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Intestinal Polypoid Adenomas Workup

  • Author: Swati G Patel, MD, MS; Chief Editor: BS Anand, MD  more...
 
Updated: Sep 22, 2015
 

Approach Considerations

2015 ACG guidelines on genetic testing and management of hereditary gastrointestinal cancer syndromes

The American College of Gastroenterology (ACG) released the following recommendations for the management of patients with hereditary gastrointestinal cancer syndromes—and they specifically discuss genetic testing and management of Lynch syndrome, familial adenomatous polyposis (FAP), attenuated familial adenomatous polyposis (AFAP), MUTYH-associated polyposis (MAP), Peutz-Jeghers syndrome, juvenile polyposis syndrome, Cowden syndrome, serrated (hyperplastic) polyposis syndrome, hereditary pancreatic cancer, and hereditary gastric cancer[32] :

  • The initial assessment is the collection of a family history of cancers and premalignant gastrointestinal conditions and should provide enough information to develop a preliminary determination of the risk of a familial predisposition to cancer.
  • Age at diagnosis and lineage (maternal and/or paternal) should be documented for all diagnoses, especially in first- and second-degree relatives.
  • When indicated, genetic testing for a germline mutation should be done on the most informative candidate(s) identified through the family history evaluation and/or tumor analysis to confirm a diagnosis and allow for predictive testing of at-risk relatives.
  • Genetic testing should be conducted in the context of pre- and post-test genetic counseling to ensure the patient's informed decision making.
  • Patients who meet clinical criteria for a syndrome as well as those with identified pathogenic germline mutations should receive appropriate surveillance measures in order to minimize their overall risk of developing syndrome-specific cancers.
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Laboratory Studies

Complete blood cell (CBC) count may be helpful because patients with an adenoma occasionally can present with a microcytic (iron deficiency) anemia due to chronic occult blood loss.

Iron studies may be needed because low serum iron and ferritin and an increased total iron-binding capacity (TIBC) can occasionally be observed as a result of blood loss in some patients with colonic adenomas and carcinomas.

Stool-based testing

Guaiac-based fecal occult blood testing (FOBT)

A small proportion of large adenomas may bleed intermittently. Depending on the age of the patients tested, 10% to 40% of asymptomatic patients with a positive result on a fecal occult blood test have an advanced adenoma. Three fresh, separate, nonhydrated stool specimens are used. FOBT screening programs are intended for the early detection of colorectal cancer (CRC) and have demonstrated decreased cancer-related and all-cause mortality.[33, 34, 35, 36]

Fecal immunochemical test (FIT)

Immunochemical testing for human globin has higher sensitivity for CRC and adenomas than traditional FOBT and is increasingly replacing guaiac-based tests as the recommended FOBT for CRC screening. In one study using 3 consecutive samples and a hemoglobin threshold of 75 ng/mL, sensitivity was 94.1% and specificity was 87.5% for cancer. Using the same testing parameters, sensitivity and specificity were 67% and 91.4%, respectively, for clinically significant neoplasia (advanced adenoma [defined as adenoma >1 cm or with villous features or high-grade dysplasia] and cancer).[37]

Many of the clinically available FITs recommend using only 1 test and a hemoglobin threshold of 100 ng/mL. This approach has been shown to still have a greater than 50% sensitivity for CRC and is associated with higher compliance than the 3-day guaiac-based testing regimens. Several issues should be considered when choosing a FIT regimen.

It is important to establish the relationship between a given quantity of hemoglobin detected in the stools and the pathology detected on colonoscopy in those with positive tests.

In CRC screening, different positivity thresholds need to be established for the immunochemical-based screening strategies. Depending on the threshold in terms of the amount of blood detected, the rates of adenoma and CRC detection vary. The positivity threshold influences the number needed to scope (NNS) to find a CRC or advanced adenoma by colonoscopy in an individual with positive FIT results.

Large differences exist in the diagnostic performance among various FITs, and the different test variances need to be carefully evaluated.

FITs increase the detection rates of advanced adenoma and CRC without generating an unacceptable number of false-positive results, which would lead to unnecessary colonoscopies.

A large, Dutch, population-based, randomized controlled trial has shown that FITs detected 2.5 times as many advanced adenomas and CRC compared with the guaiac-based FOBT, despite similar colonoscopy rates for positive screening tests. Thus, FITs appear to be superior to guaiac-based FOBTs for CRC screening.

Quantitative testing of stool for blood

This has been tried, but it does not appear to have a role for screening or diagnosis of colonic adenomas at this time.

Stool testing for genetic alterations

The analysis of fecal DNA represents an emerging area for early detection, and studies have reported 62% to 91% sensitivity for CRC and 26% to 73% sensitivity for adenomas, with a specificity ranging from 93% to 100%.[38, 39] The major drawback of current fecal DNA testing is the high cost and limited availability.

Fecal calprotectin and tumor M2-PK protein detection in stool

This test may also have better performance characteristics than guaiac-based FOBTs, but these newer tests also have low sensitivity and poor specificity.

Other biomarkers

Biomarkers in blood or urine for the detection of CRC and advanced neoplasia, such as measurement of septin 9 levels in blood and the urinary metabolite of prostaglandin E2, are being developed but are not yet ready for routine use.

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Imaging Studies

Barium enema imaging of the colon

Barium enema (BE) imaging can detect polyps and colorectal cancer (CRC). Air-contrast BE is more sensitive than the single-contrast technique for the detection of polyps. BE is included as an acceptable screening or surveillance test for colorectal cancer in the recommendations of the American Cancer Society and other organizations, but prospective controlled studies of its use in a screening program are lacking.

BE is generally regarded as less sensitive than colonoscopy in detecting adenomas smaller than 1 cm, and some studies indicate that it is not as accurate as colonoscopy for even larger lesions. As a result, BE is usually considered an alternative to colonoscopy for the evaluation of the entire colon.

The US Multi-Society Task Force (MSTF) offers double-contrast BE as an acceptable CRC screening tool; however, the US Preventative Services Task Force (USPSTF) does not.

Computed Tomography colonography (virtual colonoscopy)

This has emerged as a promising modality for the detection of adenomas and carcinomas of the colon. Thus far, computed tomography (CT) colonography has lower sensitivity than optical colonoscopy for small (<1 cm) adenomas, but the technology is improving rapidly. The advantages of virtual colonoscopy include the lack of need for sedation, the short commitment of time for the test, and its noninvasive nature. A positive test would need to be followed by a standard colonoscopy.

Most protocols still require cathartic bowel preparation, but CT colonography without bowel preparation may be possible in the future. The main disadvantages include cost, exposure to radiation, uncertainty in how to deal with extracolonic findings, and operator dependence.

The 2008 USPSTF guidelines state that there is insufficient evidence to support the use of CT colonography in routine polyp and CRC screening; however, the MSTF states CT colonography is an acceptable option.

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Procedures

Flexible sigmoidoscopy

Flexible sigmoidoscopy (FS) can be used to visualize the left colon, where over half of all colonic adenomas and cancers are located. If an adenoma is detected, a colonoscopy should then be performed. If no adenomas are detected, a repeat examination is not required for 5 years.

FS screening for average-risk patients is endorsed by all major society guidelines, including those by the US Multi-Society Task Force (MSTF) and the US Preventative Services Task Force (USPSTF). The Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial demonstrated a 26% reduction in overall colorectal cancer (CRC)–related mortality and a 21% reduction in CRC incidence with FS screening compared with standard care.[40]

The main advantages to FS include that is more widely available and less expensive than colonoscopy, has a lower risk than colonoscopy, does not require sedation, and requires a less rigorous bowel preparation (usually enema preparation alone is recommended).

The disadvantages of FS are that it does not visualize the entire colon, it can be more uncomfortable for patients since they are not sedated, and it is 2-step procedure (requires subsequent colonoscopy) if adenomas are found.

Despite its efficacy in decreasing CRC incidence and mortality, FS is diminishing as a screening tool in the United States. Critics liken FS to undertaking mammography on only one breast.

Colonoscopy

Although there are several polyp and CRC screening options, colonoscopic screening has emerged as the dominant screening strategy in the United States for average-risk patients.

Colonoscopy is the recommended screening modality for high-risk individuals, such as those with first-degree relatives with colorectal cancer/advanced adenomas, those with a hereditary colorectal cancer syndrome, and for surveillance of those with a personal history of adenomas or CRC.

Colonoscopy carries the conceptual advantage of being a 1-time test that can both visualize the entire colon and remove any adenomas in a single session. A colonoscopy can be performed at longer (10-year) intervals if no adenomas are found, and there is minimal patient discomfort since the patient is sedated during the examination.

Endoscopically, polyps can be classified as pedunculated (mucosal stalk interposed between the polyp and the colonic wall), sessile (entire base is attached to the colonic wall), flat (polyp height less than one half the diameter of the polyp) or depressed (polyps with depression into the colonic mucosal wall. See the following images.

Endoscopic view of a pedunculated polyp. Endoscopic view of a pedunculated polyp.
Endoscopic view of a sessile polyp. Endoscopic view of a sessile polyp.

Disadvantages

Disadvantages of colonoscopy are that it is an invasive examination with higher risk of complications than the other screening options (although low overall); it requires sedation; thus, patients would need to take time off work and would require a driver to and from the test. It requires a full bowel preparation and it is expensive. It is operator-dependent, and the quality of colonoscopy in the United States is highly variable. The procedure also can be time consuming. Furthermore, there is concern that the United States does not have enough trained endoscopists for all CRC screening-eligible patients to undergo high-quality colonoscopy as the primary screening tool. Complications associated with colonoscopy include perforation, bleeding, cardiopulmonary events related to sedation, and, rarely death.

Perforation rates vary depending on whether an intervention takes place (eg, polypectomy). Large database studies suggest rates ranging from 0.01% to 0.3%.[41] Risk factors for perforation during diagnostic colonoscopy include advanced age, presence of diverticulosis, female sex, and a history of pelvic/abdominal surgery.

Bleeding rates range from 0.1% to 0.6%.[41] Rates significantly depend on whether an intervention takes place (3.7 in 1000 for procedures without polypectomy and 8.7 in 1000 for procedures with polypectomy).

There is a 0.9% risk of a cardiopulmonary complication,[41] usually associated with sedation.

The complication of death is extremely low, ranging from 0.007% to 0.03%.[41]

Important considerations

No prospective randomized controlled trials available to date have demonstrated a beneficial effect of colonoscopy screening on CRC incidence or mortality. Despite this, colonoscopy is endorsed by all major society guidelines in the United States for CRC screening. The main support for the efficacy of colonoscopy lies in the conceptual advantage of visualizing the entire colon (compared to FS) and indirect evidence such as data from the National Polyp Study[3] that showed a 76% to 90% reduction in CRC incidence after polypectomy compared with historic controls. Efficacy can also be extrapolated from randomized trials examining other screening modalities such as FOBT, since a positive test triggered a subsequent colonoscopy.

More recent studies have called into question the efficacy of colonoscopy efficacy. Several large retrospective studies from Canada[5, 42] and the United States[43] have quantified the occurrence of CRC 6-36 months after reportedly a “negative” colonoscopy, ranging from 7.2% to 9% of all CRCs. In all of these studies, a significantly higher rate of postcolonoscopy CRC was seen in the right-sided compared with the left-sided colon (9.9% to 12.4% vs 4.5% to 6.8%) in these studies. A German study reported that previous colonoscopy was associated with a 67% reduction in advanced neoplasia in the left-sided colon, but no risk reduction in the right-sided colon.[6] Multiple studies (tandem colonoscopy, CT colonography studies) have demonstrated considerable miss rates of colonoscopy ranging from 2% to 12% for large adenomas. These data have highlighted the importance of colonoscopy quality.

Even at centers of excellence, there is wide variability (3- to 5-fold) in adenoma detection rates between providers.[44] Colonoscopy quality measures have emerged, although they are not uniformly tracked. All of these measures are geared towards adequate examination of the colon.[45]

Colonoscopists or their institutions should develop a continuous quality improvement process to document quality assurance (eg, percentage of cases reaching the cecum, withdrawal time, polyp detection rate, adenoma detection rate, quality of bowel preparation).

A good bowel preparation is essential for adequate visualization of the colonic mucosa. A split-dosed bowel preparation (half of the volume the evening prior to the procedure, half of the volume on the morning of the procedure) is the preferred method of bowel cleansing and results in improved visualization of the colon during colonoscopy.

Withdrawal time is a widely accepted surrogate for colonoscopy quality and should be a minimum of 6 minutes according the American Society for Gastrointestinal Endoscopy. Colonoscopy reports should identify landmarks of the cecum as well as the colonoscopy withdrawal time.

The adenoma detection rate should be at least 25% among male patients and 15% among female patients undergoing screening colonoscopy. It is widely recognized, however, that these rates are likely well under the true adenoma prevalence rate and that higher thresholds may be considered in the future.

Three randomized controlled trials are currently under way to directly examine the efficacy of colonoscopy. The VA Colonoscopy Versus Fecal Immunochemical Test in Reducing Mortality From Colorectal Cancer (CONFIRM) trial and a Spanish trial are comparing colonoscopy with FIT, and the Nordic-European Initiative on Colorectal Cancer trial will compare colonoscopy with no screening.

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Conclusions About Screening

Multiple screening options are available for colorectal polyps and colorectal cancer (CRC) in the average-risk patient, including stool-based tests (fecal occult blood test [FOBT], fecal immunochemical test [FIT]), imaging tests (barium enema [BE] imaging of the colon, computed tomography [CT] colonography), and endoscopic tests (flexible sigmoidoscopy [FS], colonoscopy).

FOBT and FS have been shown to decrease CRC-related mortality, but colonoscopy has emerged as the dominant screening modality in the United States because of its multiple conceptual advantages. Trials investigating colonoscopic screening are underway.

High-risk patients should undergo colonoscopic screening and surveillance.

Although colonoscopy is considered to be the criterion standard for screening for CRC by looking for adenomatous polyps, it is recognized that the miss rate for advanced adenomas and CRC with colonoscopy is sufficiently high to be of concern.

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Screening and Surveillance Intervals

Average-risk individuals should begin screening at age 50 years.

Those at high risk have specific recommendations based on risk, such as the following:

  • Among persons with no colorectal neoplasia on initial screening colonoscopy, repeat screening is recommended in 10 years.
  • For those with 1-2 small adenomas (≤9 mm), repeat colonoscopy is recommended in 5-10 years.
  • For those with an adenoma larger than 1 cm, 3 or more adenomas of any size, or any adenoma with advanced histology (villous features, high-grade dysplasia), colonoscopy should be repeated in 3 years.
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Histologic Findings

Adenomas are classified based on their size, architecture, and degree of dysplasia. Large size, villous content, and high-grade dysplasia in colorectal adenomas are all associated with a higher rate of finding a focus of colorectal cancer (CRC) within the adenoma. The term advanced adenoma is used for adenomas that are 1 cm or larger in diameter or that have tubulovillous or villous histologic features or high-grade dysplasia.

Size

Most adenomas are small (<1 cm). Large adenomas (>1 cm) tend to have more severe dysplasia, more worrisome architecture, and increased risk of malignant potential. However, small (6-10 mm) and diminutive adenomas (≤5 mm) may have advanced histology or carcinoma, in up to 10.1% and 1.7%, respectively.

Architecture

Traditionally, adenomas are described as tubular, tubulovillous, or villous, primarily based on the overall percentage of villous component. Risk of malignancy increases with increased villous composition of the polyp.

Tubular adenomas are variously defined as those that contain 0% to 25% villous tissue. About 70% to 85% of all adenomas are tubular; they tend to be smaller than villous adenomas. See the image below.

Tubular adenoma, low-power view. Courtesy of Georg Tubular adenoma, low-power view. Courtesy of George H. Warren, MD.

Tubulovillous adenomas contain approximately 25% to 75% villous tissue. These adenomas represent 10% to 25% of all adenomas; they tend to be intermediate in size.

Villous adenomas contain more than 75% villous tissue. These adenomas represent 5% of all adenomas; they tend to be larger and have the greatest malignancy potential.

Dysplasia

Dysplasia is a neoplastic change in histology. All adenomas are dysplastic; they display varying degrees of hyperchromasia, nucleolar prominence, nuclear pleomorphism, and increased mitoses.

Dysplasia is classified as either low-grade or high-grade. High-grade dysplasia is associated with an increased risk of malignancy. Invasive carcinoma is distinguished from high-grade dysplasia by invasion of neoplastic tissue beyond the muscularis mucosa.

The histologic criteria used to differentiate low- and high-grade dysplasia are as follows:

  • Low-grade: Basal or stratified nuclei, crowded glands, less goblet cells and mucin (See the following image.)
  • High-power view of adenomatous polyp with low-grad High-power view of adenomatous polyp with low-grade dysplasia. Courtesy of George H. Warren, MD.
  • High-grade: Loss of glandular architecture, increased mitoses (includes previously termed carcinoma in situ and intramucosal carcinoma) (See the image below.)
  • Villous adenoma with grade IV invasive carcinoma. Villous adenoma with grade IV invasive carcinoma. Courtesy of George H. Warren, MD.
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Contributor Information and Disclosures
Author

Swati G Patel, MD, MS Clinical Lecturer of Internal Medicine, Division of Gastroenterology, University of Michigan Health System; Staff Physician, Ann Arbor VA Medical Center

Swati G Patel, MD, MS is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn's and Colitis Foundation of America, Physicians for Human Rights

Disclosure: Nothing to disclose.

Coauthor(s)

Dennis J Ahnen, MD Professor of Medicine, Divisions of Gastroenterology/Medical Oncology, University of Colorado Health Science Center; Consulting Staff, Chief, Gastroenterology Section, Department of Medicine, Veteran's Affairs Medical Center, Denver

Dennis J Ahnen, MD is a member of the following medical societies: American Association for the Advancement of Science, Crohn's and Colitis Foundation of America, Gastroenterology Research Group, American College of Physicians, American Federation for Medical Research, American Gastroenterological Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, American Gastroenterological Association

Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Rajeev Vasudeva, MD Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD is a member of the following medical societies: American College of Gastroenterology, Columbia Medical Society, South Carolina Gastroenterology Association, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, South Carolina Medical Association

Disclosure: Received honoraria from Pricara for speaking and teaching; Received consulting fee from UCB for consulting.

Acknowledgements

John Riopelle, DO Fellow, Department of Medicine, Division of Gastroenterology/Hepatology, University of Colorado Health Sciences Center

Disclosure: Nothing to disclose.

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. Lash RH, Genta RM, Schuler CM. Sessile serrated adenomas: prevalence of dysplasia and carcinoma in 2139 patients. J Clin Pathol. 2010 Aug. 63(8):681-6. [Medline].

  2. Merrill RM, Anderson AE. Risk-adjusted colon and rectal cancer incidence rates in the United States. Dis Colon Rectum. 2011 Oct. 54(10):1301-6. [Medline].

  3. Winawer SJ, Zauber AG, Ho MN, et al. Prevention of colorectal cancer by colonoscopic polypectomy. The National Polyp Study Workgroup. N Engl J Med. 1993 Dec 30. 329(27):1977-81. [Medline].

  4. Singh H, Nugent Z, Mahmud SM, Demers AA, Bernstein CN. Predictors of colorectal cancer after negative colonoscopy: a population-based study. Am J Gastroenterol. 2010 Mar. 105(3):663-73; quiz 674. [Medline].

  5. Baxter NN, Sutradhar R, Forbes SS, Paszat LF, Saskin R, Rabeneck L. Analysis of administrative data finds endoscopist quality measures associated with postcolonoscopy colorectal cancer. Gastroenterology. 2011 Jan. 140(1):65-72. [Medline].

  6. Brenner H, Chang-Claude J, Seiler CM, Hoffmeister M. Interval cancers after negative colonoscopy: population-based case-control study. Gut. 2012 Nov. 61(11):1576-82. [Medline].

  7. Screening for colorectal cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2008 Nov 4. 149(9):627-37. [Medline].

  8. Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR, et al. Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology. 2012 Sep. 143(3):844-57. [Medline].

  9. Al-Sohaily S, Biankin A, Leong R, Kohonen-Corish M, Warusavitarne J. Molecular pathways in colorectal cancer. J Gastroenterol Hepatol. 2012 Sep. 27(9):1423-31. [Medline].

  10. Järvinen HJ, Aarnio M, Mustonen H, et al. Controlled 15-year trial on screening for colorectal cancer in families with hereditary nonpolyposis colorectal cancer. Gastroenterology. 2000 May. 118(5):829-34. [Medline].

  11. Schatzkin A, Freedman LS, Dawsey SM, Lanza E. Interpreting precursor studies: what polyp trials tell us about large-bowel cancer. J Natl Cancer Inst. 1994 Jul 20. 86(14):1053-7. [Medline].

  12. Williams AR, Balasooriya BA, Day DW. Polyps and cancer of the large bowel: a necropsy study in Liverpool. Gut. 1982 Oct. 23(10):835-42. [Medline].

  13. Kaneko R, Sato Y, An Y, et al. Clinico-epidemiologic study of the metabolic syndrome and lifestyle factors associated with the risk of colon adenoma and adenocarcinoma. Asian Pac J Cancer Prev. 2010. 11(4):975-83. [Medline].

  14. Lieberman DA, Prindiville S, Weiss DG, Willett W. Risk factors for advanced colonic neoplasia and hyperplastic polyps in asymptomatic individuals. JAMA. 2003 Dec 10. 290(22):2959-67. [Medline].

  15. Nguyen SP, Bent S, Chen YH, Terdiman JP. Gender as a risk factor for advanced neoplasia and colorectal cancer: a systematic review and meta-analysis. Clin Gastroenterol Hepatol. 2009 Jun. 7(6):676-81.e1-3. [Medline].

  16. Patel SG, Ahnen DJ. Familial colon cancer syndromes: an update of a rapidly evolving field. Curr Gastroenterol Rep. 2012 Oct. 14(5):428-38. [Medline]. [Full Text].

  17. Bonadona V, Boniati B, Olschwang S, et al. Cancer risks associated with germline mutations in MLH1, MSH2, and MSH6 genes in Lynch syndrome. JAMA. 2011 Jun 8. 305(22):2304-10. [Medline].

  18. Moisio AL, Jarvinen H, Peltomaki P. Genetic and clinical characterisation of familial adenomatous polyposis: a population based study. Gut. 2002 Jun. 50(6):845-50. [Medline]. [Full Text].

  19. Sieber OM, Lipton L, Crabtree M, et al. Multiple colorectal adenomas, classic adenomatous polyposis, and germ-line mutations in MYH. N Engl J Med. 2003 Feb 27. 348(9):791-9. [Medline].

  20. Woods MO, Younghusband HB, Parfrey PS, et al. The genetic basis of colorectal cancer in a population-based incident cohort with a high rate of familial disease. Gut. 2010 Oct. 59(10):1369-77. [Medline]. [Full Text].

  21. Wynder EL, Reddy BS. Metabolic epidemiology of colorectal cancer. Cancer. 1974 Sep. 34(3):suppl:801-6. [Medline].

  22. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med. 1999 Jan 21. 340(3):169-76. [Medline].

  23. Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. N Engl J Med. 1990 Dec 13. 323(24):1664-72. [Medline].

  24. Schatzkin A, Lanza E, Corle D, et al. Lack of effect of a low-fat, high-fiber diet on the recurrence of colorectal adenomas. Polyp Prevention Trial Study Group. N Engl J Med. 2000 Apr 20. 342(16):1149-55. [Medline].

  25. Schatzkin A, Mouw T, Park Y, et al. Dietary fiber and whole-grain consumption in relation to colorectal cancer in the NIH-AARP Diet and Health Study. Am J Clin Nutr. 2007 May. 85(5):1353-60. [Medline].

  26. Okabayashi K, Ashrafian H, Hasegawa H, et al. Body mass index category as a risk factor for colorectal adenomas: a systematic review and meta-analysis. Am J Gastroenterol. 2012 Aug. 107(8):1175-85; quiz 1186. [Medline].

  27. Boyle T, Keegel T, Bull F, Heyworth J, Fritschi L. Physical activity and risks of proximal and distal colon cancers: a systematic review and meta-analysis. J Natl Cancer Inst. 2012 Oct 17. 104(20):1548-61. [Medline].

  28. Kushi LH, Doyle C, McCullough M, et al; American Cancer Society 2010 Nutrition and Physical Activity Guidelines Advisory Committee. American Cancer Society Guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin. 2012 Jan-Feb. 62(1):30-67. [Medline].

  29. Martinez ME, Marshall JR et al. Colorectal Cancer: Environmental and Lifestyle Issues. Kelsen DP, Daly JM, Kern SE, Levin B, Tepper JE, eds. Gastrointestinal oncology: principles and practices. Philadelphia: Lippincott Williams and Wilkins; 2002. 665-83.

  30. Giovannucci E, Colditz GA, Stampfer MJ, et al. A prospective study of cigarette smoking and risk of colorectal adenoma and colorectal cancer in U.S. women. J Natl Cancer Inst. 1994 Feb 2. 86(3):192-9. [Medline].

  31. Giovannucci E, Rimm EB, Stampfer MJ, et al. A prospective study of cigarette smoking and risk of colorectal adenoma and colorectal cancer in U.S. men. J Natl Cancer Inst. 1994 Feb 2. 86(3):183-91. [Medline].

  32. Syngal S, Brand RE, Church JM, et al; American College of Gastroenterology. ACG clinical guideline: Genetic testing and management of hereditary gastrointestinal cancer syndromes. Am J Gastroenterol. 2015 Feb. 110(2):223-62; quiz 263. [Medline].

  33. Lindholm E, Brevinge H, Haglind E. Survival benefit in a randomized clinical trial of faecal occult blood screening for colorectal cancer. Br J Surg. 2008 Aug. 95(8):1029-36. [Medline].

  34. Scholefield JH, Moss S, Sufi F, Mangham CM, Hardcastle JD. Effect of faecal occult blood screening on mortality from colorectal cancer: results from a randomised controlled trial. Gut. 2002 Jun. 50(6):840-4. [Medline].

  35. Mandel JS, Church TR, Bond JH, et al. The effect of fecal occult-blood screening on the incidence of colorectal cancer. N Engl J Med. 2000 Nov 30. 343(22):1603-7. [Medline].

  36. Kronborg O, Jorgensen OD, Fenger C, Rasmussen M. Randomized study of biennial screening with a faecal occult blood test: results after nine screening rounds. Scand J Gastroenterol. 2004 Sep. 39(9):846-51. [Medline].

  37. Levi Z, Rozen P, Hazazi R, et al. A quantitative immunochemical fecal occult blood test for colorectal neoplasia. Ann Intern Med. 2007 Feb 20. 146(4):244-55. [Medline].

  38. Imperiale TF, Ransohoff DF, Itzkowitz SH, Turnbull BA, Ross ME, Colorectal Cancer Study Group. Fecal DNA versus fecal occult blood for colorectal-cancer screening in an average-risk population. N Engl J Med. 2004 Dec 23. 351(26):2704-14. [Medline].

  39. Ahlquist DA, Sargent DJ, Loprinzi CL, et al. Stool DNA and occult blood testing for screen detection of colorectal neoplasia. Ann Intern Med. 2008 Oct 7. 149(7):441-50, W81. [Medline].

  40. Schoen RE, Pinsky PF, Weissfeld JL, et al. Colorectal-cancer incidence and mortality with screening flexible sigmoidoscopy. N Engl J Med. 2012 Jun 21. 366(25):2345-57. [Medline].

  41. ASGE Standards of Practice Committee, Fisher DA, Maple JT, Ben-Menachem T, et al. Complications of colonoscopy. Gastrointest Endosc. 2011 Oct. 74(4):745-52. [Medline].

  42. Singh H, Nugent Z, Demers AA, Bernstein CN. Rate and predictors of early/missed colorectal cancers after colonoscopy in Manitoba: a population-based study. Am J Gastroenterol. 2010 Dec. 105(12):2588-96. [Medline].

  43. Cooper GS, Xu F, Barnholtz Sloan JS, Schluchter MD, Koroukian SM. Prevalence and predictors of interval colorectal cancers in medicare beneficiaries. Cancer. 2012 Jun 15. 118(12):3044-52. [Medline].

  44. Kahi CJ, Hewett DG, Norton DL, Eckert GJ, Rex DK. Prevalence and variable detection of proximal colon serrated polyps during screening colonoscopy. Clin Gastroenterol Hepatol. 2011 Jan. 9(1):42-6. [Medline].

  45. Rex DK, Petrini JL, Baron TH, et al. Quality indicators for colonoscopy. Am J Gastroenterol. 2006 Apr. 101(4):873-85. [Medline].

  46. Labayle D, Fischer D, Vielh P, et al. Sulindac causes regression of rectal polyps in familial adenomatous polyposis. Gastroenterology. 1991 Sep. 101(3):635-9. [Medline].

  47. Giardiello FM, Hamilton SR, Krush AJ, et al. Treatment of colonic and rectal adenomas with sulindac in familial adenomatous polyposis. N Engl J Med. 1993 May 6. 328(18):1313-6. [Medline].

  48. Steinbach G, Lynch PM, Phillips RK, et al. The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis. N Engl J Med. 2000 Jun 29. 342(26):1946-52. [Medline].

  49. Rothwell PM, Fowkes FG, Belch JF, Ogawa H, Warlow CP, Meade TW. Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. Lancet. 2011 Jan 1. 377(9759):31-41. [Medline].

 
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Endoscopic view of a pedunculated polyp.
Endoscopic view of a sessile polyp.
Tubular adenoma, low-power view. Courtesy of George H. Warren, MD.
Villous adenoma, low-power view. Courtesy of George H. Warren, MD.
High-power view of adenomatous polyp with low-grade dysplasia. Courtesy of George H. Warren, MD.
Villous adenoma with grade IV invasive carcinoma. Courtesy of George H. Warren, MD.
 
 
 
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