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.

Most juvenile polyps are benign, however, malignancy can occur. The cumulative lifetime risk of colorectal cancer is 39% in patients with juvenile polyposis syndrome.

The incidence of the mutation is between 1 in 10,000 and 1 in 15,000 births.

By age 35 years, 95% of individuals with FAP (>100 adenomas) have polyps. Without colectomy, colon cancer is virtually inevitable. The mean age of colon cancer in untreated individuals is 39 years (range 34–43 years).

Attentuated FAP arises when APC is defective but still somewhat functional. As a result, it retains part of its ability to suppress polyps. Therefore, attenuated FAP manifests as colorectal cancer unusually late (age 40–70, average=55), and typically with few, or at least far fewer polyps (typically 30), than the more usual version of FAP, at an age when FAP is no longer considered much of a likelihood or risk according to usual FAP epidemiology.

Screening for colonic polyps as well as preventing them has become an important part of the management of the condition. Medical societies have established guidelines for colorectal screening in order to prevent adenomatous polyps and to minimize the chances of developing colon cancer. It is believed that some changes in the diet might be helpful in preventing polyps from occurring but there is no other way to prevent the polyps from developing into cancerous growths than by detecting and removing them.

According to the guidelines established by the American Cancer Society, individuals who reach the age of 50 should perform an occult blood test yearly. Colon polyps as they grow can sometimes cause bleeding within the intestine, which can be detected with the help of this test. Also, persons in their 50s are recommended to have flexible sigmoidoscopies performed once in 3 to 5 years to detect any abnormal growth which could be an adenomatous polyp. If adenomatous polyps are detected during this procedure, it is most likely that the patient will have to undergo a colonoscopy. Medical societies recommend colonoscopies every ten years starting at age 50 as a necessary screening practice for colon cancer. The screening provides an accurate image of the intestine and also allows the removal of the polyp, if found. Once an adenomatous polyp is identified during colonoscopy, there are several methods of removal including using a snare or a heating device. Colonoscopies are preferred over sigmoidoscopies because they allow the examination of the entire colon; a very important aspect, considering that more than half of the colonic polyps occur in the upper colon, which is not reached during sigmoidoscopies.

It has been statistically demonstrated that screening programs are effective in reducing the number of deaths caused by colon cancer due to adenomatous polyps. While there are risks of complications associated with colonoscopies, those risks are extremely low at approximately 0.35 percent. For comparison, the lifetime risk of developing colon cancer is around 6 percent. As there is a small likelihood of recurrence, surveillance after polyp removal is recommended.

Fundic gland polyps are found in 0.8 to 1.9% of patients who undergo esophagogastroduodenoscopy, and are more common in middle aged women.

The most important consideration in evaluating patients with FGPs is distinguishing between sporadic form (patients without any other gastrointestinal condition, usually in middle age with female prevalence) and syndromic form. This is to ascertain the risk of development of gastric cancer, and to ascertain the risk of concomitant colon cancer.

FGPs can be found in association with the following genetic conditions:

- familial adenomatous polyposis

- attenuated familial adenomatous polyposis syndromes

- Zollinger-Ellison syndrome

- gastric adenocarcinoma associated with proxymal polyposis of the stomach (GAPPS): this condition, described in three families is characterized by development of antral adenomas and FGPs, with early development of severe dysplasia and gastric cancer, in absence of overt intestinal polyposis. This condition has been recently characterized by a point mutation in exon 1B of APC gene.

Sporadic FGPs have been associated with:

- chronic use of proton pump inhibitors (proposed by some authors, denied by others)

- "Helicobacter pylori" infection: there is a reverse relationship between infection and fundic gland polyps, and infection by "H pylori" causes polyps regression.

These are polyps which are associated with inflammatory conditions such as Ulcerative Colitis and Crohns disease.

Muir–Torre was observed to occur in 14 of 50 families (28%) and in 14 of 152 individuals (9.2%) with Lynch syndrome, also known as HNPCC.

The 2 major MMR proteins involved are hMLH1 and hMSH2. Approximately 70% of tumors associated with the MTS have microsatellite instability. While germline disruption of hMLH1 and hMSH2 is evenly distributed in HNPCC, disruption of hMSH2 is seen in greater than 90% of MTS patients.

Gastrointestinal and genitourinary cancers are the most common internal malignancies. Colorectal cancer is the most common visceral neoplasm in Muir–Torre syndrome patients.

Complete removal of a SSA is considered curative.

Several SSAs confer a higher risk of subsequently finding colorectal cancer and warrant more frequent surveillance. The surveillance guidelines are the same as for other colonic adenomas. The surveillance interval is dependent on (1) the number of adenomas, (2) the size of the adenomas, and (3) the presence of high-grade microscopic features.

In gastroenterology, a sessile serrated adenoma (abbreviated SSA), also known as sessile serrated polyp (abbreviated SSP), is a premalignant flat (or sessile) lesion of the colon, predominantly seen in the cecum and ascending colon.

SSAs are thought to lead to colorectal cancer through the (alternate) "serrated pathway". This differs from most colorectal cancer, which arises from mutations starting with inactivation of the APC gene.

Multiple SSAs may be part of the "serrated polyposis syndrome".

Juvenile Polyposis Syndrome can occur sporadically in families or be inherited in an autosomal dominant manner.

Two genes associated with Juvenile Polyposis Syndrome are BMPR1A and SMAD4. Gene testing may be useful when trying to ascertain which non-symptomatic family members may be at risk of developing polyps, however having a known familial mutation would be unlikely to change the course of treatment. A known mutation may also be of use for affected individuals when they decide to start a family as it allows them reproductive choices.

While mutations in the gene PTEN were also thought to have caused Juvenile Polyposis Syndrome, it is now thought that mutations in this gene cause a similar clinical picture to Juvenile Polyposis Syndrome but are actually affected with Cowden syndrome or other phenotypes of the PTEN hamartoma tumor syndrome.

The risks of progression to colorectal cancer increases if the polyp is larger than 1 cm and contains a higher percentage of villous component. Also, the shape of the polyps is related to the risk of progression into carcinoma. Polyps that are pedunculated (with a stalk) are usually less dangerous than sessile polyps (flat polyps). Sessile polyps have a shorter pathway for migration of invasive cells from the tumor into submucosal and more distant structures, and they are also more difficult to remove and to ascertain. Sessile polyps larger than 2 cm usually contain villous features, have a higher malignant potential, and tend to recur following colonoscopic polypectomy.

Although polyps do not carry significant risk of colon cancer, tubular adenomatous polyps may become cancerous when they grow larger. Larger tubular adenomatous polyps have an increased risk of malignancy when larger because then they develop more villous components and may become sessile.

It is estimated that an individual whose parents have been diagnosed with an adenomatous polyp has a 50% greater chance to develop colon cancer than individuals with no family history of colonic polyps. At this point, there is no method to establish the risks that patients with a family history of colon polyps have to develop these growths. Overall, nearly 6% of the population, regardless of the family history, is at risk of developing colon cancer.

There is a risk of development of cancer with fundic gland polyposis, but it varies based on the underlying cause of the polyposis. The risk is highest with congenital polyposis syndromes, and is lowest in acquired causes. As a result, it is recommended that patients with multiple fundic polyps have a colonoscopy to evaluate the colon. If there are polyps seen on colonoscopy, genetic testing and testing of family members is recommended.

In the gastric adenocarcinoma associated with proximal polyposis of the stomach (GAPPS), there is a high risk of early development of proximal gastric adenocarcinoma.

It is still unclear which patients would benefit with surveillance gastroscopy, but most physicians recommend endoscopy every one to three years to survey polyps for dysplasia or cancer. In the event of high grade dysplasia, polypectomy, which is done through the endoscopy, or partial gastrectomy may be recommended. One study showed the benefit of NSAID therapy in regression of gastric polyps, but the efficacy of this strategy (given the side effects of NSAIDs) is still dubious.

Monitoring involves the provision of outpatient colonoscopy, and occasionally upper gastric tract esophagogastroduodenoscopy (EGD, to search for premalignant gastric or duodenal tumors), typically once every 1–3 years, and/or a genetic blood test to definitively confirm or deny susceptibility. A small number of polyps can often be excised (removed) during the procedure, if found, but if there are more severe signs or numbers, in patient surgery may be required.

NCBI states that when an individual is identified as having FAP, or the mutations resulting in FAP: "It is appropriate to evaluate the parents of an affected individual (a) with molecular genetic testing of APC if the disease-causing mutation is known in the proband [person first identified with the condition] or (b) for clinical manifestations of APC-associated polyposis conditions".

Villous adenoma is a type of polyp that grows in the colon and other places in the gastrointestinal tract and sometimes in other parts of the body. These adenomas may become malignant (cancerous). Villous adenomas have been demonstrated to contain malignant portions in about one third of affected persons, and invasive malignancy in another one third of removed specimens. Colonic resection may be required for large lesions. These can also lead to secretory diarrhea with large volume liquid stools with few formed elements. They are commonly described as secreting large amounts of mucus, resulting in hypokalaemia in patients. On endoscopy a "cauliflower' like mass is described due to villi stretching. Being an adenoma, the mass is covered in columnar epithelial cells.

This is a very rare neoplasm accounting for approximately 0.0003% of all tumors and about 2.5% of all external ear neoplasms. There is a wide age range at initial presentation, although the mean age is about 50 years of age. Females are affected slightly more often (1.5:1).

Verruciform xanthoma is uncommon, with a female:male ratio of 1:1.1

Gardner syndrome, also known as Gardner's syndrome or familial colorectal polyposis, is an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon. The extracolonic tumors may include osteomas of the skull, thyroid cancer, epidermoid cysts, fibromas, as well as the occurrence of desmoid tumors in approximately 15% of affected individuals.

Desmoid tumors are fibrous tumors which usually occur in the tissue covering the intestines and may be provoked by surgery to remove the colon. The countless polyps in the colon predispose to the development of colon cancer; if the colon is not removed, the chance of colon cancer is considered to be very significant. Polyps may also grow in the stomach, duodenum, spleen, kidneys, liver, mesentery and small bowel. In a small number of cases, polyps have also appeared in the cerebellum. Cancers related to Gardner syndrome commonly appear in the thyroid, liver and kidneys. The number of polyps increases with age, and hundreds to thousands of polyps can develop in the colon.

The syndrome was first described in 1951. There is no cure at this time, and in its more advanced forms, it is considered a terminal diagnosis with a life expectancy of 35–45 years; treatments are surgery and palliative care, although some chemotherapy has been tried with limited success.

Gardner syndrome is inherited in an autosomal dominant manner. Typically, one parent has Gardner syndrome. Each of their children, male and female alike, are at 50% risk of inheriting the gene for Gardner syndrome.

While there is a wide age range at clinical presentation (12–85 years), most patients come to clinical attention at 55 years (mean). There is no gender difference.

Most individuals come to clinical attention during the 5th decade, although the age range is broad (20 to 80 years). There is an equal gender distribution.

Muir–Torre syndrome (MTS) is a rare hereditary, autosomal dominant cancer syndrome that is thought to be a subtype of HNPCC. Individuals are prone to develop cancers of the colon, genitourinary tract, and skin lesions, such as keratoacanthomas and sebaceous tumors. The genes affected are MLH1, MSH2, and more recently, MSH6, and are involved in DNA mismatch repair.

The colorectal adenoma is a benign glandular tumor of the colon and the rectum. It is a precursor lesion of the colorectal adenocarcinoma (colon cancer).

Some morphological variants have been described:

- tubular adenoma

- tubulovillous adenoma

- villous adenoma

- sessile serrated adenoma (SSA)

Nipple adenomas most commonly occur in 30- to 40-year-old women, but can also occur in men. They can also occur at any age, including in the elderly, in adolescence, and in infants.

This is a very rare tumor, since only about 1 in 35,000 to 40,000 people have VHL, of whom about 10% have endolymphatic sac tumors. Patients usually present in the 4th to 5th decades without an gender predilection. The tumor involves the endolymphatic sac, a portion of the intraosseous inner ear of the posterior petrous bone.

A sebaceous adenoma, a type of adenoma, a cutaneous condition characterized by a slow-growing tumor usually presenting as a pink, flesh-coloured, or yellow papule or nodule.