Adenoma. Medical search

A benign epithelial tumor with a glandular organization.

A benign, slow-growing tumor, most commonly of the salivary gland, occurring as a small, painless, firm nodule, usually of the parotid gland, but also found in any major or accessory salivary gland anywhere in the oral cavity. It is most often seen in women in the fifth decade. Histologically, the tumor presents a variety of cells: cuboidal, columnar, and squamous cells, showing all forms of epithelial growth. (Dorland, 27th ed)

An adenoma of the large intestine. It is usually a solitary, sessile, often large, tumor of colonic mucosa composed of mucinous epithelium covering delicate vascular projections. Hypersecretion and malignant changes occur frequently. (Stedman, 25th ed)

Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.

A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.

A benign epithelial tumor of the LIVER.

A benign tumor of the anterior pituitary in which the cells do not stain with acidic or basic dyes.

A pituitary tumor that secretes GROWTH HORMONE. In humans, excess HUMAN GROWTH HORMONE leads to ACROMEGALY.

Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.

Discrete tissue masses that protrude into the lumen of the COLON. These POLYPS are connected to the wall of the colon either by a stalk, pedunculus, or by a broad base.

A pituitary adenoma which secretes ADRENOCORTICOTROPIN, leading to CUSHING DISEASE.

A benign tumor, usually found in the anterior lobe of the pituitary gland, whose cells stain with acid dyes. Such pituitary tumors may give rise to excessive secretion of growth hormone, resulting in gigantism or acromegaly. A specific type of acidophil adenoma may give rise to nonpuerperal galactorrhea. (Dorland, 27th ed)

Endoscopic examination, therapy or surgery of the luminal surface of the colon.

Benign neoplasms derived from glandular epithelium. (From Stedman, 25th ed)

A pituitary adenoma which secretes PROLACTIN, leading to HYPERPROLACTINEMIA. Clinical manifestations include AMENORRHEA; GALACTORRHEA; IMPOTENCE; HEADACHE; visual disturbances; and CEREBROSPINAL FLUID RHINORRHEA.

A small tumor of the anterior lobe of the pituitary gland whose cells stain with basic dyes. It may give rise to excessive secretion of ACTH, resulting in CUSHING SYNDROME. (Dorland, 27th ed)

Tumors or cancers of the ADRENAL CORTEX.

A polyposis syndrome due to an autosomal dominant mutation of the APC genes (GENES, APC) on CHROMOSOME 5. The syndrome is characterized by the development of hundreds of ADENOMATOUS POLYPS in the COLON and RECTUM of affected individuals by early adulthood.

A condition caused by prolonged exposure to excessive HUMAN GROWTH HORMONE in adults. It is characterized by bony enlargement of the FACE; lower jaw (PROGNATHISM); hands; FEET; HEAD; and THORAX. The most common etiology is a GROWTH HORMONE-SECRETING PITUITARY ADENOMA. (From Joynt, Clinical Neurology, 1992, Ch36, pp79-80)

A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.

Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. The mutation of these genes is associated with familial adenomatous polyposis (ADENOMATOUS POLYPOSIS COLI) and GARDNER SYNDROME, as well as some sporadic colorectal cancers.

A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.

Tumors or cancer of the SALIVARY GLANDS.

Tumors or cancer of the COLON.

Tumors or cancer of the INTESTINES.

An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.

Two or more abnormal growths of tissue occurring simultaneously and presumed to be of separate origin. The neoplasms may be histologically the same or different, and may be found in the same or different sites.

Tumors or cancer of the ADRENAL GLANDS.

A disease of the PITUITARY GLAND characterized by the excess amount of ADRENOCORTICOTROPIC HORMONE secreted. This leads to hypersecretion of cortisol (HYDROCORTISONE) by the ADRENAL GLANDS resulting in CUSHING SYNDROME.

Tumors or cancer of the PAROTID GLAND.

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)

A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.

An irregular unpaired bone situated at the SKULL BASE and wedged between the frontal, temporal, and occipital bones (FRONTAL BONE; TEMPORAL BONE; OCCIPITAL BONE). Sphenoid bone consists of a median body and three pairs of processes resembling a bat with spread wings. The body is hollowed out in its inferior to form two large cavities (SPHENOID SINUS).

Tumors or cancer of the DUODENUM.

An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).

A small, unpaired gland situated in the SELLA TURCICA. It is connected to the HYPOTHALAMUS by a short stalk which is called the INFUNDIBULUM.

A malignant epithelial tumor with a glandular organization.

A condition of abnormally elevated output of PARATHYROID HORMONE due to parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. It is characterized by the combination of HYPERCALCEMIA, phosphaturia, elevated renal 1,25-DIHYDROXYVITAMIN D3 synthesis, and increased BONE RESORPTION.

Tumors or cancer of the THYROID GLAND.

Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)

A bony prominence situated on the upper surface of the body of the sphenoid bone. It houses the PITUITARY GLAND.

Endoscopic examination, therapy or surgery of the sigmoid flexure.

A mass of histologically normal tissue present in an abnormal location.

Tumors or cancer of the RECTUM.

The sudden loss of blood supply to the PITUITARY GLAND, leading to tissue NECROSIS and loss of function (PANHYPOPITUITARISM). The most common cause is hemorrhage or INFARCTION of a PITUITARY ADENOMA. It can also result from acute hemorrhage into SELLA TURCICA due to HEAD TRAUMA; INTRACRANIAL HYPERTENSION; or other acute effects of central nervous system hemorrhage. Clinical signs include severe HEADACHE; HYPOTENSION; bilateral visual disturbances; UNCONSCIOUSNESS; and COMA.

A 191-amino acid polypeptide hormone secreted by the human adenohypophysis (PITUITARY GLAND, ANTERIOR), also known as GH or somatotropin. Synthetic growth hormone, termed somatropin, has replaced the natural form in therapeutic usage such as treatment of dwarfism in children with growth hormone deficiency.

The segment of LARGE INTESTINE between the CECUM and the RECTUM. It includes the ASCENDING COLON; the TRANSVERSE COLON; the DESCENDING COLON; and the SIGMOID COLON.

Hormones secreted by the PITUITARY GLAND including those from the anterior lobe (adenohypophysis), the posterior lobe (neurohypophysis), and the ill-defined intermediate lobe. Structurally, they include small peptides, proteins, and glycoproteins. They are under the regulation of neural signals (NEUROTRANSMITTERS) or neuroendocrine signals (HYPOTHALAMIC HORMONES) from the hypothalamus as well as feedback from their targets such as ADRENAL CORTEX HORMONES; ANDROGENS; ESTROGENS.

A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.

Excision of one or more of the parathyroid glands.

Antineoplastic agent that is also used as a veterinary anesthetic. It has also been used as an intermediate in organic synthesis. Urethane is suspected to be a carcinogen.

Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.

A benign tumor of the intrahepatic bile ducts.

A lactogenic hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). It is a polypeptide of approximately 23 kD. Besides its major action on lactation, in some species prolactin exerts effects on reproduction, maternal behavior, fat metabolism, immunomodulation and osmoregulation. Prolactin receptors are present in the mammary gland, hypothalamus, liver, ovary, testis, and prostate.

The segment of LARGE INTESTINE between TRANSVERSE COLON and the SIGMOID COLON.

Expression of CD44 in Apc and Tcf mutant mice implies regulation by the WNT pathway. (1/4752)

Overexpression of cell surface glycoproteins of the CD44 family is an early event in the colorectal adenoma-carcinoma sequence. This suggests a link with disruption of APC tumor suppressor protein-mediated regulation of beta-catenin/Tcf-4 signaling, which is crucial in initiating tumorigenesis. To explore this hypothesis, we analyzed CD44 expression in the intestinal mucosa of mice and humans with genetic defects in either APC or Tcf-4, leading to constitutive activation or blockade of the beta-catenin/Tcf-4 pathway, respectively. We show that CD44 expression in the non-neoplastic intestinal mucosa of Apc mutant mice is confined to the crypt epithelium but that CD44 is strongly overexpressed in adenomas as well as in invasive carcinomas. This overexpression includes the standard part of the CD44 (CD44s) as well as variant exons (CD44v). Interestingly, deregulated CD44 expression is already present in aberrant crypt foci with dysplasia (ACFs), the earliest detectable lesions of colorectal neoplasia. Like ACFs of Apc-mutant mice, ACFs of familial adenomatous polyposis (FAP) patients also overexpress CD44. In sharp contrast, Tcf-4 mutant mice show a complete absence of CD44 in the epithelium of the small intestine. This loss of CD44 concurs with loss of stem cell characteristics, shared with adenoma cells. Our results indicate that CD44 expression is part of a genetic program controlled by the beta-catenin/Tcf-4 signaling pathway and suggest a role for CD44 in the generation and turnover of epithelial cells. (+info)

MTHFR polymorphism, methyl-replete diets and the risk of colorectal carcinoma and adenoma among U.S. men and women: an example of gene-environment interactions in colorectal tumorigenesis. (2/4752)

Our studies on interactions of a folate-metabolizing gene polymorphism and dietary intake in colorectal tumorigenesis demonstrate the potential importance of studying interactions between genotype and environmental exposure in relation to cancer risk. We observed an inverse association of a polymorphism (667C --> T, ala --> val) in the methylenetetrahydrofolate reductase (MTHFR) gene with colorectal cancer but not with colorectal adenomas. The inverse association of methionine and adverse association of alcohol with colorectal cancer were stronger among val/val individuals. These interactions were not present in studies of colorectal adenomas. Our studies illustrate that studying gene-environment interactions in relation to cancer can be of importance in clarifying cancer etiology as well as pointing to preventive dietary modifications. (+info)

Expression of relaxin-like factor is down-regulated in human testicular Leydig cell neoplasia. (3/4752)

In addition to their role in steroidogenesis in the male, testicular Leydig cells constitutively express large amounts of the peptide relaxin-like factor (RLF), also known as Ley-IL. The Leydig cell-derived RLF belongs to the insulin-like superfamily, which also includes relaxin, insulin and the insulin-like growth factors, and within the testis is a specific marker of Leydig cells. Little information is available either on the regulation of gene expression or on the function of this Leydig cell-derived peptide. In the present study we have investigated the expression pattern of human RLF in patients with rare Leydig cell hyperplasia and adenoma. The expression of both mRNA and protein appear to be decreased in hyperplastic Leydig cells, whereas in the Leydig cell adenomas studied, large central areas of the adenoma were devoid of RLF mRNA and protein. Only Leydig cells located at the periphery of the adenoma displayed expression of RLF, with full agreement between in-situ hybridization and immunohistochemistry. It thus appears that the expression of the RLF gene and its products are down-regulated in Leydig cell hyperplasia and adenoma, consistent with a concomitant dedifferentiation of these cells. (+info)

Effect of retinoids on AOM-induced colon cancer in rats: modulation of cell proliferation, apoptosis and aberrant crypt foci. (4/4752)

We have previously reported that the retinoids, 4-(hydroxyphenyl)retinamide (4-HPR) and 9-cis-retinoic acid (RA) prevented azoxymethane (AOM)-induced colon tumors and along with 2-(carboxyphenyl)retinamide (2-CPR) prevented aberrant crypt foci (ACF). In this study, we evaluated the effect of 2-CPR on AOM-induced colon tumors and the effect of the three retinoids on apoptosis and cell proliferation. Male F344 rats were administrated 15 mg/kg AOM at weeks 7 and 8 of age. 2-CPR (315 mg/kg) was administered in the diet starting either 1 week before or at week 12 after the first dose of AOM. The rats continued to receive the 2-CPR until killed at week 46. Unlike the demonstrated prevention of colon cancer by the other two retinoids, both dosing schedules of 2-CPR resulted in an approximate doubling of the yield of colon tumors. In adenomas, 2-CPR, 4-HPR and 9-cis-RA were equally effective in reducing mitotic activity, while only 4-HPR and 9-cis-RA but not 2-CPR enhanced apoptosis. When administered for only the 6 days prior to killing 4-HPR but not 2-CPR decreased the Mitotic Index and increased the Apoptotic Index in adenomas. In non-involved crypts, chronic exposure to 4-HPR and 9-cis-RA in contrast to 2-CPR reduced the Mitotic Index and enhanced the Apoptotic Index. In concurrence with our previous study, both 2-CPR and 4-HPR were very potent in preventing ACF when administered in the diet starting 1 week before the first dose of AOM and continuing for the 5 weeks of the study. Hence, unlike the other two retinoids, 2-CPR, although very potent in preventing ACF, enhanced rather than prevented AOM-induced colon cancer. Furthermore, our results suggest that the effect of 2-CPR on tumor yield is different from 4-HPR and 9-cis-RA because, unlike them, it does not enhance apoptosis. (+info)

Reduced lung tumorigenesis in human methylguanine DNA--methyltransferase transgenic mice achieved by expression of transgene within the target cell. (5/4752)

Human methylguanine-DNA methyltransferase (MGMT) transgenic mice expressing high levels of O6-alkylguanine-DNA alkyltransferase (AGT) in lung were crossbred to A/J mice that are susceptible to pulmonary adenoma to study the impact of O6-methylguanine (O6mG)-DNA adduct repair on NNK-induced lung tumorigenesis. Expression of the chimeric human MGMT transgene in lung was identified by northern and western blot analysis, immunohistochemistry assay and enzymatic assay. AGT activity was 17.6 +/- 3.2 versus 1.2 +/- 0.4 fmol/microg DNA in lung of MGMT transgenic mice compared with non-transgenic mice. Immunohistochemical staining with anti-human AGT antibody showed that human AGT was expressed throughout the lung. However, some epithelial cells of bronchi and alveoli did not stain for human AGT, suggesting that the human MGMT transgene expression was heterogeneous. After 100 mg/kg NNK i.p. injection in MGMT transgenic mice, lung AGT activity remained much higher and levels of lung O6mG-DNA adducts in MGMT transgenic mice were lower than those of non-transgenic mice. In the tumorigenesis study, mice received 100 mg/kg NNK at 6 weeks of age and were killed 44 weeks later. Ten of 17 MGMT transgenic mice compared with 16 of 17 non-transgenic mice had lung tumors, P < 0.05. MGMT transgenic mice had lower multiplicity and smaller sized lung tumors than non-transgenic mice. Moreover, a reduction in the frequency of K-ras mutations in lung tumors was found in MGMT transgenic mice (6.7 versus 50% in non-transgenic mice). These results indicate that high levels of AGT expressed in mouse lung reduce lung tissue susceptibility to NNK-induced tumorigenesis due to increased repair capacity for O6mG, subsequently, decreased mutational activation of K-ras oncogene. Heterogeneity in the level of AGT expressed in different lung cell populations or other forms of carcinogenic DNA damage caused by NNK may explain the residual incidence of lung tumors in MGMT transgenic mice. (+info)

Possible carcinogenic effects of X-rays in a transgenerational study with CBA mice. (6/4752)

A lifetime experiment using 4279 CBA/J mice was carried out to investigate whether the pre-conceptual exposure of sperm cells to X-ray radiation or urethane would result in an increased cancer risk in the untreated progeny, and/or increased susceptibility to cancer following exposure to a promoting agent. The study consisted of four main groups, namely a control group (saline), a urethane group (1 mg/g body wt) and two X-ray radiation groups (1 Gy, 2 Gy). At 1, 3 and 9 weeks after treatment, the males of these four parental groups were mated with untreated virgin females. The offspring of each parental group was divided into two subgroups: one received s.c. urethane (0.1 mg/g body wt once) as a promoter, the other saline, at the age of 6 weeks. All animals were evaluated for the occurrence of tumours. K-ras oncogene and p53 tumour suppressor gene mutations were investigated in frozen lung tumour samples. The female offspring of male parents exposed to X-rays 1 week before their mating showed a trend towards a higher tumour incidence of the haematopoietic system than the F1 controls. In addition, a higher percentage of bronchioloalveolar adenocarcinomas in male offspring born to irradiated paternals mated 1 week after X-ray treatment points to a plausible increased sensitivity of post-meiotic germ cell stages towards transgenerational carcinogenic effects. On the other hand, no increased tumour incidence and malignancy were observed in the offspring born to irradiated paternals mated 3 and 9 weeks after X-ray treatment. Paternal urethane treatment 1, 3 and 9 weeks prior to conception did not result in significantly altered incidence or malignancy of tumours of the lung, liver and haematopoietic tissue in the offspring. K-ras mutations increased during tumour progression from bronchioloalveolar hyperplasia to adenoma. Codon 61 K-ras mutations were more frequent in lung tumours of urethane-promoted progeny from irradiated parents than from control parents. P53 mutations were absent from these lung alterations. (+info)

Epithelial thyroid tumors in cows. (7/4752)

From 1964 to 1973, 370 tumors were collected from cows of unknown age. Ten (2.7%) of these were primary thyroid tumors. Three were malignant. The benign tumors were solitary encapsulated adenomas in the parenchyma with more or less defined trabeculae, tubular, and microfollicular pattern. One of the malignant tumors was a cystic papillary adenocarcinoma, and two were small cell carcinomas consisting of small, sometimes binuclear, pleomorphic cells. (+info)

The elevated serum alkaline phosphatase--the chase that led to two endocrinopathies and one possible unifying diagnosis. (8/4752)

A 39-year-old Chinese man with hypertension being evaluated for elevated serum alkaline phosphatase (SAP) levels was found to have an incidental right adrenal mass. The radiological features were characteristic of a large adrenal myelolipoma. This mass was resected and the diagnosis confirmed pathologically. His blood pressure normalised after removal of the myelolipoma, suggesting that the frequently observed association between myelolipomas and hypertension may not be entirely coincidental. Persistent elevation of the SAP levels and the discovery of hypercalcaemia after surgery led to further investigations which confirmed primary hyperparathyroidism due to a parathyroid adenoma. The patient's serum biochemistry normalised after removal of the adenoma. The association of adrenal myelolipoma with primary hyperparathyroidism has been reported in the literature only once previously. Although unconfirmed by genetic studies this association may possibly represent an unusual variation of the multiple endocrine neoplasia type 1 syndrome. (+info)

Adenoma yes [35] Mucinous adenocarcinoma [18] Squamous papilloma yes vaginal micropapillomatosis [16][17][18] ...

https://en.wikipedia.org/wiki/List_of_vaginal_tumors

Summary: Associated Cancers: colorectal and ovarian cancer; pilomatrixoma; medulloblastoma; pleomorphic adenomas; malignant ... pleomorphic adenomas, and malignant mesothelioma. While less is known about the exact mechanism of α-catenin, its presence in ... "The influence of 5-aminosalicylic acid on the progression of colorectal adenomas via the β-catenin signaling pathway". ...

https://en.wikipedia.org/wiki/Catenin

Nipple adenoma. Related subjects. *Main article. *Classification. *Risk factors (Alcohol, Hereditary breast-ovarian cancer ...

https://en.wikipedia.org/wiki/Inflammatory_breast_cancer

Mutations have been associated with increased risk of developing any kind of invasive cancer, including stomach cancer, pancreatic cancer, prostate cancer, and colon cancer.[14] Carriers have the normal risks of developing cancer (and other diseases) associated with increased age, smoking, alcohol consumption, poor diet, lack of exercise, and other known risk factors, plus the additional risk from the genetic mutations and an increased susceptibility to damage from ionizing radiation, including natural background radiation.[8]:39-50 Men with BRCA mutations cannot get ovarian cancer, but they may be twice as likely as non-carriers to develop prostate cancer at a younger age.[8]:Ch8 The risk is smaller and disputed for BRCA1 carriers; up to one-third of BRCA2 mutation carriers are expected to develop prostate cancer before age 65. Prostate cancer in BRCA mutation carriers tends to appear a decade earlier than normal, and it tends to be more aggressive than normal. As a result, annual prostate ...

https://en.wikipedia.org/wiki/BRCA_mutation

... to the point of suppressing the activity of the rest of the gland-is usually a thyrotoxic adenoma, a surgically curable form of ... nodule or lobe of the thyroid is sometimes removed for biopsy or because of the presence of an autonomously functioning adenoma ...

https://en.wikipedia.org/wiki/Thyroid_disease

Awareness has also led to increased anxiety for women. Early detection efforts result in overdiagnosis of precancerous and cancerous tumors that would never risk the woman's life (about one-third of breast cancers diagnosed through screening programs), and result in her being subjected to invasive and sometimes dangerous radiological and surgical procedures.[93] In recent years, the definition of breast cancer has expanded to include non-invasive, non-cancerous conditions like lobular carcinoma in situ (LCIS) and pre-cancerous or "stage 0" conditions like ductal carcinoma in situ (DCIS). Despite the now-regretted decision to use the word carcinoma in these relatively common conditions (almost a quarter of "breast cancer" diagnoses in the USA), they are not life-threatening cancers.[94] Women with these conditions are promoted as breast cancer survivors due to the fear they experienced before they became educated about their condition, rather than in respect of any real threat to their lives. ...

https://en.wikipedia.org/wiki/Breast_cancer_awareness

The older names, "multiple endocrine adenomas" and "multiple endocrine adenomatosis" (MEA), have been replaced by the current ... In 1903 Erdheim described the case of an acromegalic patient with a pituitary adenoma and three enlarged parathyroid glands. ... In 1961 Sipple described a combination of a pheochromocytoma, medullary thyroid carcinoma and parathyroid adenoma. ...

https://en.wikipedia.org/wiki/Multiple_endocrine_neoplasia

Pleomorphic adenoma. References[edit]. *^ Witt, Robert L., ed. (2005). "Chapter 9 "Benign tumors, cysts, and tumor-like ... Though much less likely to occur than pleomorphic adenoma, Warthin's tumor is the second most common benign parotid tumor. ...

https://en.wikipedia.org/wiki/Warthin's_tumor

Canalicular adenoma • Canine tooth • Cantilever mechanics • Carbon dioxide laser • Caries vaccine • Carnassial • Case School of ... Pleomorphic adenoma • Pleurodont • Plica fimbriata • Polk E. Akers • Polymorphous low-grade adenocarcinoma • Polynoxylin • ...

https://en.wikipedia.org/wiki/Index_of_oral_health_and_dental_articles

... or parathyroid adenoma). It is used by surgeons to locate ectopic parathyroid adenomas, most commonly found in the anterior ... Parathyroid adenomas have been linked with DDT although a causal link has not yet been established. Normal parathyroid glands ... "Parathyroid Adenoma". BrighamRAD Teaching Case Database. Archived from the original on 2011-07-16. Carroll MF, Schade DS (May ... Parathyroid adenomas are very rarely detectable on clinical examination. Surgical removal of a parathyroid tumor eliminates the ...

https://en.wikipedia.org/wiki/Hyperparathyroidism