Cystadenoma: A benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. In some instances, considerable portions of the neoplasm, or even the entire mass, may be cystic. (Stedman, 25th ed)Cystadenoma, Mucinous: A multilocular tumor with mucin secreting epithelium. They are most often found in the ovary, but are also found in the pancreas, appendix, and rarely, retroperitoneal and in the urinary bladder. They are considered to have low-grade malignant potential.Cystadenoma, Serous: A cystic tumor of the ovary, containing thin, clear, yellow serous fluid and varying amounts of solid tissue, with a malignant potential several times greater than that of mucinous cystadenoma (CYSTADENOMA, MUCINOUS). It can be unilocular, parvilocular, or multilocular. It is often bilateral and papillary. The cysts may vary greatly in size. (Dorland, 27th ed; from Hughes, Obstetric-Gynecologic Terminology, 1972)Cystadenoma, Papillary: A benign neoplasm of the ovary.Cystadenocarcinoma: A malignant neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. The neoplastic cells manifest varying degrees of anaplasia and invasiveness, and local extension and metastases occur. Cystadenocarcinomas develop frequently in the ovaries, where pseudomucinous and serous types are recognized. (Stedman, 25th ed)Appendiceal Neoplasms: Tumors or cancer of the APPENDIX.Mucocele: A retention cyst of the salivary gland, lacrimal sac, paranasal sinuses, appendix, or gallbladder. (Stedman, 26th ed)Biliary Tract Neoplasms: Tumors or cancer in the BILIARY TRACT including the BILE DUCTS and the GALLBLADDER.Bile Duct Neoplasms: Tumors or cancer of the BILE DUCTS.Appendix: A worm-like blind tube extension from the CECUM.Adenoma, Bile Duct: A benign tumor of the intrahepatic bile ducts.Cysts: Any fluid-filled closed cavity or sac that is lined by an EPITHELIUM. Cysts can be of normal, abnormal, non-neoplastic, or neoplastic tissues.Sertoli-Leydig Cell Tumor: A sex cord-gonadal stromal tumor consists of LEYDIG CELLS; SERTOLI CELLS; and FIBROBLASTS in varying proportions and degree of differentiation. Most such tumors produce ANDROGENS in the Leydig cells, formerly known as androblastoma or arrhenoblastoma. Androblastomas occur in the TESTIS or the OVARY causing precocious masculinization in the males, and defeminization, or virilization (VIRILISM) in the females. In some cases, the Sertoli cells produce ESTROGENS.Bile Ducts, Intrahepatic: Passages within the liver for the conveyance of bile. Includes right and left hepatic ducts even though these may join outside the liver to form the common hepatic duct.Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).Adenolymphoma: A benign tumor characterized histologically by tall columnar epithelium within a lymphoid tissue stroma. It is usually found in the salivary glands, especially the parotid.Cystadenocarcinoma, Mucinous: A malignant cystic or semisolid tumor most often occurring in the ovary. Rarely, one is solid. This tumor may develop from a mucinous cystadenoma, or it may be malignant at the onset. The cysts are lined with tall columnar epithelial cells; in others, the epithelium consists of many layers of cells that have lost normal structure entirely. In the more undifferentiated tumors, one may see sheets and nests of tumor cells that have very little resemblance to the parent structure. (Hughes, Obstetric-Gynecologic Terminology, 1972, p184)Cecal Diseases: Pathological developments in the CECUM.Hepatic Duct, Common: Predominantly extrahepatic bile duct which is formed by the junction of the right and left hepatic ducts, which are predominantly intrahepatic, and, in turn, joins the cystic duct to form the common bile duct.Spermatocele: A cystic dilation of the EPIDIDYMIS, usually in the head portion (caput epididymis). The cyst fluid contains dead SPERMATOZOA and can be easily differentiated from TESTICULAR HYDROCELE and other testicular lesions.Endocrine Gland Neoplasms: Tumors or cancer of the ENDOCRINE GLANDS.Ovarian Neoplasms: Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.Aspermia: A condition characterized by the complete absence of SEMEN. This disorder should be differentiated from AZOOSPERMIA, absence of sperm in the semen.Pseudomyxoma Peritonei: A condition characterized by poorly-circumscribed gelatinous masses filled with malignant mucin-secreting cells. Forty-five percent of pseudomyxomas arise from the ovary, usually in a mucinous cystadenocarcinoma (CYSTADENOCARCINOMA, MUCINOUS), which has prognostic significance. Pseudomyxoma peritonei must be differentiated from mucinous spillage into the peritoneum by a benign mucocele of the appendix. (Segen, Dictionary of Modern Medicine, 1992)Salivary Gland Neoplasms: Tumors or cancer of the SALIVARY GLANDS.Pancreatic Cyst: A true cyst of the PANCREAS, distinguished from the much more common PANCREATIC PSEUDOCYST by possessing a lining of mucous EPITHELIUM. Pancreatic cysts are categorized as congenital, retention, neoplastic, parasitic, enterogenous, or dermoid. Congenital cysts occur more frequently as solitary cysts but may be multiple. Retention cysts are gross enlargements of PANCREATIC DUCTS secondary to ductal obstruction. (From Bockus Gastroenterology, 4th ed, p4145)Urologic Surgical Procedures, Male: Surgery performed on the male genitalia.Neoplasms, Multiple Primary: 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.Retroperitoneal NeoplasmsSalivary Glands, Minor: Accessory salivary glands located in the lip, cheek, tongue, floor of mouth, palate and intramaxillary.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Pancreatic Pseudocyst: Cyst-like space not lined by EPITHELIUM and contained within the PANCREAS. Pancreatic pseudocysts account for most of the cystic collections in the pancreas and are often associated with chronic PANCREATITIS.Ovarian Cysts: General term for CYSTS and cystic diseases of the OVARY.Cholangiopancreatography, Magnetic Resonance: Non-invasive diagnostic technique for visualizing the PANCREATIC DUCTS and BILE DUCTS without the use of injected CONTRAST MEDIA or x-ray. MRI scans provide excellent sensitivity for duct dilatation, biliary stricture, and intraductal abnormalities.Pancreatic Diseases: Pathological processes of the PANCREAS.Bile Ducts, Extrahepatic: Passages external to the liver for the conveyance of bile. These include the COMMON BILE DUCT and the common hepatic duct (HEPATIC DUCT, COMMON).Appendectomy: Surgical removal of the vermiform appendix. (Dorland, 28th ed)Pancreatectomy: Surgical removal of the pancreas. (Dorland, 28th ed)Cystadenocarcinoma, Serous: A malignant cystic or semicystic neoplasm. It often occurs in the ovary and usually bilaterally. The external surface is usually covered with papillary excrescences. Microscopically, the papillary patterns are predominantly epithelial overgrowths with differentiated and undifferentiated papillary serous cystadenocarcinoma cells. Psammoma bodies may be present. The tumor generally adheres to surrounding structures and produces ascites. (From Hughes, Obstetric-Gynecologic Terminology, 1972, p185)Adenocarcinoma, Mucinous: An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Lacrimal Apparatus Diseases: Diseases of the lacrimal apparatus.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases.von Hippel-Lindau Disease: An autosomal dominant disorder caused by mutations in a tumor suppressor gene. This syndrome is characterized by abnormal growth of small blood vessels leading to a host of neoplasms. They include HEMANGIOBLASTOMA in the RETINA; CEREBELLUM; and SPINAL CORD; PHEOCHROMOCYTOMA; pancreatic tumors; and renal cell carcinoma (see CARCINOMA, RENAL CELL). Common clinical signs include HYPERTENSION and neurological dysfunctions.MassachusettsVon Hippel-Lindau Tumor Suppressor Protein: A ubiquitin-protein ligase that mediates OXYGEN-dependent polyubiquitination of HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT. It is inactivated in VON HIPPEL-LINDAU SYNDROME.Hemangioblastoma: A benign tumor of the nervous system that may occur sporadically or in association with VON HIPPEL-LINDAU DISEASE. It accounts for approximately 2% of intracranial tumors, arising most frequently in the cerebellar hemispheres and vermis. Histologically, the tumors are composed of multiple capillary and sinusoidal channels lined with endothelial cells and clusters of lipid-laden pseudoxanthoma cells. Usually solitary, these tumors can be multiple and may also occur in the brain stem, spinal cord, retina, and supratentorial compartment. Cerebellar hemangioblastomas usually present in the third decade with INTRACRANIAL HYPERTENSION, and ataxia. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2071-2)Hospitals, General: Large hospitals with a resident medical staff which provides continuous care to maternity, surgical and medical patients.BostonRetinal Neoplasms: Tumors or cancer of the RETINA.

Third International Meeting on von Hippel-Lindau disease. (1/27)

Five years after the identification of the von Hippel-Lindau (VHL) gene, physicians, scientists and concerned VHL family members met to review the current state of knowledge on the diagnosis and treatment of VHL and to summarize the latest information on the biochemistry of the VHL protein (pVHL). The NIH and University of Pennsylvania groups reported the detection of germ-line mutations in 100% (93 of 93) of VHL families studied. Several studies determined the frequency of VHL germ-line mutations in individuals with a single manifestation of VHL without a family history of VHL. National groups to improve the diagnosis and treatment of individuals with VHL disease have been established in Great Britain, Denmark, France, Holland, Italy, Japan, Poland, and the United States. Evidence for the existence of genes that modify the expression of VHL was presented. The VHL protein appears to have several distinct functions: (a) down-regulation of hypoxia-inducible mRNAs; (b) proper assembly of the extracellular fibronectin matrix; (c) regulation of exit from the cell cycle; and (d) regulation of expression of carbonic anhydrases 9 and 12.  (+info)

CDKN2A gene inactivation in epithelial sporadic ovarian cancer. (2/27)

The tumour suppressor gene CDKN2A, located on chromosome 9p21, encodes the cell cycle regulatory protein p16. Inactivation of the CDKN2A gene could lead to uncontrolled cell growth. In order to determine the role of CDKN2A in the development of sporadic ovarian cancer, loss of heterozygosity at 9p21-22, homozygous deletion, mutation and methylation status of the CDKN2A gene as well as CDKN2A expression were examined in a panel of serous papillary ovarian cancer. The frequency of loss of heterozygosity (LOH) for one or more informative markers at 9p21-22 was 65% (15/23). The most common deleted region was located between interferon (IFN)-alpha and D9S171. Homozygous deletions and mutations of the CDKN2A gene were not found. There was no evidence of methylation in exon 1, but methylation in exon 2 of CDKN2A gene was found in 26% (6/23). Absence of CDKN2A gene expression was shown in 27% (6/22) at mRNA level and 21% (4/19) at protein level. These data suggest that the CDKN2A gene is involved in the tumorigenesis of ovarian cancer, but the mechanisms of CDKN2A gene inactivation in serous papillary ovarian cancer remains unclear.  (+info)

Ovarian micropapillary serous borderline tumors. Clinicopathologic features and outcome of seven surgically staged patients. (3/27)

We report the clinicopathologic findings for 7 patients with completely staged ovarian micropapillary serous borderline tumors (MSBTs) to further clarify tumor behavior. None of the MSBTs had microinvasion in the ovarian neoplasm. The MSBT pattern constituted 25% to almost all of the neoplasm. Four were bilateral, and 6 involved the ovarian surface. Five patients had peritoneal implants; 2 were invasive, and 3 were noninvasive MSBTs. Distribution of stages among patients was as follows: IA, 1; IC, 1; IIC, 2; IIIB, 2; and IIIC, 1. Median follow-up was 8.5 years. Four patients were alive and well at the last follow-up visit, including 1 patient with stage IIIC (lymph node metastases) disease who had noninvasive implants (12 years after surgery). One patient who was free of disease died of complications of chemotherapy and abdominal surgery. Two patients died of intra-abdominal neoplastic growth (stages IIC and IIIB) 5 and 9 years after surgery, respectively; both had invasive implants. Without invasive peritoneal implants, MSBTs seem to behave as similar staged nonmicropapillary serous borderline tumors without invasive peritoneal implants. With invasive peritoneal implants, they seem to behave as low-grade carcinomas. Pathologists should recognize MSBT as a neoplasm that can have adverse prognostic features, including invasive peritoneal implants.  (+info)

Expression of laminin-5-gamma-2 chain in intraductal papillary-mucinous and invasive ductal tumors of the pancreas. (4/27)

The laminin-5-gamma-2 chain is expressed in various invasive carcinoma cells. To clarify the relationship between laminin-5 expression and the development of intraductal papillary-mucinous tumors (IPMTs), we performed an immunohistochemical study of 26 IPMTs and 30 invasive ductal adenocarcinomas. Cases were classified into five groups: intraductal papillary-mucinous adenoma (Group A; n = 8), adenocarcinoma without invasion (Group B; n = 3), adenocarcinoma with minimal invasion (Group C; n = 5), adenocarcinoma with macroscopically evident invasion (Group D; n = 10), and invasive ductal adenocarcinoma (conventional type; Group E; n = 30). In the invasive components of Groups D and E, laminin-5 was expressed in 80% and 100% of cases, respectively. In the intraductal components of IPMTs, expression of laminin-5 was not seen in Groups A and B, whereas they were seen in one case in Group C (20%) and in seven in Group D (70%). Most of the staining patterns of the intraductal components were focal and scattered. Laminin-5-gamma-2 expression in the intraductal components of IPMTs tends to increase as tumors develop and may be a indicator of the potential invasiveness of the tumor cells.  (+info)

Solid-pseudopapillary tumors of the pancreas are genetically distinct from pancreatic ductal adenocarcinomas and almost always harbor beta-catenin mutations. (5/27)

Solid-pseudopapillary tumors (SPTs) are unusual pancreatic neoplasms of low malignant potential that most frequently affect young women. Genetic events contributing to the development of SPTs are unknown. Whereas the more common ductal adenocarcinomas of the pancreas essentially never harbor beta-catenin or APC gene mutations, we have recently identified alterations of the APC/beta-catenin pathway in other nonductal pancreatic neoplasms including pancreatoblastomas and acinar cell carcinomas. We analyzed a series of 20 SPTs for somatic alterations of the APC/beta-catenin pathway using immunohistochemistry for beta-catenin protein accumulation, direct DNA sequencing of beta-catenin exon 3, and direct DNA sequencing of the mutation cluster region in exon 15 of the APC gene in those SPTs that did not harbor beta-catenin mutations. Immunohistochemical labeling for cyclin D1 was performed to evaluate the overexpression of this cell-cycle protein as one of the putative downstream effectors of beta-catenin dysregulation. In addition, we analyzed the SPTs for genetic alterations commonly found in pancreatic ductal adenocarcinomas, including mutations in the K-ras oncogene and p53 and DPC4 tumor suppressor genes, using direct DNA sequencing of K-ras and immunostaining for p53 and Dpc4. Almost all SPTs harbored alterations in the APC/beta-catenin pathway. Nuclear accumulation of beta-catenin protein was present in 95% (19 of 20), and activating beta-catenin oncogene mutations were identified in 90% (18 of 20) of the SPTs. Seventy-four percent (14 of 19) showed overexpression of cyclin D1, ranging from 10 to 70% of tumor nuclei. In contrast, no K-ras mutations were present in any of the 20 SPTs, and Dpc4 expression was intact in all 16 SPTs for which immunohistochemical labeling was successful. Overexpression of p53 was limited to only 3 of 19 (15.8%) SPTs. These results emphasize the two distinct, divergent genetic pathways of neoplastic progression in pancreatic ductal and nonductal neoplasms.  (+info)

Solid--cystic papillary tumor of pancreas. (6/27)

A case of Solid and Cystic Papillary Epithelial Tumor of Pancreas displaying low grade malignancy occurring in a 38 years old female is presented. It is a rare condition and could be diagnosed histopathologically after complete excision.  (+info)

Differential diagnosis of benign and malignant intraductal papillary mucinous tumors of the pancreas: MR cholangiopancreatography and MR angiography. (7/27)

OBJECTIVE: To compare the usefulness of magnetic resonance cholangiopancreatography (MRCP) and MR angiography (MRA) in differentiating malignant from benign intraductal papillary mucinous tumors of the pancreas (IPMTs), and to determine the findings which suggest malignancy. MATERIALS AND METHODS: During a 6-year period, 46 patients with IPMT underwent MRCP. Morphologically, tumor type was classified as main duct, branch duct, or combined. The diameter of the main pancreatic duct (MPD), the extent of the dilated MPD, and the location and size of the cystic lesion, septum, and communicating channel were assessed. For all types of IPMTs, enhanced mural nodules and portal vein narrowing were evaluated at MRA. RESULTS: Combined-type IPMTs were more frequently malignant (78%) than benign (42%) (p < 0.05). Compared with benign lesions, malignant lesions were larger, and the caliber of the communicating channel was also larger (p < 0.05). Their dilated MPD was more extensive and of greater diameter (p < 0.05), and the presence of mural nodules was more frequent (p < 0.001). CONCLUSION: Combined MRCP and MRA might be useful for the differential diagnosis of malignant and benign IPMTs of the pancreas.  (+info)

Papillary cystadenoma arising from the upper lip: a case report. (8/27)

We report a rare case of a papillary cystadenoma arising from the upper lip. This tumor was not distinctly encapsulated and had proliferated replacing the ductal epithelium. Mast cells were found not only in the stroma but also in the oncocytic epithelial layer. There was a strong immunoreaction with mitochondrial antibody in the epithelial layer. Only one case (0.9%) of papillary cystadenoma has occurred among the 110 benign intraoral salivary gland tumors seen in our hospital from 1966 through September 2003.  (+info)

  • Disorders under investigation are: Autosomal dominant inherited urologic malignant disorders including: von Hippel- Lindau (VHL), hereditary papillary renal cancer (HPRC), Birt Hogg Dube (BHD) and hereditary leiomyomatosis and renal cell acarcinoma (HLRCC) as well as familial renal cancer. (
  • We tested atorvastatin as a therapy for ( a ) ethylnitrosourea (ENU)-enhanced renal cystadenoma and ( b ) spontaneous liver hemangioma in 129Sv/Jae Tsc2 +/− mice. (
  • Pathologic analyses revealed a predominance of renal cystadenoma in ENU-treated and liver hemangioma in non-ENU-treated 129Sv/Jae Tsc2 +/− mice. (
  • Following atorvastatin treatment, no significant reduction in tumor size, morphology, or phosphorylated S6 levels was observed for either ENU-associated renal cystadenoma or spontaneous liver hemangioma as compared with the untreated groups. (
  • Columnar epithelial cells lining the papillary structures stained variably and weakly for this distal respiratory cell marker. (