Disease relevance of Cystadenoma

• Conservative management of the Zollinger-Ellison syndrome. Ectopic gastrin production by an ovarian cystadenoma [1].
• METHODS: We used immunohistochemical and DNA-sequencing techniques to analyze 46 ovarian carcinomas, 21 ovarian tumors of low malignant potential, and 16 solitary cystadenomas for the presence of p53 mutations [2].
• These differences between rates of telomerase expression in either carcinomas or LMP tumors and those in cystadenomas were statistically significant (P<.0001) [3].
• All five of the telomerase-positive cystadenomas belonged to a variant called papillary cystadenomas, whereas none of the telomerase-negative cystadenomas belonged to this variant (P<.0001) [3].
• Tsc1 heterozygotes develop kidney cystadenomas and liver hemangiomas at high frequency, but the incidence of kidney tumors is somewhat lower than in Tsc2 heterozygote mice [4].

High impact information on Cystadenoma

• The renal cystadenomas develop from intercalated cells of the cortical collecting duct and uniformly express gelsolin at high levels, enabling detection of early neoplastic lesions [5].
• Lack of telomerase expression in ovarian cystadenomas raises questions about the alleged immortality of these tumors because expression of this enzyme is thought to be essential for continuous growth in adult tumors [3].
• Our findings provide cogent evidence that mutations of BRAF and KRAS occur in the epithelium of cystadenomas adjacent to SBTs and strongly suggest that they are very early events in tumorigenesis, preceding the development of SBT [6].
• Here we show that a subset of cultured ovarian cystadenoma cells expressing SV40 large T-antigen, which allows bypassing of M1, develop a specific type of genomic instability, characterized by numerical (as opposed to structural) chromosomal alterations, that leads to non-telomere-based premature growth arrest/crisis [7].
• Expression of COX-2 was detected in 42% of 86 ovarian carcinomas and in 37% of 19 low malignant potential tumors, but not in 12 cystadenomas or 2 normal ovaries [8].

Chemical compound and disease context of Cystadenoma

• This report is concerned with identification of a new class of oligosaccharide ligand--sulfate-containing--for the human E-selectin molecule from among oligosaccharides on an ovarian cystadenoma glycoprotein [9].
• In the ovary, corpora lutea were lacking while cysts were quite common in Tamoxifen-exposed mice at all doses; cystadenomas were seen in two mice [10].
• Thirteen of 19 benign ovarian cystadenomas also expressed the epitope, but staining was weak and restricted to the luminal surface of the cell membrane [11].
• A case of hepatobiliary cystadenoma with mesenchymal stroma is documented in which unequivocal immunostaining for progesterone receptors was observed in mesenchymal cells [12].
• Hepatobiliary cystadenoma with mesenchymal stroma: expression of oestrogen receptors in formalin-fixed tissue [13].

Biological context of Cystadenoma

• These findings suggest that the K-ras mutation occurs during the transformation from benign cystadenomas to LMP or malignant lesions, providing molecular genetic support for the hypothesis of the "adenoma-carcinoma sequence" in some mucinous ovarian tumors, but in other cases an alternative pathway may also be possible [14].
• Changes in DNA methylation may be more important for inactivation of this gene (and perhaps other tumor suppressor genes) in LMP tumors, which lack many of the alternative mechanisms present in carcinomas. p16 expression is primarily related to mucinous differentiation in cystadenomas [15].
• Semi-quantitative reverse transcription (RT)-PCR analysis showed that expression of LTBP-1 and TGF-beta 1 mRNAs was much higher in both serous and mucinous adenocarcinomas than in their benign counterparts, including serous and mucinous cystadenomas and cystadenomas of low malignant potential (LMPs) [16].

Anatomical context of Cystadenoma

• Telomerase activity was examined in 12 ex vivo brushing samples of the pancreatic duct, and 8 of 8 with pancreatic cancer had detectable telomerase activity, whereas 0 of 4 of benign lesions (cystadenoma and pancreatitis) did [17].
• Microcystic adenoma of the pancreas (glycogen-rich cystadenoma) with stromal amyloid deposits [18].
• High peritoneal fluid activin A levels (>2 multiples of the mean) distinguished carcinoma from cystadenoma with a sensitivity of 72% and a specificity of 80% [19].
• We describe an asymptomatic case of a mucin secreting biliary cystadenoma in which the mucin presented as an amorphous intraluminal filling defect in the common hepatic duct on endoscopic retrograde cholangiopancreatography (ERCP) [20].
• Intrahepatic biliary cystadenoma causing luminal common bile duct obstruction [21].

Gene context of Cystadenoma

• RESULTS: Benign cystadenomas exhibited promoter hypermethylation in only two genes, p16 (13%) and E-cadherin (13%) [22].
• Tight junction proteins claudin-3 and claudin-4 are frequently overexpressed in ovarian cancer but not in ovarian cystadenomas [23].
• In this study, the expression of PLK1 and PLK3 was determined immunohistochemically in tissue specimen of normal ovaries (n=9), cystadenomas (n=17), borderline tumours (n=13) and ovarian carcinomas (n=77) [24].
• PLK 1 and PLK3 expression was low in normal ovarian surface epithelium and borderline tumours, with moderately higher expression levels in cystadenomas [24].
• Most serous borderline tumors expressed higher levels of MDM2 compared with the benign cystadenomas and carcinomas [25].

Analytical, diagnostic and therapeutic context of Cystadenoma

• EXPERIMENTAL DESIGN: Expression of HIF-1alpha protein was studied by immunohistochemistry in 102 specimens of epithelial ovarian cancers, in 50 borderline tumors, and in 20 cystadenomas [26].
• EXPERIMENTAL DESIGN: Paraffin embedded tissues from 7 normal ovaries, 22 cystadenomas and 42 borderline lesions were analyzed using standard immunoperoxidase and in situ hybridization techniques to assess ARHI expression [27].
• METHODS: In 32 women with endometriomas (17 untreated and 15 treated with GnRH analogue) and 21 with ovarian cystadenomas, we examined the expression of secretory leukocyte protease inhibitor messenger RNA (mRNA) by Northern blot analysis; protein distribution was measured immunohistochemically [28].
• Among O-glycans from an ovarian cystadenoma mucin, isomeric oligosaccharide sequences, sialyl-Lea- and sialyl-Lex-active, could be resolved by HPLC as fluorescent neoglycolipids, and sequenced by liquid secondary-ion mass spectrometry [29].
• Methylation-specific PCR was used to analyze the p16 gene for DNA methylation in 20 ovarian cystadenomas, 15 low malignant potential (LMP) tumors, and 37 carcinomas. p16 expression was determined immunohistochemically in 58 of these tumors (16 cystadenomas, 13 LMP tumors, 29 carcinomas) [15].

References