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Colon polyps
Polyp of sigmoid colon as revealed by colonoscopy. Approximately 1 cm in diameter. The polyp was removed by snare cautery.
SpecialtyGastroenterology Edit this on Wikidata
Adenomatous colon polyp with malignant focus at apex

A colorectal polyp is a polyp (fleshy growth) occurring on the lining of the colon or rectum.[1] Untreated colorectal polyps can develop into colorectal cancer.[2]

Colorectal polyps are often classified by their behaviour (i.e. benign vs. malignant) or cause (e.g. as a consequence of inflammatory bowel disease). They may be benign (e.g. hyperplastic polyp), pre-malignant (e.g. tubular adenoma) or malignant (e.g. colorectal adenocarcinoma).

Signs and symptoms

[edit]

Colorectal polyps are not usually associated with symptoms.[2] When they occur, symptoms include bloody stools; changes in frequency or consistency of stools (such as a week or more of constipation or diarrhoea);[3] and fatigue arising from blood loss.[2] Anemia arising from iron deficiency can also present due to chronic blood loss, even in the absence of bloody stools.[3][4] Another symptom may be an increased mucus production especially those involving villous adenomas.[4] Copious production of mucus causes loss of potassium that can occasionally result in symptomatic hypokalemia.[4] Occasionally, if a polyp is big enough to cause a bowel obstruction, there may be nausea, vomiting and severe constipation.[3]

Structure

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Polyps are either pedunculated (attached to the intestinal wall by a stalk) or sessile (grow directly from the wall).[5][6]: 1342  In addition to the gross appearance categorization, they are further divided by their histologic appearance as tubular adenoma which are tubular glands, villous adenoma which are long finger like projections on the surface, and tubulovillous adenoma which has features of both.[6]: 1342 

Genetics

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Hereditary syndromes causing increased colorectal polyp formation include:

Several genes have been associated with polyposis, such as GREM1, MSH3, MLH3, NTHL1, RNF43 and RPS20.[8]

Familial adenomatous polyposis

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Main article: Familial adenomatous polyposis

Familial adenomatous polyposis (FAP) is a form of hereditary cancer syndrome involving the APC gene located on chromosome q521.[9] The syndrome was first described in 1863 by Virchow on a 15-year-old boy with multiple polyps in his colon.[9] The syndrome involves development of multiple polyps at an early age and those left untreated will all eventually develop cancer.[9] The gene is expressed 100% in those with the mutation and it is autosomal dominant.[9] 10–20% of patients have negative family history and acquire the syndrome from spontaneous germline mutation.[9] The average age of newly diagnosed patient is 29 and the average age of newly discovered colorectal cancer is 39.[9] It is recommended that those affected undergo colorectal cancer screening at younger age with treatment and prevention are surgical with removal of affected tissues.[9]

Hereditary nonpolyposis colorectal cancer (Lynch Syndrome)

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Main article: Hereditary nonpolyposis colorectal cancer

Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) is a hereditary colorectal cancer syndrome.[9] It is the most common hereditary form of colorectal cancer in the United States and accounts for about 3% of all cases of cancer.[9] It was first recognized by Alder S. Warthin in 1885 at the University of Michigan.[9] It was later further studied by Henry Lynch who recognized an autosomal dominant transmission pattern with those affected having relatively early onset of cancer (mean age 44 years), greater occurrence of proximal lesions, mostly mucinous or poorly differentiated adenocarcinoma, greater number of synchronous and metachronous cancer cells, and good outcome after surgical intervention.[9] The Amsterdam Criteria were initially used to define Lynch syndrome before the underlying genetic mechanism had been worked out.[9] The Criteria required that the patient has three family members all first-degree relatives with colorectal cancer that involves at least two generations with at least one affected person being younger than 50 years of age when the diagnosis was made.[9] The Amsterdam Criteria is too restrictive and was later expanded to include cancers of endometrial, ovarian, gastric, pancreatic, small intestinal, ureteral, and renal pelvic origin.[9] The increased risk of cancer seen in patients with by the syndrome is associated with dysfunction of DNA repair mechanism.[9] Molecular biologists have linked the syndrome to specific genes such as hMSH2, hMSH1, hMSH6, and hPMS2.[9]

Peutz–Jeghers syndrome

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Main article: Peutz–Jeghers syndrome

Peutz–Jeghers syndrome is an autosomal dominant syndrome that presents with hamartomatous polyps, which are disorganized growth of tissues of the intestinal tract, and hyperpigmentation of the interlining of the mouth, lips and fingers.[9] The syndrome was first noted in 1896 by Hutchinson, and later separately described by Peutz, and then again in 1940 by Jeghers.[9] The syndrome is associated with malfunction of serine-threonine kinase 11 or STK 11 gene, and has a 2–10% increase in risk of developing cancer of the intestinal tract.[9] The syndrome also causes increased risk of extraintestinal cancer such as that involving breast, ovary, cervix, fallopian tubes, thyroid, lung, gallbladder, bile ducts, pancreas, and testicles.[9] The polyps often bleeds and may cause obstruction that would require surgery.[9] Any polyp larger than 1.5 cm needs removal and patients should be monitored closely and screen every two years for malignancy.[9]

Juvenile polyposis syndrome

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Main article: Juvenile polyposis syndrome

Juvenile polyposis syndrome is an autosomal dominant syndrome characterized by increased risk of cancer of intestinal tract and extraintestinal cancer.[9] It often presents with bleeding and obstruction of the intestinal tract along with low serum albumin due to protein loss in the intestine.[9] The syndrome is linked to malfunction of SMAD4 a tumor suppression gene that is seen in 50% of cases.[9] Individuals with multiple juvenile polyps have at least 10% chance of developing malignancy and should undergo abdominal colectomy with ileorectal anastomosis, and close monitoring via endoscopy of rectum.[9] For individuals with few juvenile polyps, patients should undergo endoscopic polypectomy.[9]

Types

[edit]
Incidences and malignancy risks of various types of colorectal polyps

Colorectal polyps can broadly be classified as follows:

  • hyperplastic,
  • neoplastic (adenomatous and malignant),
  • hamartomatous and,
  • inflammatory.

Comparison table

[edit]
Colorectal polyps
Type Risk of containing malignant cells Histopathology Image
Hyperplastic polyp 0% No dysplasia.[10]
  • Mucin-rich type: Serrated ("saw tooth") appearance, containing glands with star-shaped lumina.[11] Crypts that are elongated but straight, narrow and hyperchromatic at the base. All crypts reach to the muscularis mucosae.[11]
  • Goblet cell-rich type: Elongated, fat crypts and little to no serration. Filled with goblet cells, extending to surface, which commonly has a tufted appearance.[11]
Tubular adenoma 2% at 1.5 cm[12] Low to high grade dysplasia[13] Over 75% of volume has tubular appearance.[14]
Tubulovillous adenoma 20% to 25%[15] 25–75% villous[14]
Villous adenoma 15%[16] to 40%[15] Over 75% villous[14]
Sessile serrated adenoma (SSA)[17]
  • Basal dilation of the crypts
  • Basal crypt serration
  • Crypts that run horizontal to the basement membrane (horizontal crypts)
  • Crypt branching.
Colorectal adenocarcinoma 100%
  • In carcinoma in situ (Tis): cancer cells invading into the lamina propria, and may involve but not penetrate the muscularis mucosae. Can be classified as "high-grade dysplasia", because prognosis and management are essentially the same.[10]
  • Invasive adenocarcinoma: Extending through the muscularis mucosae into the submucosa and beyond.[10]

Hyperplastic polyp

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Main article: Hyperplastic polyp

Most hyperplastic polyps are found in the distal colon and rectum.[18] They have no malignant potential,[18] which means that they are no more likely than normal tissue to eventually become a cancer.

Neoplastic polyp

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A neoplasm is a tissue whose cells have lost normal differentiation. They can be either benign growths or malignant growths. The malignant growths can either have primary or secondary causes. Adenomatous polyps are considered precursors to cancer and cancer becomes invasive once malignant cells cross the muscularis mucosa and invade the cells below.[9] Any cellular changes seen above the lamina propria are considered non-invasive and are labeled atypia or dysplasia. Any invasive carcinoma that has penetrated the muscularis mocos has the potential for lymph node metastasis and local recurrence which will require more aggressive and extensive resection.[9] The Haggitt's criteria is used for classification of polyps containing cancer and is based on the depth of penetration.[9] The Haggitt's criteria has level 0 through level 4, with all invasive carcinoma of sessile polyp variant by definition being classified as level 4.[9]

  • Level 0: Cancer does not penetrate through the muscularis mucosa.[9]
  • Level 1: Cancer penetrates through the muscularis mucosa and invades the submucosa below but is limited to the head of the polyp.[9]
  • Level 2: Cancer invades through with involvement of the neck of polyp.[9]
  • Level 3: Cancer invades through with involvement of any parts of the stalk.[9]
  • Level 4: Cancer invades through the submucosa below the stalk of the polyp but above the muscularis propria of the bowel wall.[9]

Adenomas

[edit]
Main article: Colorectal adenoma

Neoplastic polyps of the bowel are often benign hence called adenomas. An adenoma is a tumor of glandular tissue, that has not (yet) gained the properties of cancer.[citation needed]

The common adenomas of the colon (colorectal adenoma) are the tubular, tubulovillous, villous, and sessile serrated (SSA).[18] A large majority (65–80%) are of the benign tubular type with 10–25% being tubulovillous, and villous being the most rare at 5–10%.[9]

As is evident from their name, sessile serrated and traditional serrated adenomas (TSAs) have a serrated appearance and can be difficult to distinguish microscopically from hyperplastic polyps.[18] Making this distinction is important, however, since SSAs and TSAs have the potential to become cancers,[19] while hyperplastic polyps do not.[18]

The villous subdivision is associated with the highest malignant potential because they generally have the largest surface area. (This is because the villi are projections into the lumen and hence have a bigger surface area.) However, villous adenomas are no more likely than tubular or tubulovillous adenomas to become cancerous if their sizes are all the same.[18]

Hamartomatous polyp

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Hamartomatous polyps are tumours, like growths found in organs as a result of faulty development. They are normally made up of a mixture of tissues. They contain mucus-filled glands, with retention cysts, abundant connective tissue, and chronic cellular infiltration of eosinophils.[20] They grow at the normal rate of the host tissue and rarely cause problems such as compression. A common example of a hamartomatous lesion is a strawberry naevus. Hamartomatous polyps are often found by chance; occurring in syndromes such as Peutz–Jegher syndrome or Juvenile polyposis syndrome.

Peutz–Jeghers syndrome is associated with polyps of the GI tract and also increased pigmentation around the lips, genitalia, buccal mucosa, feet, and hands. People are often diagnosed with Peutz–Jegher after presenting at around the age of nine with an intussusception. The polyps themselves carry little malignant potential but because of potential coexisting adenomas there is a 15% chance of colonic malignancy.

Juvenile polyps are hamartomatous polyps that often become evident before twenty years of age, but can also be seen in adults. They are usually solitary polyps found in the rectum which most commonly present with rectal bleeding. Juvenile polyposis syndrome is characterised by the presence of more than five polyps in the colon or rectum, or numerous juvenile polyps throughout the gastrointestinal tract, or any number of juvenile polyps in any person with a family history of juvenile polyposis. People with juvenile polyposis have an increased risk of colon cancer.[19]

Inflammatory polyp

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These are polyps that are associated with inflammatory conditions such as ulcerative colitis and Crohn's disease.[citation needed]

Prevention

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Diet and lifestyle are believed to play a large role in whether colorectal polyps form. Studies show there to be a protective link between consumption of cooked green vegetables, brown rice, legumes, and dried fruit and decreased incidence of colorectal polyps.[21]

Diagnosis

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Colorectal polyps can be detected using a faecal occult blood test, flexible sigmoidoscopy, colonoscopy, virtual colonoscopy, digital rectal examination, barium enema or a pill camera.[3][failed verification]

Malignant potential is associated with

  • degree of dysplasia
  • Type of polyp (e.g. villous adenoma):
    • Tubular adenoma: 5% risk of cancer
    • Tubulovillous adenoma: 20% risk of cancer
    • Villous adenoma: 40% risk of cancer
  • Size of polyp:
    • <1 cm =<1% risk of cancer[22]
    • 1–2 cm=10% risk of cancer[22]
    • >2 cm=50% risk of cancer[22]

Normally an adenoma that is greater than 0.5 cm is treated.

[edit]

NICE classification

[edit]

In colonoscopy, colorectal polyps can be classified by NICE (Narrow-band imaging International Colorectal Endoscopic):[24]

Type 1 Type 2 Type 3
Color Same or lighter than background Browner than background Browner or darkly browner than background, sometimes patchy whiter areas
Vessels None, or isolated lacy vessels coursing across the lesion Brown vessels surrounding white structures Area of disrupted or missing vessels
Surface Pattern Homogenous, or dark or white spots of uniform size Oval, tubular or branched white structures surrounded by brown vessels Amorphous or absent surface pattern
Most likely pathology Hyperplasia Adenoma Deep submucosal invasive cancer
Treatment Follow up Mucosal or submucosal polypectomy Surgical operation

Treatment

[edit]

Polyps can be removed during a colonoscopy or sigmoidoscopy using a wire loop that cuts the stalk of the polyp and cauterises it to prevent bleeding.[3][failed verification] Many "defiant" polyps—large, flat, and otherwise laterally spreading adenomas—may be removed endoscopically by a technique called endoscopic mucosal resection (EMR), which involves injection of fluid underneath the lesion to lift it and thus facilitate endoscopic resection. Saline water may be used to generate lift, though some injectable solutions such as SIC 8000 may be more effective.[25] Minimally invasive surgery is indicated for polyps that are too large or in unfavorable locations, such as the appendix, that cannot be removed endoscopically.[26] These techniques may be employed as an alternative to the more invasive colectomy.[27]

Follow-up

[edit]

By United States guidelines, the following follow-up is recommended:[28]

Baseline colonoscopy finding Recommended time until next colonoscopy
Normal 10 years
1–2 tubular adenomas <10 mm 7–10 years
3–4 tubular adenomas <10 mm 3–5 years
  • 5–10 tubular adenomas <10 mm and/or
  • Adenoma 10 mm and/or
  • Adenoma with tubulovillous or villous histology and/or
  • Adenoma with high-grade dysplasia
 3 years
>10 adenomas on single examination 1 year
Piecemeal resection of adenoma 20 mm 6 months

References

[edit]
[edit]
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Colorectal polyp

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from Grokipedia
A colorectal polyp is a small clump of cells that forms on the lining of the colon or , often protruding into the intestinal lumen. Most colorectal polyps are benign and , but certain types can develop into over time if not removed. They affect approximately 20% of adults, with prevalence rising to 40% in those over age 50. Colorectal polyps are classified into several types based on their shape, histology, and potential for malignancy. Neoplastic polyps, such as adenomas (including tubular, villous, and tubulovillous subtypes) and serrated polyps (like sessile serrated lesions), are precancerous and account for about 80% of cases, with roughly 5% already malignant at detection. In contrast, non-neoplastic polyps, including hyperplastic, inflammatory, and juvenile types, are typically harmless and do not progress to cancer. Polyps may appear as pedunculated (stalked, resembling a ) or sessile (flat and broad-based), with the latter often harder to detect. Most individuals with colorectal polyps experience no symptoms, leading to their discovery primarily through routine screening. When present, symptoms may include (manifesting as blood on , in the stool, or black/tarry stools), changes in bowel habits such as or , , from , or excess in the stool. The absence of symptoms underscores the importance of screening, such as starting at age 45 for average-risk individuals, which can detect and remove polyps to prevent cancer progression. The exact cause of colorectal polyps remains unclear, but they arise from genetic mutations leading to abnormal in the intestinal lining. Risk factors include advancing age (most common after 45), a personal or family history of polyps or , inflammatory bowel diseases like or , , , heavy alcohol use, , and diets low in fiber or high in red/processed meats. Hereditary syndromes, such as (FAP) or Lynch syndrome, significantly elevate risk by causing multiple polyps. Certain populations, including Black individuals in the United States, face higher incidence rates. Treatment typically involves endoscopic removal (polypectomy) during for polyps larger than 5 mm or those with concerning features, which reduces the risk of developing by up to 80%. Larger or sessile polyps may require advanced techniques like endoscopic mucosal resection. Surveillance are recommended based on polyp number, size, and to monitor for recurrence. While prevention is not absolute, lifestyle measures—such as maintaining a healthy weight, exercising regularly, consuming a high-fiber diet rich in fruits and vegetables, limiting alcohol, and avoiding —can lower risk.

Overview

Definition and characteristics

A colorectal polyp is defined as an abnormal growth that protrudes from the lining the colon or . These growths are typically benign, though some have the potential to become malignant over time. Polyps can occur anywhere along the , including the proximal colon (, ascending, and transverse segments), distal colon (descending and sigmoid segments), or , with their location influencing detection and management approaches. Colorectal polyps vary in size, commonly classified as (less than 5 mm in diameter), small (6-9 mm), or large (10 mm or greater), which helps assess . Morphologically, they appear as either pedunculated, with a stalk connecting the growth to the mucosal surface, or sessile, featuring a broad-based attachment without a stalk. In the general , the of colorectal polyps is approximately 25-30% among adults aged 50 years and older, based on screening data, while autopsy studies indicate rates up to 50% by age 70. The understanding of colorectal polyps advanced significantly with the introduction of colonoscopy in the 1960s, enabling direct visualization and removal, which marked a shift from earlier indirect diagnostic methods. Certain polyps, particularly adenomatous ones, play a key role in the adenoma-carcinoma sequence leading to colorectal cancer.

Epidemiology and risk factors

Colorectal polyps are detected in approximately 20-30% of screening colonoscopies in Western countries, with prevalence rates reaching up to 30% in population and autopsy studies among middle-aged and elderly individuals. In contrast, detection rates are lower in Asia and Africa, estimated at 10-15%. Globally, the prevalence of colorectal adenomas, a common type of polyp, is about 23.9% based on systematic reviews of screening data. These geographic variations reflect differences in dietary habits, screening practices, and genetic factors. The incidence of colorectal polyps increases with age, remaining rare under 40 years but rising sharply thereafter, with detection rates of 21-28% in individuals aged 50-59 years, 41-45% in those aged 60-69 years, and 53-58% in those over 70 years. Recent expansions in screening to age 45 have led to increased polyp detection in younger adults, with rates of approximately 25-27% in ages 45-54 as of 2025, aligning with rising early-onset trends. Demographic patterns show higher in males compared to females, with men exhibiting an of approximately 1.68 for distal lesions. Racial and ethnic differences also influence risk, with higher rates observed among Caucasians and relative to or Asian populations; for instance, have a 1.2- to 2-fold increased risk for proximal lesions. Familial clustering is evident, where a family history of polyps elevates individual risk independent of specific syndromes. Modifiable risk factors significantly contribute to polyp development. , particularly with a BMI greater than 30 kg/m², increases the risk by 1.5- to 2-fold, with even higher odds (up to 4.26) for severe (BMI ≥40). , especially with 20 or more pack-years, approximately doubles the risk, with relative risks around 2.14 for current smokers. Dietary factors play a key role, as high consumption of red and processed meats is associated with a of 1.2-1.5, while low intake exacerbates this vulnerability. include regular , which can reduce polyp risk by about 30%. Recent trends indicate declining rates of advanced neoplasia and in populations with widespread screening programs, attributed to the preventive effect of polypectomy. In the United States, post-2000 screening initiatives contributed to a 20-30% drop in advanced neoplasia rates (as observed in early 2010s studies), though overall incidence declines have slowed to approximately 1% per year as of 2023.

Clinical Presentation

Signs and symptoms

Most colorectal polyps are , especially when small, and are typically discovered incidentally during routine screening for . The vast majority—over 90%—of such polyps are detected in asymptomatic individuals via procedures like . When symptoms arise, they often stem from bleeding or the physical presence of larger polyps. is the most frequent manifestation, appearing as bright red blood on toilet paper or in the stool for distal polyps located in the or , while proximal polyps in the may cause (hidden) bleeding or dark, tarry stools () due to slower blood transit and degradation. Changes in bowel habits, including persistent or lasting more than a week, can occur with sizable polyps that partially obstruct the bowel lumen or produce excess . Chronic, low-grade blood loss from any polyps may lead to , presenting with symptoms such as fatigue, pallor, and . Chronic or acute bleeding from polyp ulceration may result in severe . Rare acute presentations are associated with giant polyps exceeding 4 cm, which can trigger intestinal obstruction or intussusception—a condition where one segment of bowel telescopes into another—resulting in crampy , , , and . Pedunculated polyps, with their stalk-like attachment, may also cause localized if they twist or become torsed. Symptom profiles differ by polyp location: distal lesions more commonly produce noticeable bright red owing to their nearer position to the , whereas proximal polyps are generally less likely to cause overt symptoms and instead contribute to insidious issues like from undetected blood loss.

Complications

Colorectal polyps, particularly adenomatous types, pose a significant of via the adenoma-carcinoma , where benign growths progressively accumulate genetic alterations leading to invasive cancer. This process typically spans 7 to 15 years from adenoma inception to cancer development, though high- adenomas—such as those with villous , high-grade , or size greater than 1 cm—may progress within 5 to 10 years. The malignancy escalates with polyp size: approximately 1% for lesions under 1 cm, 10% for those 1 to 2 cm, and up to 50% for polyps exceeding 2 cm in diameter. Non-malignant complications from untreated polyps are less common but can be serious. Chronic or acute from polyp ulceration may result in severe . Intestinal obstruction occurs rarely, though it is more frequent in juvenile polyps or polyposis syndromes due to polyp bulk or multiplicity. during polyp growth is extremely rare, typically limited to isolated case reports involving large or inflammatory lesions. Sessile serrated lesions follow a distinct serrated neoplastic pathway to cancer, often driven by early BRAF mutations, which promote CpG island methylator phenotype progression and . These polyps contribute to 15-30% of colorectal cancers and carry a slower but insidious if undetected. Undetected colorectal polyps account for over 95% of colorectal cancers, underscoring their role in preventable mortality when screening and removal are neglected.

Pathology

Histological structure

Colorectal polyps arise from the epithelial lining of the colonic mucosa, forming exophytic or sessile projections that can be neoplastic or non-neoplastic in nature. Neoplastic polyps, primarily adenomas, exhibit glandular architecture derived from dysplastic colonic epithelium, while non-neoplastic polyps display reactive or disorganized mucosal components without dysplasia. Microscopically, these lesions are evaluated for architectural patterns and cellular atypia to distinguish their potential behavior. In adenomatous polyps, the hallmark is a proliferation of dysplastic glands resembling colonic mucosa but with aberrant growth. Tubular adenomas feature closely packed, branching tubular glands with round to oval lumina, often showing a pedunculated or sessile configuration. Villous adenomas display elongated, finger-like villous fronds with fibrovascular cores lined by tall columnar cells, whereas tubulovillous adenomas combine both patterns, with 25-75% villous component. Dysplasia is graded using a two-tiered system: low-grade dysplasia involves mild architectural distortion, such as pseudostratification and loss of nuclear polarity, with cytological features like hyperchromasia and small nucleoli; high-grade dysplasia shows marked atypia, including complex glandular crowding, cribriforming, increased nuclear-to-cytoplasmic ratios, and prominent nucleoli, indicating a higher risk of progression. Non-neoplastic polyps lack dysplastic changes and include hyperplastic, inflammatory, and hamartomatous types. Hyperplastic polyps demonstrate a serrated glandular architecture with saw-tooth-like crypts confined to the upper half of the , featuring microvesicular in cells and no basal crypt branching. Inflammatory pseudopolyps consist of inflamed and eroded surface mucosa with expanded containing mixed inflammatory infiltrates, crypt abscesses, and featuring dilated thin-walled vessels and . Hamartomatous polyps, such as juvenile polyps, are characterized by disorganized, cystically dilated glands filled with and inflammatory debris, embedded in edematous stroma rich in lymphocytes and plasma cells. Histological diagnosis relies primarily on hematoxylin and eosin (H&E) , which highlights epithelial architecture, glandular patterns, and cytological for routine evaluation. Special stains, such as Ki-67 , assess proliferative activity by revealing nuclear in epithelial cells, often showing an expanded basal proliferative zone in adenomas or irregular foci in serrated lesions to aid in distinguishing subtle .

Genetic and molecular basis

The development of colorectal polyps involves a series of somatic genetic mutations that drive initiation and progression, particularly in sporadic adenomas. Inactivating mutations in the gene occur in approximately 80% of sporadic adenomas and represent an early initiating event by disrupting the , leading to uncontrolled . Progression to advanced adenomas is often marked by activating mutations in the in 30-50% of cases, which enhance downstream signaling in the MAPK pathway and promote growth. In late-stage lesions approaching carcinoma, loss-of-function mutations in the TP53 tumor suppressor gene accumulate, impairing and , further destabilizing the genome. Two primary molecular pathways underlie polyp formation and : the classic adenoma-carcinoma driven by chromosomal (CIN) and the serrated neoplasia pathway characterized by epigenetic alterations. The CIN pathway, responsible for most conventional adenomas, features progressive accumulation of chromosomal aberrations, including and , often initiated by APC inactivation and culminating in widespread genomic . In contrast, the serrated pathway predominates in sessile serrated lesions and involves the CpG island methylator phenotype (CIMP), where hypermethylation silences tumor suppressor genes, combined with the BRAF V600E mutation in about 80% of sessile serrated polyps, activating the MAPK pathway independently of . This pathway frequently leads to through MLH1 promoter methylation. Hereditary syndromes account for a subset of polyps with distinct genetic bases, predisposing individuals to polyposis through mutations. Familial adenomatous polyposis (FAP) arises from APC mutations, resulting in hundreds to thousands of adenomas typically by the second decade of life, with near-certain progression to if untreated. Lynch syndrome, caused by defects in genes such as MLH1 or MSH2, confers a 70-80% lifetime risk of , often through fewer but rapidly progressing adenomas exhibiting . Peutz-Jeghers syndrome stems from mutations, leading to hamartomatous polyps throughout the accompanied by mucocutaneous melanin pigmentation. Juvenile polyposis syndrome involves mutations in SMAD4 or BMPR1A, which disrupt TGF-β signaling and cause multiple (typically 5 or more, but ranging from a few to hundreds) hamartomatous polyps primarily in the colorectum, increasing cancer risk over time. Recent advances highlight the interplay of environmental factors and emerging detection technologies in polyp pathogenesis. By 2025, studies have elucidated the gut microbiome's role in promoting serrated lesion formation, with dysbiotic communities enriched in and certain species fostering and BRAF activation in susceptible individuals. Additionally, liquid biopsy techniques detecting (ctDNA) have shown promise for non-invasive polyp surveillance, with reported sensitivities for advanced adenomas around 23% in recent multimodal assays through or profiling, though specificity remains a challenge for early lesions.

Classification

Major types

Colorectal polyps are broadly classified into neoplastic and non-neoplastic categories based on their histological features and potential for . Neoplastic polyps, which are precancerous, include adenomas and serrated lesions, while non-neoplastic polyps lack this malignant potential and arise from various benign processes. Adenomas represent the most common neoplastic polyps and are subclassified by into tubular, villous, and tubulovillous types. Tubular adenomas account for approximately 70% of cases, characterized by simple glandular structures with low malignant potential in small lesions but increasing risk with size and villous components. Villous adenomas comprise 5-15% and feature elongated, finger-like projections, conferring the highest risk of progression to among adenomas. Tubulovillous adenomas make up 20-25%, blending features of both and exhibiting intermediate risk. Serrated polyps form another key neoplastic subgroup, distinguished by a saw-tooth glandular and varying cancer risk. Hyperplastic polyps, the most frequent serrated type, are typically small, distal, and carry a very low risk of (<1%). In contrast, sessile serrated lesions (also called sessile serrated adenomas or polyps) are larger, right-sided, and have a higher progression risk of 5-15% due to their precursor role in the serrated neoplasia pathway. Traditional serrated adenomas, rarer and often left-sided, show mixed serrated and adenomatous features with elevated malignant potential. Non-neoplastic polyps include hamartomatous and inflammatory variants, which do not typically progress to cancer. Hamartomatous polyps, such as juvenile polyps (often solitary in children) and Peutz-Jeghers polyps (multiple and associated with a hereditary syndrome), consist of disorganized normal tissue elements like cystic glands and smooth muscle. Inflammatory pseudopolyps arise in inflammatory bowel disease, representing islands of regenerating mucosa amid ulceration rather than true neoplasms. Rare non-neoplastic types encompass lipomatous polyps, composed of adipose tissue and usually asymptomatic, and lymphoid polyps, which are nodular aggregates of immune cells. Metaplastic polyps, sometimes termed mucosal prolapse polyps, feature fibromuscular changes due to mechanical stress and are not true polyps but reactive proliferations. The World Health Organization's 2019 classification, which remains the standard as of 2025, refined polyp taxonomy, particularly elevating sessile serrated lesions as a distinct entity from hyperplastic polyps owing to their differing molecular profiles and cancer risks, aiding in targeted surveillance. This update underscores the role of BRAF mutations and CpG island methylator phenotype in serrated pathways, distinct from the APC-driven adenoma-carcinoma sequence.

Comparison of histological features

Colorectal polyps exhibit diverse histological features that distinguish their types and inform clinical risk assessment. Non-neoplastic polyps, including hyperplastic, inflammatory, and hamartomatous variants, generally lack dysplasia and show benign architectural patterns, whereas neoplastic polyps such as conventional adenomas and certain serrated lesions demonstrate cytological atypia and structural abnormalities indicative of malignant potential. These differences are critical for determining progression risk, with neoplastic types progressing through the adenoma-carcinoma sequence or serrated pathway to colorectal cancer. Key histological differentiators center on the presence of dysplasia and architectural complexity. Neoplastic polyps like adenomas feature dysplastic epithelium—ranging from low-grade in tubular forms to high-grade in villous subtypes—arranged in glandular or frond-like patterns, conferring substantial malignant potential that escalates with villous components or size exceeding 1 cm (approximately 10-20% risk of harboring invasive cancer). In contrast, non-neoplastic polyps such as hyperplastic types display uniform serration without dysplasia, while inflammatory polyps exhibit stromal inflammation and surface erosion, both with negligible progression risk (<1%). Hamartomatous polyps, characterized by malformed but mature tissues, also lack dysplasia but may signal syndromic associations elevating overall cancer susceptibility. Among serrated polyps, sessile serrated lesions stand out with boot-shaped crypts and lateral growth, bridging non-neoplastic and neoplastic categories due to their potential for dysplasia development. Prevalence among endoscopically detected polyps reflects these distinctions: conventional adenomas comprise 60-70%, hyperplastic polyps 20-30%, inflammatory polyps around 10-20% in inflammatory bowel disease contexts, hamartomatous polyps less than 1%, and serrated lesions (including sessile subtypes) approximately 20-30% overall, with traditional serrated adenomas rarer at 1-5%. Diagnostic challenges are prominent in borderline cases, particularly differentiating hyperplastic polyps from sessile serrated lesions, where subtle features like crypt base serration or dilation may be overlooked in superficial sections, leading to interobserver disagreement rates of 20-40%; exhaustive sectioning and immunohistochemical aids are often necessary for accurate classification. Multidisciplinary review is recommended for complex or diagnostically challenging polyps, prioritizing histological confirmation to guide risk stratification without over-resection.
Polyp TypeHistological FeaturesMalignancy RiskLocation PreferenceApproximate Prevalence
Hyperplastic polypSerrated crypts with regular architecture, no Low (<1%)Distal colon/rectum20-30%
Sessile serrated lesionSerrated architecture with crypt dilation, horizontal extension, possible low-grade Intermediate (5-15% if ≥1 cm or dysplastic)Proximal colon3-9%
Tubular adenomaBranched tubular glands with low- to high-grade Variable (1% if <1 cm; 10-20% if >1 cm)Throughout (distal for small)50-60%
Villous adenomaLeaf-like villous projections with high-grade High (20-40%)Distal colon5-10%
Hamartomatous polyp (e.g., juvenile)Disorganized admixture of glands, stroma, and cysts; no Low (<1%)Variable<1%
Inflammatory polypSurface erosion with inflammatory granulation tissue and fibrosis; no Very low (<1%)Areas of inflammation (e.g., IBD)10-20% in IBD contexts
Molecular markers, such as BRAF V600E mutations prevalent in sessile serrated lesions, can support histological differentiation in ambiguous cases.

Diagnosis

Screening and detection methods

Screening for colorectal polyps is a cornerstone of early detection strategies aimed at preventing colorectal cancer, focusing on asymptomatic individuals at average risk. The United States Preventive Services Task Force (USPSTF) recommends initiating screening at age 45 years and continuing through age 75 years, with a grade A recommendation for adults aged 50 to 75 and grade B for those aged 45 to 49, based on evidence of substantial net benefit in reducing colorectal cancer incidence and mortality. For adults aged 76 to 85 years, screening should be selectively offered based on individual health status and prior screening history. These guidelines, established in 2021 and unchanged as of 2025, endorse multiple modalities, including colonoscopy every 10 years or annual fecal immunochemical testing (FIT), with the choice depending on patient preferences, access, and local resources. Non-invasive screening methods prioritize accessibility and patient compliance by detecting markers of potential neoplasia without direct visualization. FIT, which identifies hidden hemoglobin in stool samples, is recommended annually and demonstrates high sensitivity for colorectal cancer (74% to 92%) but lower sensitivity for advanced adenomas (approximately 24%), making it effective for triaging patients who require follow-up colonoscopy. Multitarget stool DNA testing, such as Cologuard, combines DNA biomarkers and FIT, achieving 92.3% sensitivity for colorectal cancer and 42.4% for advanced precancerous lesions (including adenomas ≥1 cm), though it has a higher false-positive rate (13%) compared to FIT alone (5%). CT colonography, also known as virtual colonoscopy, offers 90% per-patient sensitivity for adenomas or cancers ≥10 mm, with the advantage of imaging the entire colon non-invasively every five years, though it requires bowel preparation and may detect extracolonic findings necessitating additional evaluation. Invasive methods provide direct visualization and the opportunity for immediate intervention. Colonoscopy remains the gold standard, with per-patient sensitivity exceeding 95% for large polyps (≥10 mm) and the capability to resect detected lesions during the procedure, recommended at 10-year intervals for average-risk individuals. Flexible sigmoidoscopy, which examines the distal colon, detects approximately 60% to 70% of advanced neoplasms (primarily in the rectosigmoid) and is performed every five to 10 years, often combined with FIT for comprehensive coverage. Emerging technologies aim to enhance detection rates and reduce procedural burdens. AI-assisted capsule endoscopy, involving ingestible devices that capture colonic images analyzed by machine learning algorithms, has shown promising results in recent trials (2023–2025), with sensitivity rates around 84% to 92% for polyps ≥6 mm, potentially improving polyp yield and diagnostic accuracy while minimizing reading times. Blood-based tests, such as the FDA-approved Shield test (multitarget cell-free DNA assay) introduced in 2024, offer another non-invasive option for average-risk adults, with 83% sensitivity for colorectal cancer and 13% for advanced adenomas, recommended every three years, though with lower detection of precancerous lesions compared to stool-based methods. Despite these advances, disparities in screening access and uptake persist, particularly among racial and ethnic minorities. For instance, as of 2023, colorectal cancer screening rates are lower among Hispanic (approximately 53%), Black (66%), and many Asian subgroups (50-60%) adults compared to non-Hispanic Whites (70-80%), attributed to barriers such as limited healthcare access, language challenges, and socioeconomic factors, which exacerbate inequities in early polyp detection.

Endoscopic evaluation and classification

Endoscopic evaluation of colorectal polyps is primarily performed via colonoscopy, which allows direct visualization and characterization of lesions within the colon and rectum. Adequate bowel preparation is essential, typically involving a split-dose regimen of oral polyethylene glycol-based laxatives administered the day before and morning of the procedure to ensure clear visualization of the mucosa. Conscious sedation, often with a combination of midazolam and fentanyl, is commonly used to enhance patient comfort during the procedure, which lasts 20-30 minutes on average. The colonoscope, a flexible tube with a camera, is advanced from the anus through the rectum, sigmoid, descending, transverse, ascending colon, and into the cecum, with air or carbon dioxide insufflation to distend the lumen for optimal inspection. During colonoscopy, polyps are characterized and often removed via polypectomy techniques tailored to their morphology. Pedunculated polyps, which have a stalk, are typically resected using hot snare polypectomy, where an electrocautery snare is looped around the stalk and current is applied to cut and coagulate, reducing bleeding risk for lesions larger than 10 mm. Sessile polyps, which lack a stalk and are flat-based, often require endoscopic mucosal resection (EMR), involving submucosal injection of saline or a lifting agent to elevate the lesion, followed by en bloc or piecemeal snare resection to ensure complete removal while minimizing perforation risk. These methods allow for both diagnostic sampling and therapeutic intervention in a single procedure. Classification systems facilitate real-time assessment of polyp morphology and histology during endoscopy. The Paris classification describes superficial neoplastic lesions based on endoscopic appearance: type 0-Ip denotes pedunculated polyps with a narrow stalk, while 0-Is indicates sessile polyps with a broad base; flat lesions are categorized as 0-IIa (slightly elevated), 0-IIb (non-protruding), or 0-IIc (slightly depressed), aiding in risk stratification for submucosal invasion. The Narrow-band Imaging International Colorectal Endoscopic (NICE) classification, used with narrow-band imaging, differentiates polyp types by color, vascular pattern, and surface structure: type 1 (hyperplastic-like) features a colorless or brownish hue with straight, dark vessels and indistinct surface patterns; type 2 (adenoma-like) shows a brownish color with tubular or branched vessels surrounding white structures; and type 3 (deep submucosal invasive cancer-like) exhibits disrupted vessels and amorphous surfaces. This system enables optical diagnosis with high accuracy for diminutive polyps. Advanced imaging enhances polyp characterization beyond white-light endoscopy. Narrow-band imaging (NBI) filters light to emphasize vascular and mucosal patterns, improving adenoma detection; meta-analyses report sensitivity exceeding 90% and negative predictive value over 90% for high-confidence predictions of histology in small polyps. Chromoendoscopy involves spraying dyes such as indigo carmine or methylene blue onto the mucosa to highlight pit patterns and borders, increasing adenoma detection rates by accentuating subtle lesions, particularly in high-risk patients. These techniques support "resect-and-discard" strategies for low-risk polyps when optical diagnosis aligns with histopathology. Histopathological confirmation follows endoscopic sampling, with protocols ensuring adequate tissue for analysis. For large or sessile lesions undergoing EMR, biopsies are often taken from the resection margins in a 4-quadrant fashion to assess completeness and rule out residual neoplasia. Resected polyps or biopsy specimens are fixed in formalin, processed, and examined microscopically for features like dysplasia or invasion. Turnaround time for histopathology reports typically ranges from 3 to 7 days, though complex cases may extend to 1-2 weeks, guiding subsequent management decisions.

Management

Treatment approaches

Treatment of colorectal polyps primarily involves endoscopic removal to prevent progression to malignancy, with techniques selected based on polyp size, histology, location, and accessibility. Polypectomy is the standard approach for most polyps encountered during colonoscopy, aiming for complete resection with clear margins to minimize recurrence. The choice of method balances efficacy, safety, and the endoscopist's expertise, guided by international society recommendations.35122-2/fulltext) For diminutive polyps (≤5 mm), cold snare polypectomy (CSP) is recommended, incorporating a 1-2 mm margin of normal tissue to ensure complete removal, achieving high success rates with minimal tissue distortion for histological assessment. This technique avoids electrocautery, reducing the risk of thermal injury while effectively resecting small lesions in a single pass. For slightly larger polyps (6-9 mm), either cold or hot snare polypectomy may be used, with cold snare preferred in scenarios prioritizing simplicity and lower complication risk. Larger sessile or flat polyps (≥10 mm) typically require more advanced endoscopic techniques such as endoscopic mucosal resection (EMR), which involves submucosal injection of fluid to lift the lesion before snare excision, enabling en bloc or piecemeal removal. EMR achieves complete resection in approximately 89% of cases in a single session, with local recurrence rates as low as 1-2% when adequate margins are obtained and sites are inspected post-procedure.00274-5/fulltext) For non-pedunculated polyps with suspected early invasive cancer or requiring en bloc resection for precise staging, endoscopic submucosal dissection (ESD) is employed, offering curative rates of 86-90% through meticulous dissection of the submucosa. ESD is particularly advantageous in the right colon for large lesions but demands specialized training due to its technical complexity. In cases of giant polyps (>20-30 mm) that are unresectable endoscopically due to size, location, or , or those exhibiting deep submucosal on imaging or , surgical resection via or transanal excision is indicated to achieve curative intent. For residual or recurrent polyp tissue post-polypectomy, ablative methods like (APC) can be applied to achieve and eradicate remnants, particularly in piecemeal resections. Treatment strategies vary by polyp type: low-risk hyperplastic polyps, especially small distal ones, may be managed conservatively if confirmed histologically benign with negligible malignant potential, though removal is often performed to avoid diagnostic uncertainty. In contrast, adenomatous polyps, including those with high-grade , warrant aggressive endoscopic removal regardless of size, as they harbor significant neoplastic risk and complete excision is essential for . , such as distinguishing adenomas from hyperplastic lesions, informs this tailored approach. Overall outcomes for polypectomy are favorable, with bleeding occurring in 0.5-1.5% of cases—most commonly immediate and manageable endoscopically—and perforation rates ranging from 0.1-0.6 per 1,000 procedures, higher with larger lesions or right-sided resections. Recent advancements as of 2025 incorporate (AI)-assisted colonoscopy, which enhances polyp detection and characterization, reducing adenoma miss rates by up to 20-30% and incomplete resection rates to below 10% through real-time guidance during polypectomy. Systems like ENDOANGEL have demonstrated superior efficacy in improving complete resection metrics compared to standard techniques.

Surveillance and follow-up

Surveillance after polypectomy for colorectal polyps is guided by risk stratification to detect metachronous lesions or recurrence, with recommendations primarily from the U.S. Multi-Society Task Force (USMSTF) on . Low-risk findings, such as no polyps or 1-2 tubular adenomas smaller than 10 mm, warrant a repeat in 7-10 years, aligning with average-risk screening intervals; this interval reflects the very low risk of colorectal cancer for at least 10 years following a normal or nearly normal colonoscopy. Intermediate-risk cases, including 3-4 tubular adenomas smaller than 10 mm or a sessile serrated polyp smaller than 10 mm without , recommend surveillance in 3-5 years. High-risk features—defined by polyp size ≥10 mm, villous , high-grade , or 5-10 adenomas—necessitate closer monitoring with in 3 years, while more than 10 adenomas at baseline may require evaluation within 1 year to assess for incomplete removal or missed lesions. The report plays a pivotal role in tailoring these protocols, as it determines risk category based on adenoma number, size, , and grade, ensuring personalized follow-up to balance detection of advanced neoplasia with procedural burden. Repeat remains the cornerstone method for , allowing direct visualization and resection of new polyps, though non-invasive options like fecal immunochemical testing (FIT) may supplement or substitute in average-risk patients post-polypectomy when is contraindicated or declined, particularly for extending intervals in low-risk scenarios.05458-1/fulltext) For patients with hereditary syndromes such as (FAP), lifetime surveillance is essential due to near-certain polyp development, with guidelines recommending annual or biennial starting in the early teens (ages 10-15) for classic FAP to monitor polyp burden and timing for prophylactic colectomy.30054-7/fulltext) Adherence to these surveillance recommendations varies, with studies reporting rates around 50-60%, influenced by barriers including access to care, patient anxiety, sedation concerns, and socioeconomic factors that contribute to both under- and over-utilization of procedures.

Prevention

Lifestyle and dietary strategies

Adopting a diet rich in is associated with a reduced of developing colorectal polyps. Meta-analyses of cohort studies indicate that high intake, typically exceeding 25 grams per day, is linked to a 20-30% lower of colorectal adenomas compared to low intake, with a summary (SRR) of approximately 0.72 for the highest versus lowest categories.01586-2/fulltext) This protective effect is attributed to mechanisms such as the fermentation of by , producing short-chain fatty acids like butyrate, which inhibits and promotes in colonic epithelial cells, thereby preventing polyp formation. The World Cancer Research Fund (WCRF) International's 2025 report on dietary and lifestyle patterns reinforces these findings, recommending fiber-rich foods as part of a broader strategy for prevention, noting consistent associations across large-scale studies. Increased consumption of fruits and vegetables also contributes to polyp risk reduction. Cohort studies suggest that of at least five servings per day is associated with a (RR) of about 0.8 for colorectal adenomas, particularly for fruits, due to their and anti-inflammatory properties that mitigate in the colonic mucosa. In contrast, limiting to less than 500 grams per week (cooked weight) is advised, as higher consumption is linked to elevated polyp risk through mechanisms involving iron and heterocyclic amines that promote DNA damage and ; meta-analyses show that adhering to this limit can reduce precursor risks by up to 24%. Regular and are key lifestyle interventions. Engaging in at least 150 minutes of moderate-intensity exercise per week, such as brisk walking, is associated with approximately a 25% reduction in colorectal polyp incidence, as evidenced by meta-analyses of observational studies showing dose-dependent benefits on insulin sensitivity and gut . For , achieving a 5-10% body in individuals correlates with a 15-46% decrease in incidence, likely by lowering chronic and levels that foster polyp development. Moderating alcohol and quitting smoking further support prevention. Limiting alcohol to less than one per day (equivalent to under seven drinks weekly) appears protective against adenomas, with studies showing no increased risk and potential modest benefits from low intake via effects, though higher consumption elevates risk. significantly lowers polyp risk over time; former smokers who quit for 10 or more years experience roughly a 50% reduction in serrated polyp odds compared to current smokers, as tobacco carcinogens like nitrosamines diminish in the colonic environment post-cessation.30149-1/fulltext) These strategies, when combined, amplify benefits, as highlighted in the WCRF's comprehensive of meta-analyses confirming their role in reducing polyp formation through synergistic effects on gut and .

Screening guidelines and chemoprevention

Screening guidelines for colorectal polyps emphasize early detection to prevent progression to cancer, with major organizations recommending initiation at age 45 for average-risk individuals. The (ACS) 2023 guidelines advocate starting multitiered screening options at age 45, including annual fecal immunochemical testing (FIT), guaiac-based fecal occult blood testing (gFOBT), multitarget stool DNA testing every three years, every 10 years, computed tomography colonography every five years, or every five years, tailored to patient preferences and access. In , 2024 guidelines from the Initiative on Colorectal Cancer promote organized, population-based FIT screening programs starting at age 50 in most countries, which have achieved 20-40% reductions in incidence in implemented nations through high participation and early polyp detection. Chemoprevention strategies target pharmacological agents to inhibit polyp formation or progression, particularly in high-risk groups. Low-dose aspirin (75-100 mg daily) has demonstrated a 50% risk reduction for colorectal neoplasia in individuals with Lynch syndrome, as shown in the 2025 CaPP3 trial, building on earlier CAPP2 findings of 20-30% reduction with higher doses (600 mg) over long-term follow-up. For select high-risk patients, such as those with Lynch syndrome or elevated cardiovascular risk, the U.S. Preventive Services Task Force (USPSTF) 2022 statement notes insufficient evidence for broad aspirin use in prevention but supports individualized consideration based on bleeding risks. Nonsteroidal anti-inflammatory drugs (NSAIDs) like (150 mg twice daily) reduce polyp burden by approximately 40% in (FAP), with sustained effects on polyp number and size in rectal segments post-surgery. Emerging agents show promise but require further validation. Observational studies in diabetic patients indicate metformin use is associated with 15-25% lower risk of recurrence, independent of glycemic control, through mechanisms like AMPK activation inhibiting . supplementation (up to 4000 IU/day) has mixed evidence; the VITAL found no significant reduction in adenoma incidence at 2000 IU/day over five years, though subgroup analyses suggest potential benefits in deficient populations. Personalized prevention is advancing with polygenic risk scores (PRS) in 2025 research, which identify 10-20% of individuals as high-risk for colorectal neoplasia, enabling targeted screening intensification beyond family history alone and improving risk stratification in diverse populations. These approaches synergize with modifications to enhance overall polyp prevention efficacy.

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