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.

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.

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

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

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.

Polypoid lesions of the gallbladder affect approximately 5% of the adult population. The causes are uncertain, but there is a definite correlation with increasing age and the presence of gallstones (cholelithiasis). Most affected individuals do not have symptoms. The gallbladder polyps are detected during abdominal ultrasonography performed for other reasons.

The incidence of gallbladder polyps is higher among men than women. The overall prevalence among men of Chinese ancestry is 9.5%, higher than other ethnic types.

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.

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".

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.

In the United States, about 160,000 new cases of colorectal cancer are diagnosed each year. Hereditary nonpolyposis colorectal cancer is responsible for approximately 2 percent to 7 percent of all diagnosed cases of colorectal cancer. The average age of diagnosis of cancer in patients with this syndrome is 44 years old, as compared to 64 years old in people without the syndrome.

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.

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.

Most polyps are benign and do not need to be removed. Polyps larger than 1 cm with co-occurring gallstones occurring in people over the age of 50 may have the gallbladder removed (cholecystectomy), especially if the polyps are several or appear malignant. Laparoscopic surgery is an option for small or solitary polyps.

The exact cause of nasal polyps is unclear. They are, however, commonly associated with conditions that cause long term inflammation of the sinuses. This includes chronic rhinosinusitis, asthma, aspirin sensitivity, and cystic fibrosis.

Various additional diseases associated with polyp formation include:

Chronic rhinosinusitis is a common medical condition characterized by symptoms of sinus inflammation lasting at least 12 weeks. The cause is unknown and the role of microorganisms remains unclear. It can be classified as either with or without nasal polyposis.

Cystic fibrosis (CF) is the most common cause of nasal polyps in children. Therefore, any child under 12 to 20 years old with nasal polyps should be tested for CF. Half of people with CF will experience extensive polyps leading to nasal obstruction and requiring aggressive management.

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".

Little research is conducted on these cancers due to their relative rarity when compared to the more common colorectal cancers. APC-min mice which carry a gene deficiency corresponding to that of humans with FAP also go on to develop small intestinal tumors, though humans do not.

Safety regulations from US accreditor the Joint Commission may have unintentionally decreased digital rectal examination and FOBT in hospital settings such as Emergency Departments.

Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome is an autosomal dominant genetic condition that has a high risk of colon cancer as well as other cancers including endometrial cancer (second most common), ovary, stomach, small intestine, hepatobiliary tract, upper urinary tract, brain, and skin. The increased risk for these cancers is due to inherited mutations that impair DNA mismatch repair. It is a type of cancer syndrome.

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.

There are two primary types of nasal polyps: ethmoidal and antrochoanal. Ethmoidal polyps arise from the ethmoid sinuses and extend through the middle meatus into the nasal cavity. Antrochoanal polyps usually arise in the maxillary sinus and extend into the nasopharynx and represent only 4-6% of all nasal polyps. However, antrochoanal polyps are more common in children comprising one-third of all polyps in this population. Ethmoidal polyps are usually smaller and multiple while antrochoanal polyps are usually single and larger.

Risk factors for small intestine cancer include:

- Crohn's disease

- Celiac disease

- Radiation exposure

- Hereditary gastrointestinal cancer syndromes: familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, Peutz-Jeghers syndrome

- Males are 25% more likely to develop the disease

Benign tumours and conditions that may be mistaken for cancer of the small bowel:

- Hamartoma

- Tuberculosis

Conditions such as ulcerative colitis or certain types of relapsing infectious diarrhea can vary in severity over time, and FOBT may assist in assessing the severity of the disease. Medications associated with gastrointestinal bleeding such as Bortezomib are sometimes monitored by FOBT.

Attenuated familial adenomatous polyposis is a form of familial adenomatous polyposis, a cancer syndrome. It is a pre-malignant disease that can develop into colorectal cancer. A patient will have fewer than a hundred polyps located typically in right side of the colon. Cancer might develop as early as the age of five, though typically presents later than classical FAP.

Inflammatory fibroid polyp, abbreviated IFP, is a benign abnormal growth of tissue projecting into the lumen of the gastrointestinal tract.

99% of cervical polyps will remain benign and 1% will at some point show neoplastic change. Cervical polyps are unlikely to regrow.