The most common general classification is:

- hyperplastic,

- neoplastic (adenomatous & malignant),

- hamartomatous and,

- inflammatory.

Colorectal polyps are not usually associated with symptoms. When they occur, symptoms include rectal bleeding, bloody stools, abdominal pain and fatigue. A change in bowel habits may occur including constipation and diarrhoea. Occasionally, if a polyp is big enough to cause a bowel obstruction, there may be nausea, vomiting and severe constipation.

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)

SSAs, generally, are asymptomatic. They are typically identified on a colonoscopy and excised for a definitive diagnosis and treatment.

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.

From early adolescence, patients with this condition gradually (and much of the time 'silently') develop hundreds to thousands of colorectal polyps (and sometimes polyps elsewhere)—small abnormalities at the surface of the intestinal tract, especially in the large intestine including the colon or rectum. These may bleed, leading to blood in the stool. If the blood is not visible, it is still possible for the patient to develop anemia due to gradually developing iron deficiency. If malignancy develops, this may present with weight loss, altered bowel habit, or even metastasis to the liver or elsewhere. FAP can also develop 'silently' in some individuals, giving few or no signs until it has developed into advanced colorectal cancer.

Because familial polyposis develops very gradually over years, and can also manifest in an 'attenuated' form even more gradually, polyps resulting from FAP can lead to cancer developing at any point from adolescence to old age.

Depending on the nature of the defect in the APC gene, and whether it is the full or attenuated form, familial polyposis may manifest as polyps in colon or in the duodenal tract, or in any combination of these. Therefore, an absence of polyps in, for example, the rectum, may not of itself be sufficient to confirm absence of polyps. It may be necessary to consider and visually examine other possible parts of the intestinal tract. Colonoscopy is preferred over sigmoidoscopy for this, as it provides better observation of the common right-side location of polyps.

The genetic determinant in familial polyposis may also predispose carriers to other malignancies, e.g., of the duodenum and stomach (particularly ampullary adenocarcinoma). Other signs that may point to FAP are pigmented lesions of the retina ("CHRPE—congenital hypertrophy of the retinal pigment epithelium"), jaw cysts, sebaceous cysts, and osteomata (benign bone tumors). The combination of polyposis, osteomas, fibromas and sebaceous cysts is termed "Gardner's syndrome" (with or without abnormal scarring).

SSAs are diagnosed by their microscopic appearance; histomorphologically, they are characterized by (1) basal dilation of the crypts, (2) basal crypt serration, (3) crypts that run horizontal to the basement membrane (horizontal crypts), and (4) crypt branching. The most common of these features is basal dilation of the crypts.

Unlike traditional colonic adenomas (e.g. tubular adenoma, villous adenoma), they do not (typically) have nuclear changes (nuclear hyperchromatism, nuclear crowding, elliptical/cigar-shaped nuclei).

An adenoma (from Greek αδένας, "", "gland" + -ώμα, "", "tumor") (; plural adenomas or adenomata ) is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both. Adenomas can grow from many glandular organs, including the adrenal glands, pituitary gland, thyroid, prostate, and others. Some adenomas grow from epithelial tissue in nonglandular areas but express glandular tissue structure (as can happen in familial polyposis coli). Although adenomas are benign, over time they may transform to become malignant, at which point they are called adenocarcinomas. Most adenomas do not transform. But even while benign, they have the potential to cause serious health complications by compressing other structures (mass effect) and by producing large amounts of hormones in an unregulated, non-feedback-dependent manner (causing paraneoplastic syndromes). Some adenomas are too small to be seen macroscopically but can still cause clinical symptoms.

Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated. Three variants are known to exist, FAP and attenuated FAP (originally called hereditary flat adenoma syndrome) are caused by APC gene defects on chromosome 5 while autosomal recessive FAP (or MYH-associated polyposis) is caused by defects in the "MUTYH" gene on chromosome 1. Of the three, FAP itself is the most severe and most common; although for all three, the resulting colonic polyps and cancers are confined to the colon wall and removal can greatly reduce the spread of cancer.

The root cause of FAP is understood to be a genetic mutation—a flaw in the body's tumour suppressor genes that prevent development of tumours. The flaw allows numerous cells of the intestinal wall to develop into potentially cancerous polyps when they would usually reach the end of their life; inevitably one or more will eventually progress and give rise to cancer (7% risk by age 21, rising to 87% by age 45 and 93% by age 50). The flawed genes do not trigger cancer, but rather, they reduce the body's ability to protect against the risk of aged cells becoming cancerous. Even with the flawed gene, it may still take time before a cell actually does develop that is cancerous as a result, and the gene may in some cases still partially operate to control tumours, therefore cancer from FAP takes many years to develop and is almost always an adult-onset disease.

The second form of FAP, known as attenuated familial adenomatous polyposis has the APC gene functional but slightly impaired. It is therefore somewhat able to operate as usual. Attenuated FAP still presents a high 70% lifetime risk of cancer (as estimated), but typically presents with far fewer polyps (typically 30) rather than the hundreds or thousands usually found in FAP, and arises at an age when FAP is usually no longer considered likely—typically between 40 and 70 years old (average 55) rather than the more usual 30's upward. Because it has far fewer polyps, options for management may be different.

The third variant, autosomal recessive familial adenomatous polyposis or MYH-associated polyposis, is also milder and, as its name suggests, requires both parents to be 'carriers' to manifest the condition.

In some cases FAP can manifest higher in the colon than usual (for example, the ascending colon, or proximal to the splenic flexure, or in the gastric or duodenal tracts) where they show no symptoms until cancer is present and greatly advanced. APC mutations have been linked to certain other cancers such as thyroid cancer. As the mutation causing FAP is genetic, it can be inherited hereditarily from either parent, and passed to children. A genetic blood test of the APC gene exists that can determine whether it is deficient, and therefore can predict the possibility of FAP. Individuals at risk (due to family links or genetic testing) are usually offered routine monitoring of the intestinal tract every 1 – 5 years for life, from early adulthood, to detect the slow-forming polyps and act if found, before they can pose a threat. International polyposis registries exists that track known cases of FAP or APC gene defects, for research and clinical purposes. Mutation of APC also occurs commonly in incident cases of colorectal carcinoma, emphasizing its importance in this form of cancer.

An adenoma of a parathyroid gland may secrete inappropriately high amounts of parathyroid hormone and thereby cause primary hyperparathyroidism.

About 25–50% of hepatic adenomas cause pain in the right upper quadrant or epigastric region of the abdomen. Since hepatic adenomas can be large (8–15 cm), patients may notice a palpable mass. However, hepatic adenomas are usually asymptomatic, and may be discovered incidentally on imaging ordered for some unrelated reason. Large hepatic adenomas have a tendency to rupture and bleed massively inside the abdomen. If not treated, there is a 30% risk of bleeding. Bleeding may lead to hypotension, tachycardia, and sweating (diaphoresis).

Salivary gland oncocytomas are most common in ages 70–80, females, the parotid gland (85–90%), and are firm, slowly growing, painless masses of less than 4 cm. They may be bilateral.

Medullary carcinoma may refer to one of several different tumors of epithelial origin. As the term "" is a generic anatomic descriptor for the mid-layer of various organ tissues, a medullary tumor usually arises from the "mid-layer tissues" of the relevant organ.

Medullary carcinoma most commonly refers to:

- Medullary thyroid cancer

- Medullary carcinoma of the breast

Medullary carcinoma may also refer to tumors of:

- Pancreas

- Ampulla of Vater

- Gallbladder

- Stomach

- Large intestine

- Kidney — Renal medullary carcinoma

Due to the diverse nature of salivary gland tumours, many different terms and classification systems have been used. Perhaps the most widely used currently is that system proposed by the World Health Organization in 2004, which classifies salivary neoplasms as primary or secondary, benign or malignant, and also by tissue of origin. This system defines five broad categories of salivary gland neoplasms:

Benign epithelial tumors

- Pleomorphic adenoma

- Warthin's tumor

- Myoepithelioma

- Basal cell adenoma

- Oncocytoma

- Canalicular adenoma

- Lymphadenoma

- "Sebaceous lymphadenoma"

- "Nonsebaceous lymphadenoma"

- Ductal papilloma

- "Inverted ductal papilloma"

- "Intraductal papilloma"

- "Sialadenoma papilliferum"

- Cystadenoma

- Malignant epithelial tumors

- Acinic cell carcinoma

- Mucoepidermoid carcinoma

- Adenoid cystic carcinoma

- Polymorphous low-grade adenocarcinoma

- Epithelial-myoepithelial carcinoma

- Clear cell carcinoma, not otherwise specified

- Basal cell adenocarcinoma

- Sebaceous carcinoma

- Sebaceous lymphadenocarcinoma

- Cystadenocarcinoma

- Low-grade cribriform cystadenocarcinoma

- Mucinous adenocarcinoma

- Oncocytic carcinoma

- Salivary duct carcinoma

- Salivary duct carcinoma, not otherwise specified

- Adenocarcinoma, not otherwise specified

- Myoepithelial carcinoma

- Carcinoma ex pleomorphic adenoma

- Mammary analogue secretory carcinoma

- Carcinosarcoma

- Metastasizing pleomorphic adenoma

- Squamous cell carcinoma

- Large cell carcinoma

- Lymphoepithelial carcinoma

- Sialoblastoma

- Soft tissue tumors

- Hemangioma

- Hematolymphoid tumors

- Hodgkin lymphoma

- Diffuse large B-cell lymphoma

- Extranodal marginal zone B cell lymphoma

- Secondary tumors (i.e. a tumor which has metastasized to the salivary gland from a distant location)

Others, not included in the WHO classification above, include:

- Intraosseous (central) salivary gland tumors

- Hybrid tumors (i.e. a tumor displaying combined forms of histologic tumor types)

- Hybrid carcinoma

- Others

- Others

- Keratocystoma

- Sialolipoma

Salivary gland tumours usually present as a lump or swelling in the affected gland which may or may not have been present for a long time. The lump may be accompanied by symptoms of duct blockage (e.g. xerostomia). Usually, in their early stages it is not possible to distinguish a benign tumour from a malignant one. One of the key differentiating symptoms of a malignant growth is nerve involvement. For example signs of facial nerve damage (e.g facial palsy) are associated with malignant parotid tumours. Facial pain, and paraesthesia are also very often associated with a malignant tumours. Other red flag symptoms which may suggest malignancy and warrant further investigation are fixation of the lump to the overlying skin, ulceration and induration of the mucosa.

An oncocytoma is an epithelial tumor composed of oncocytes, large eosinophilic cells having small, round, benign-appearing nuclei with large nucleoli.

Oncocytoma can arise in a number of organs.

Hepatocellular adenoma (also known as hepatic adenoma or hepadenoma) is a rare, benign liver tumor. It most commonly occurs in people with elevated systemic levels of estrogen, classically in women taking estrogen-containing oral contraceptive medication.

Ceruminous adenoma are rare tumors, accounting for less than 1% of all external ear tumors. The patients will present with a mass, perhaps associated pain, and may have changes in hearing (usually a sensorineural or a conductive hearing loss). Some patients have tinnitus. Nerve paralysis is very uncommon.

The signs and symptoms are similar to other malignant salivary gland tumours; however, it may have been preceded by an appreciable mass that was long-standing and did not appear to be growing.

Findings that suggest a malignant salivary gland tumour include rapid growth, facial weakness (due to facial nerve compression), pain, skin ulceration, fixation of the mastoid tip

and parasthesias.

Most patients present clinically with progressive, one sided hearing loss, much more often of the sensorineural rather than conductive type. Patients may also experience tinnitus, vertigo, and loss of vestibular function (ataxia). Symptoms are usually present for a long time, which supports the slow growth of these tumors. Patients may also present with other symptoms related to von Hippel-Lindau syndrome in other anatomic sites, which will result in imaging evaluation of the head.

Nipple adenomas may be felt as a lump under the nipple or areola. They may come to attention because of nipple pain, ulceration, swelling or discharge.

Mucinous cystadenoma is a benign cystic tumor lined by a mucinous epithelium. It is a type of cystic adenoma (cystadenoma).

Mucinous cystadenoma may arise in a number of locations; however, mucinous cystadenoma at different locations are not generally considered to be related to one another.

A ceruminous adenoma (also known as adenoma of the ceruminous gland and ceruminoma) is a benign glandular neoplasm which arises from the ceruminous glands located within the external auditory canal. These glands are found within the outer one third to one half of the external auditory canal, more common along the posterior surface; therefore, the tumor develops within a very specific location.

Carcinoma ex pleomorphic adenoma, abbreviated ca ex PA, is a type of cancer typically found in the parotid gland. It arises from the benign tumour pleomorphic adenoma.

Its prognosis depends on the stage. Early tumour have essentially a benign behaviour.

Mucinous cystadenomas may be found in the:

- Ovary - ovarian mucinous cystadenoma

- Pancreas - pancreatic mucinous cystadenoma

- Peritoneum - peritoneal mucinous cystadenoma

- Liver - mucinous cystadenoma of the liver

- Vermiform appendix - appendiceal mucinous cystadenoma (see cystadenoma)