquired, and most probably occur in the intestinal crypt stem cell.[15][16][not in citation given] The most commonly mutated gene in all colorectal cancer is the APC gene, which produces the APC protein. The APC protein is a "brake" on the accumulation of β-catenin protein; without APC, β-catenin accumulates to high levels and translocates (moves) into the nucleus, binds to DNA, and activates the transcription of genes that are normally important for stem cell renewal and differentiation but when inappropriately expressed at high levels can cause cancer. While APC is mutated in most colon cancers, some cancers have increased β-catenin because of mutations in β-catenin (CTNNB1) that block its degradation, or they have mutation(s) in other genes with function analogous to APC such as AXIN1, AXIN2, TCF7L2, or NKD1.[17]
Beyond the defects in the Wnt-APC-beta-catenin 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 an adenoma into an invasive carcinoma. (Sometimes the gene encoding p53 is not mutated, but another protective protein named BAX is.)[17]
Other apoptotic proteins commonly deactivated in colorectal cancers are TGF-β and DCC (Deleted in Colorectal Cancer). TGF-β has a deactivating mutation in at least half of colorectal cancers. Sometimes TGF-β is not deactivated, but a downstream protein named SMAD is.[17] DCC commonly has deletion of its chromosome segment in colorectal cancer.[18]
Some genes are oncogenes - they are overexpressed in colorectal cancer. 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. The chronological order of mutations is sometimes important, with a primary KRAS mutation generally leading to a self-limiting hyperplastic or borderline lesion, but if occurring after a previous APC mutation it often progresses to cancer.[19] PTEN, a tumor suppressor, normally inhibits PI3K, but can sometimes become mutated and deactivated.[17]
Comprehensive, genome-scale analysis has revealed that colorectal carcinomas are clearly separable into hypermutated and non-hypermutated tumor types.[20] In addition to the oncogenic and inactivating mutations described for the genes above, non-hypermutated samples also contain mutated CTNNB1, FAM123B, SOX9, ATM, and ARID1A. Progressing through a distinct set of genetic events, hypermutated tumors display mutated forms of ACVR2A, TGFBR2, MSH3, MSH6, SLC9A9, TCF7L2, and BRAF. The common theme among these genes, across both tumor types, is their involvement in WNT and TGF-β signaling pathways, which in turn results in increased activity of MYC, a central player in colorectal cancer.[20]
Diagnosis[edit]
Diagnosis of colorectal cancer is via tumor biopsy typically done during sigmoidoscopy or colonoscopy. The extent of the disease is then usually determined by a CT scan of the chest, abdomen and pelvis. There are other potential imaging test such as PET and MRI which may be used in certain cases. Colon cancer staging is done next and based on the TNM system which is determined by how much the initial tumor has spread, if and where lymph nodes are involved, and if and how many metastases there are.[7]
Pathology[edit]
The pathology of the tumor is usually reported from the analysis of tissue taken from a biopsy or surgery. A pathology report will usually contain a description of cell type and grade. The most common colon cancer cell type is adenocarcinoma which accounts for 95% of cases. Other, rarer types include lymphoma and squamous cell carcinoma.
Cancers on the right side (ascending colon and cecum) tend to be exophytic, that is, the tumour grows outwards from one location in the bowel wall. This very rarely causes obstruction of feces, and presents with symptoms such as anemia. Left-sided tumours tend to be circumferential, and can obstruct the bowel much like a napkin ring which can present with thinner calibre stools.
Adenocarcinoma is a malignant epithelial tumor, originating from glandular epithelium of the colorectal mucosa. It invades the wall, infiltrating the muscularis mucosae, the submucosa and thence 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/colloid (optically "empty" spaces) - mucinous (colloid) adenocarcinoma, poorly differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery - "signet-ring cell." Depending on glandular architecture, cellular pleomorphism, and mucosecretion of the predominant pattern, adenocarcinoma may present three degrees of differentiation: well, moderately, and poorly differentiated.[21]
Most colorectal cancer tumors are thought to be cyclooxygenase-2 (COX-2) positive.[citation needed] This enzyme is generally not found in healthy colon tissue, but is thought to fuel abnormal cell growth.
Colorectal lesions
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Appearance of the inside of the colon showing one invasive colorectal carcinoma (the crater-like, reddish, irregularly shaped tumor).
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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).
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Endoscopic image of colon cancer identified in sigmoid colon on screening colonoscopy in the setting of Crohn's disease.
-
PET/CT of a staging exam of colon carcinoma. Besides the primary tumor a lot of lesions can be seen. On cursor position: lung nodule.
Micrographs (H&E stain)
-
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.
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Cancer — Histopathologic image of colonic carcinoid.
-
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.
Prevention[edit]
Most colorectal cancers should be preventable, through increased surveillance, improved lifestyle, and, probably, the use of dietary chemopreventative agents[citation needed].
Lifestyle[edit]
Current dietary recommendations to prevent colorectal cancer include increasing the consumption of whole grains, fruits and vegetables, and reducing the intake of red meat.[22][23] The evidence for fiber and fruits and vegetables however is poor.[23] Physical activity can moderately reduce the risk of colorectal cancer.[24]
Medication[edit]
Aspirin and celecoxib appear to decrease the risk of colorectal cancer in those at high risk.[25] However it is not recommended in those at average risk.[26] There is tentative evidence for calcium supplementation but it is not sufficient to make a recommendation.[27] Vitamin D intake and blood levels are associated with a lower risk of colon cancer.[28][29]
Screening[edit]
More than 80% of colorectal cancers arise from adenomatous polyps making this cancer amenable to screening. Diagnosis of cases of colorectal cancer through screening tends to occur 2–3 years before diagnosis of cases with symptoms.[7] Screening has the potential to reduce colorectal cancer deaths by 60%.[30]
The three main screening tests are fecal occult blood testing, flexible sigmoidoscopy and colonoscopy.[7] Of the three, only sigmoidoscopy cannot screen the right side of the colon where 42% of malignancies are found.[31] 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.[7]
A new screening method is the M2-PK Test. The enzyme biomarker M2-PK has been identified as a key enzyme in colorectal cancers and polyps. M2-PK does not depend on blood in the stool and is specifically related to changes in the tumour metabolism. It does not require any special preparation prior to testing. Only a small stool sample is needed. M2-PK features a high sensitivity for colorectal cancer and polyps and is able to detect bleeding and non-bleeding colorectal cancer and polyps.[32] In the event of a positive result people would be asked to undergo further examination e.g. colonoscopy.
Fecal occult blood testing of the stool is typically recommended every two years and can be either guaiac based or immunochemical.[7] Medical societies recommend screening between the age of 50 and 75 years with sigmoidoscopy every 5 years and colonoscopy every 10 years. For those at high risk, screenings usually begin at around 40.[7][33] For people with average risk who have had a high-quality colonoscopy with normal results, the American Gastroenterological Association does not recommend any type of screening in the 10 years following the colonoscopy.[34][35] For people over 75 or those with a life expectancy of less than 10 years, screening is not recommended.[36]
Management[edit]
The treatment of colorectal cancer depends on how advanced it is.[37] When colorectal cancer is caught early surgery can be curative. However, when it is detected at later stages (metastases are present), this is less likely and treatment is often directed more at extending life and keeping people comfortable.[7]
Surgery[edit]
For people with localized cancer the preferred treatment is complete surgical removal with the attempt of achieving a cure. 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 if it occurs is in the liver and lungs.[7]
Chemotherapy[edit]
Chemotherapy may be used in addition to surgery in certain cases[7] as adjuvant therapy. If cancer has entered the lymph nodes, adding the chemotherapy agents fluorouracil or capecitabine 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 case, a couple of different chemotherapy medications are used.[7] Chemotherapy drugs may include combinations of agents including fluorouracil, capecitabine, UFT, leucovorin, irinotecan, or oxaliplatin.[38]
Radiation[edit]
While a combination of radiation and chemotherapy may be useful for rectal cancer,[7] its use in colon cancer is not routine due to the sensitivity of the bowels to radiation.[39]
Palliative care[edit]
In people with incurable colorectal cancer, palliative care can be considered for improving quality of life. Surgical options may include non-curative surgical removal of some of the cancer tissue, bypassing part of the intestines, or stent placement. These procedures can be considered to improve symptoms and reduce complications such as bleeding from the tumor, abdominal pain and intestinal obstruction.[40] Non-operative methods of symptomatic treatment include radiation therapy to decrease tumor size as well as pain medications.[41]
Prognosis[edit]
In Europe the five-year survival for colorectal cancer is less than 60%. In the developed world about a third of people who get the disease die from it.[7]
Survival is directly related to detection and the type of cancer involved, but overall is poor for symptomatic cancers, as they are typically quite advanced. Survival rates for early stage detection is about 5 times that of late stage cancers. For example, patients with a tumor that has not breached the muscularis mucosa (TNM stage Tis, N0, M0) have an average 5-year survival of 100%, while those with an invasive cancer, i.e. T1 (within the submucosal layer) or T2 (within the muscular layer) cancer have an average 5-year survival of approximately 90%. Those with a more invasive tumor, yet without node involvement (T3-4, N0, M0) have an average 5-year survival of approximately 70%. Patients with positive regional lymph nodes (any T, N1-3, M0) have an average 5-year survival of approximately 40%, while those with distant metastases (any T, any N, M1) have an average 5-year survival of approximately 5%.[42]
According to the American Cancer Society statistics in 2006,[43] over 20% of patients present with metastatic (stage IV) colorectal cancer at the time of diagnosis, and up to 25% of this group will have isolated liver metastasis that is potentially resectable. Lesions which undergo curative resection have demonstrated 5-year survival outcomes now exceeding 50%.[44]
Follow-up[edit]
The aims of follow-up are to diagnose, in the earliest possible stage, any metastasis or tumors that develop later, but did not originate from the original cancer (metachronous lesions).
The U.S. National Comprehensive Cancer Network and American Society of Clinical Oncology provide guidelines for the follow-up of colon cancer.[45][46] A medical history and physical examination are recommended every 3 to 6 months for 2 years, then every 6 months for 5 years. Carcinoembryonic antigen blood level measurements follow the same timing, but are only advised for patients with T2 or greater lesions who are candidates for intervention. A CT-scan of the chest, abdomen and pelvis can be considered annually for the first 3 years for patients who are at high risk of recurrence (for example, patients who had poorly differentiated tumors or venous or lymphatic invasion) and are candidates for curative surgery (with the aim to cure). A colonoscopy can be done after 1 year, except if it could not be done during the initial staging because of an obstructing mass, in which case it should be performed after 3 to 6 months. If a villous polyp, a polyp >1 centimeter or high grade dysplasia is found, it can be repeated after 3 years, then every 5 years. For other abnormalities, the colonoscopy can be repeated after 1 year.
Routine PET or ultrasound scanning, chest X-rays, complete blood count or liver function tests are not recommended.[45][46] These guidelines are based on recent meta-analyses showing intensive surveillance and close follow-up can reduce the 5-year mortality rate from 37% to 30%.[47][48][49]
Epidemiology[edit]
Age-standardized death from colorectal cancer per 100,000 inhabitants in 2004.[50]
no data
<2.5
2.5-5
5-7.5
7.5-10
10-12.5
12.5-15
|
15-17.5
17.5-20
20-22.5
22.5-25
25-27.5
>27.5
|
Globally more than 1 million people get colorectal cancer every year[7] resulting in about 0.5 million deaths.[51] As of 2008 it is the second most common cause of cancer in women and the third most common in men[52] with it being the fourth most common cause of cancer death after lung, stomach, and liver cancer.[53] It is more common in developed than developing countries.[51] Globally incidences vary 10-fold with highest rates in the Australia, New Zealand, Europe and the US and lowest rates in Africa and South-Central Asia.[2]
United States[edit]
Based on rates from 2007-2009, 4.96% of US men and women born today will be diagnosed with colorectal cancer during their lifetime.[54] From 2005-2009, the median age at diagnosis for cancer of the colon and rectum in the US was 69 years of age. Approximately 0.1% were diagnosed under age 20; 1.1% between 20 and 34; 4.0% between 35 and 44; 13.4% between 45 and 54; 20.4% between 55 and 64; 24.0% between 65 and 74; 25.0% between 75 and 84; and 12.0% 85+ years of age. Rates are higher among males (54 per 100,000 c.f. 40 per 100,000 for females).
Society and culture[edit]
In the United States, March is colorectal cancer awareness month.[30]
Notable cases[edit]
Main article: List of people diagnosed with colorectal cancer
- Corazon Aquino, former president of the Philippines[55]
- Pope John Paul II[56]
- Ronald Reagan[57]
- Harold Wilson, former Prime Minister of the United Kingdom[58]
- Robin Gibb, musician and member of the Bee Gees[59]
- Humayun Ahmed, Bengali writer and film maker[60]
Research[edit]
- Bowel & Cancer Research
- Mouse models of colorectal and intestinal cancer
- The Cancer Genome Atlas[20]
References[edit]
- ^ Cancer Genome Atlas Network (19 July 2012). "Comprehensive molecular characterization of human colon and rectal cancer.". Nature 487: 330–337.
- ^ a b Colorectal Cancer Incidence, Mortality and Prevalence Worldwide in 2008 — Summary. Available from: Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. (2010) GLOBOCAN 2008 v2.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 10 [Internet]. Lyon, France: International Agency for Research on Cancer. Accessed on 11 Oct 2012.
- ^ al.], edited by Tadataka Yamada ; associate editors, David H. Alpers ... [et (2008). Principles of clinical gastroenterology. Chichester, West Sussex: Wiley-Blackwell. p. 381. ISBN 978-1-4051-6910-3.
- ^ a b Astin M, Griffin, T, Neal, RD, Rose, P, Hamilton, W (May 2011). "The diagnostic value of symptoms for colorectal cancer in primary care: a systematic review". The British journal of general practice : the journal of the Royal College of General Practitioners 61 (586): 231–43. doi:10.3399/bjgp11X572427. PMC 3080228. PMID 21619747.
- ^ Adelstein BA, Macaskill, P, Chan, SF, Katelaris, PH, Irwig, L (2011). "Most bowel cancer symptoms do not indicate colorectal cancer and polyps: a systematic review.". BMC gastroenterology 11: 65. doi:10.1186/1471-230X-11-65. PMC 3120795. PMID 21624112.
- ^ a b Watson AJ, Collins, PD (2011). "Colon cancer: a civilization disorder.". Digestive diseases (Basel, Switzerland) 29 (2): 222–8. doi:10.1159/000323926. PMID 21734388.
- ^ a b c d e f g h i j k l m n o p Cunningham D, Atkin W, Lenz HJ, Lynch HT, Minsky B, Nordlinger B, Starling N (2010). "Colorectal cancer.". Lancet 375 (9719): 1030–47. doi:10.1016/S0140-6736(10)60353-4. PMID 20304247.
- ^ Lee, I-Min; Shiroma, Eric J; Lobelo, Felipe; Puska, Pekka; Blair, Steven N; Katzmarzyk, Peter T (1 July 2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". The Lancet 380 (9838): 219–29. doi:10.1016/S0140-6736(12)61031-9. PMID 22818936.
- ^ Fedirko V, Tramacere, I, Bagnardi, V, Rota, M, Scotti, L, Islami, F, Negri, E, Straif, K, Romieu, I, La Vecchia, C, Boffetta, P, Jenab, M (Sep 2011). "Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies.". Annals of oncology : official journal of the European Society for Medical Oncology / ESMO 22 (9): 1958–72. doi:10.1093/annonc/mdq653. PMID 21307158.
- ^ Jawad N, Direkze, N, Leedham, SJ (2011). "Inflammatory bowel disease and colon cancer.". Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer 185: 99–115. doi:10.1007/978-3-642-03503-6_6. PMID 21822822.
- ^ a b Xie J, Itzkowitz, SH (2008). "Cancer in inflammatory bowel disease.". World journal of gastroenterology : WJG 14 (3): 378–89. PMC 2679126. PMID 18200660.
- ^ a b c d Triantafillidis JK, Nasioulas, G, Kosmidis, PA (Jul 2009). "Colorectal cancer and inflammatory bowel disease: epidemiology, risk factors, mechanisms of carcinogenesis and prevention strategies.". Anticancer research 29 (7): 2727–37. PMID 19596953.
- ^ Juhn E, Khachemoune, A (2010). "Gardner syndrome: skin manifestations, differential diagnosis and management.". American journal of clinical dermatology 11 (2): 117–22. doi:10.2165/11311180-000000000-00000. PMID 20141232.
- ^ Half E, Bercovich, D, Rozen, P (2009). "Familial adenomatous polyposis.". Orphanet journal of rare diseases 4: 22. doi:10.1186/1750-1172-4-22. PMC 2772987. PMID 19822006.
- ^ Ionov Y, Peinado MA, Malkhosyan S, Shibata D, Perucho M (1993). "Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis". Nature 363 (6429): 558–61. doi:10.1038/363558a0. PMID 8505985.
- ^ Srikumar Chakravarthi, Baba Krishnan, Malathy Madhavan (1999). "Apoptosis and expression of p53 in colorectal neoplasms". Indian J Med Res 86 (7): 95–102.
- ^ a b c d Markowitz SD, Bertagnolli MM (December 2009). "Molecular Origins of Cancer: Molecular Basis of Colorectal Cancer". N. Engl. J. Med. 361 (25): 2449–60. doi:10.1056/NEJMra0804588. PMC 2843693. PMID 20018966.
- ^ Mehlen P, Fearon ER (August 2004). "Role of the dependence receptor DCC in colorectal cancer pathogenesis". J. Clin. Oncol. 22 (16): 3420–8. doi:10.1200/JCO.2004.02.019. PMID 15310786.
- ^ Vogelstein, B.; Kinzler, K. W. (2004). "Cancer genes and the pathways they control". Nature Medicine 10 (8): 789–799. doi:10.1038/nm1087. PMID 15286780. edit
- ^ a b c Muzny, DM.; Bainbridge, MN.; Chang, K.; Dinh, HH.; Drummond, JA.; Fowler, G.; Kovar, CL.; Lewis, LR. et al. (Jul 2012). "Comprehensive molecular characterization of human colon and rectal cancer.". Nature 487 (7407): 330–7. doi:10.1038/nature11252. PMID 22810696.
- ^ Pathology atlas
- ^ Campos FG, Logullo Waitzberg, AG, Kiss, DR, Waitzberg, DL, Habr-Gama, A, Gama-Rodrigues, J (Jan 2005). "Diet and colorectal cancer: current evidence for etiology and prevention.". Nutricion hospitalaria : organo oficial de la Sociedad Espanola de Nutricion Parenteral y Enteral 20 (1): 18–25. PMID 15762416.
- ^ a b Doyle VC, Logullo Waitzberg, AG, Kiss, DR, Waitzberg, DL, Habr-Gama, A, Gama-Rodrigues, J (May 2007). "Nutrition and colorectal cancer risk: a literature review.". Gastroenterology nursing : the official journal of the Society of Gastroenterology Nurses and Associates 30 (3): 178–82; quiz 182–3. doi:10.1097/01.SGA.0000278165.05435.c0. PMID 17568255.
- ^ Harriss DJ, Atkinson, G, Batterham, A, George, K, Cable, NT, Reilly, T, Haboubi, N, Renehan, AG, Colorectal Cancer, Lifestyle, Exercise And Research, Group (Sep 2009). "Lifestyle factors and colorectal cancer risk (2): a systematic review and meta-analysis of associations with leisure-time physical activity.". Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland 11 (7): 689–701. doi:10.1111/j.1463-1318.2009.01767.x. PMID 19207713.
- ^ Cooper K, Squires, H, Carroll, C, Papaioannou, D, Booth, A, Logan, RF, Maguire, C, Hind, D, Tappenden, P (Jun 2010). "Chemoprevention of colorectal cancer: systematic review and economic evaluation.". Health technology assessment (Winchester, England) 14 (32): 1–206. doi:10.3310/hta14320. PMID 20594533.
- ^ Agency for Healthcare Research and Quality (2010/2011). "Aspirin or Nonsteroidal Anti-inflammatory Drugs for the Primary Prevention of Colorectal Cancer". United States Department of Health & Human Services.
- ^ Weingarten MA, Zalmanovici, A, Yaphe, J (2008). "Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps.". Cochrane database of systematic reviews (Online) (1): CD003548. doi:10.1002/14651858.CD003548.pub4. PMID 18254022.
- ^ Ma Y, Zhang, P, Wang, F, Yang, J, Liu, Z, Qin, H (2011). "Association between vitamin D and risk of colorectal cancer: a systematic review of prospective studies.". Journal of clinical oncology : official journal of the American Society of Clinical Oncology 29 (28): 3775–82. doi:10.1200/JCO.2011.35.7566. PMID 21876081.
- ^ Yin L, Grandi, N, Raum, E, Haug, U, Arndt, V, Brenner, H (Jul 2011). "Meta-analysis: Serum vitamin D and colorectal adenoma risk.". Preventive medicine 53 (1-2): 10–6. doi:10.1016/j.ypmed.2011.05.013. PMID 21672549.
- ^ a b He J, Efron, JE (2011). "Screening for colorectal cancer.". Advances in surgery 45: 31–44. PMID 21954677.
- ^ Siegel RL, Ward EM, Jemal A (Mar 2012). "Trends in Colorectal Cancer Incidence Rates in the United States by Tumor Location and Stage, 1992–2008". Cancer Epidemiology, Biomarkers & Prevention 21 (3). 411–6 (See Introduction). doi:10.1158/1055-9965.EPI-11-1020. PMID 22219318. Retrieved 2012-09-16.
- ^ C. Tonus, M. Sellinger u. a.: Faecal pyruvate kinase isoenzyme type M2 for colorectal cancer screening: A meta-analysis. In: World journal of gastroenterology : WJG. Band 18, Nummer 30, August 2012, S. 4004–4011, ISSN 1007-9327. doi:10.3748/wjg.v18.i30.4004. PMID 22912551. PMC 3419997.
- ^ "Screening for Colorectal Cancer". U.S. Preventive Services Task Force. 2008.
- ^ American Gastroenterological Association, "Five Things Physicians and Patients Should Question", Choosing Wisely: an initiative of the ABIM Foundation (American Gastroenterological Association), retrieved August 17, 2012
- ^ Winawer, S; Fletcher, R; Rex, D; Bond, J; Burt, R; Ferrucci, J; Ganiats, T; Levin, T; Woolf, S; Johnson, D; Kirk, L; Litin, S; Simmang, C; Gastrointestinal Consortium, Panel (2003 Feb). "Colorectal cancer screening and surveillance: clinical guidelines and rationale-Update based on new evidence.". Gastroenterology 124 (2): 544–60. doi:10.1053/gast.2003.50044. PMID 12557158.
- ^ Qaseem A, Denberg TD, Hopkins RH Jr, et al. (2012). "Screening for Colorectal Cancer: A Guidance Statement From the American College of Physicians". Annals of internal medicine 156 (5): 378–386. doi:10.1059/0003-4819-156-5-201203060-00010. PMID 22393133.
- ^ Stein A, Atanackovic, D, Bokemeyer, C (Sep 2011). "Current standards and new trends in the primary treatment of colorectal cancer.". European journal of cancer (Oxford, England : 1990). 47 Suppl 3: S312–4. doi:10.1016/S0959-8049(11)70183-6. PMID 21943995.
- ^ "Chemotherapy of metastatic colorectal cancer". Prescrire Int 19 (109): 219–24. October 2010. PMID 21180382.
- ^ authors, editors, Vincent T. DeVita, Jr., Theodore S. Lawrence, Steven A. Rosenberg ; associate scientific advisors, Robert A. Weinberg, Ronald A. DePinho ; with 421 contributing (2008). DeVita, Hellman, and Rosenberg's cancer : principles & practice of oncology (8th ed. ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 1258. ISBN 978-0-7817-7207-5.
- ^ Wasserberg N, Kaufman HS (December 2007). "Palliation of colorectal cancer". Surg Oncol 16 (4): 299–310. doi:10.1016/j.suronc.2007.08.008. PMID 17913495.
- ^ Amersi F, Stamos MJ, Ko CY (July 2004). "Palliative care for colorectal cancer". Surg. Oncol. Clin. N. Am. 13 (3): 467–77. doi:10.1016/j.soc.2004.03.002. PMID 15236729.
- ^ Box 3-1, Page 107 in: Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.
- ^ http://www.cancer.org/docroot/PRO/content/PRO_1_1_Cancer_Statistics_2006_Presentation.asp
- ^ Simmonds PC, Primrose JN, Colquitt JL, Garden OJ, Poston GJ, Rees M (April 2006). "Surgical resection of hepatic metastases from colorectal cancer: A systematic review of published studies". Br. J. Cancer 94 (7): 982–99. doi:10.1038/sj.bjc.6603033. PMC 2361241. PMID 16538219.
- ^ a b NCCN Clinical Practice Guidelines in Oncology - Colon Cancer (version 1, 2008: September 19, 2007).
- ^ a b Desch CE, Benson AB 3rd, Somerfield MR, et al.; American Society of Clinical Oncology (2005). "Colorectal cancer surveillance: 2005 update of an American Society of Clinical Oncology practice guideline". J Clin Oncol 23 (33): 8512–9. doi:10.1200/JCO.2005.04.0063. PMID 16260687.
- ^ Jeffery M, Hickey BE, Hider PN (2002). "Follow-up strategies for patients treated for non-metastatic colorectal cancer". Cochrane Database Syst Rev (1): CD002200. doi:10.1002/14651858.CD002200. PMID 11869629.
- ^ Renehan AG, Egger M, Saunders MP, O'Dwyer ST (2002). "Impact on survival of intensive follow up after curative resection for colorectal cancer: systematic review and meta-analysis of randomised trials". BMJ 324 (7341): 831–8. doi:10.1136/bmj.324.7341.813. PMC 100789. PMID 11934773.
- ^ Figueredo A, Rumble RB, Maroun J, et al.; Gastrointestinal Cancer Disease Site Group of Cancer Care Ontario's Program in Evidence-based Care (2003). "Follow-up of patients with curatively resected colorectal cancer: a practice guideline". BMC Cancer 3: 26. doi:10.1186/1471-2407-3-26. PMC 270033. PMID 14529575.
- ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009.
- ^ a b Merika E, Saif, MW, Katz, A, Syrigos, K, Morse, M (Sep 2010). "Review. Colon cancer vaccines: an update.". In vivo (Athens, Greece) 24 (5): 607–28. PMID 20952724.
- ^ Jemal A, Bray, F, Center, MM, Ferlay, J, Ward, E, Forman, D (2011). "Global cancer statistics". CA: a cancer journal for clinicians 61 (2): 69–90. doi:10.3322/caac.20107. PMID 21296855.
- ^ WHO (February 2010). "Cancer". World Health Organization. Retrieved 2011-01-05.
- ^ Howlader N, Noone AM, Krapcho M, Neyman N, Aminou R, Altekruse SF, Kosary CL, Ruhl J, Tatalovich Z, Cho H, Mariotto A, Eisner MP, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). "SEER Cancer Statistics Review, 1975-2009 (Vintage 2009 Populations).". National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2009_pops09/, based on November 2011 SEER data submission, posted to the SEER web site, 2012.
- ^ http://www.abs-cbnnews.com/storypage.aspx?StoryID=112887
- ^ "Pope John Paul II". ABC News Online.
- ^ "Reagan turns 90". BBC News: Americas. 6 February 2001.
- ^ Daily Mail
- ^ Klein, Sarah (2012-04-23). "12 Famous Faces Touched By Colorectal Cancer". Huffington Post.
- ^ "Humayun Ahmed dies". Bdnews24.com. 2012-07-19. Retrieved 2012-07-19.
External links[edit]
- Colorectal cancer at the Open Directory Project
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Tumors: digestive system neoplasia (C15–C26/D12–D13, 150–159/211)
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| GI tract |
| Upper GI tract |
| Esophagus |
- Squamous cell carcinoma
- Adenocarcinoma
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|
| Stomach |
- Gastric carcinoma
- Signet ring cell carcinoma
- Gastric lymphoma
- Linitis plastica
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|
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| Lower GI tract |
| Small intestine |
|
|
| Appendix |
- Carcinoid
- Pseudomyxoma peritonei
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| Colon/rectum |
- colorectal polyp: Peutz–Jeghers syndrome
- Juvenile polyposis syndrome
- Familial adenomatous polyposis/Gardner's syndrome
- Cronkhite–Canada syndrome
- neoplasm: Adenocarcinoma
- Familial adenomatous polyposis
- Hereditary nonpolyposis colorectal cancer
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| Anus |
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| Upper and/or lower |
- Gastrointestinal stromal tumor
- Krukenberg tumor (metastatic)
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| Accessory |
| Liver |
- malignant: Hepatocellular carcinoma
- Hepatoblastoma
- benign: Hepatocellular adenoma
- Cavernous hemangioma
- hyperplasia: Focal nodular hyperplasia
- Nodular regenerative hyperplasia
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| Biliary tract |
- bile duct: Cholangiocarcinoma
- Klatskin tumor
- gallbladder: Gallbladder cancer
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| Pancreas |
- exocrine pancreas: Adenocarcinoma
- Pancreatic ductal carcinoma
- cystic neoplasms: Serous microcystic adenoma
- Intraductal papillary mucinous neoplasm
- Mucinous cystic neoplasm
- Solid pseudopapillary neoplasm
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| Peritoneum |
- Primary peritoneal carcinoma
- Peritoneal mesothelioma
- Desmoplastic small round cell tumor
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anat (t, g, p)/phys/devp/enzy
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noco/cong/tumr, sysi/epon
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proc, drug (A2A/2B/3/4/5/6/7/14/16), blte
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