This study immunohistochemically evaluated (by Ki-67 and p53 staining) the presence of p53 signature, TILT lesions, and STIC in 14 consecutive cases of prophylactic salpingo-oophorectomy in women with BRCA-1/2 mutation (bilateral salpingo-oophorectomy), 11 cases of macroscopically inconspicuous adnexae of patients with primary contralateral tubal cancer (TC), 9 cases of primary peritoneal cancer (PPC), and 10 cases of serous ovarian borderline tumors, evaluating the fallopian tubes (using the Sectioning and Extensively Examining the FIMbria protocol), ovarian surface epithelium, and ovarian cortical inclusion cysts.
BRCA1/2 mutation rate was 1/76 (1.3%) in the endometriotic cyst study group and 1/50 (2%) in the control non-endometriotic cysts, showing no statistically significant difference between the groups (p=0.84).
No visible movement in the cleft was defined as type A, fluid displaced into the cleft as type BI, displacement of the flava ligaments at the level of the cleft as type BII, and intraspinal cysts arising from the spondylolytic cleft as type BIII.
We evaluated immunohistochemical markers of sex-steroid differentiation and steroidogenesis (calretinin, inhibin, steroidogenic factor 1), steroid enzymes involved in hormone biosynthesis (CYP17, CYP19, HSD17β1, AKR1C3), and hormone receptors (estrogen receptor, progesterone receptor, and androgen receptor) in 101 epithelial ovarian tumors and in normal structures implicated in ovarian carcinogenesis (ovarian surface epithelium and cortical inclusion cysts) in an attempt to elucidate this process.
We postulate that the appearance of the Fas system and its related proteins in sequestered columnar OSE cells of irregularly shaped inclusion cysts may contribute to balance cell growth with cell death, although little active caspase-3 expression was observed.
Despite normal in vitro differentiation, the exotic strains CAST and GPHT also showed decreased oral transmission, due to formation of smaller cysts and a lower tissue burden during chronic infection, traits also shared by MAS and FOU.
By 12 months of age approximately 18% of Cav1-/- females developed single or multiple dilated endometrial cysts lined by a flattened, simple low epithelium.
The objective of the study was evaluation of the indicators of the inflammatory state, including RANTES and the levels of C-reactive protein, leukocytes, fibrinogen and iron in the blood serum of patients with endometrial cysts (n=48) and benign ovarian tumours of mature teratoma type (n=38).
Specific PCR was performed and followed by DNA sequencing for mitochondrial 12S ribosomal RNA gene and BLAST analysis.The sheep cysts were not hydatid cysts.
We used lineage tracing, conditional deletion, mosaic analysis and ligand stimulation in mice to determine that both villous protrusions and floating cysts contribute to PEC translocation to myocardium in a CDC42-dependent manner.
Using hyperimmune anti-p57 serum combined with immunolabeling, we found that p57 was expressed by small trophic forms and intracystic bodies, whereas it was not expressed on larger trophic forms or externally by cysts.
Detailed morphological analysis using immunofluorescence microscopy with both confocal and two-photon microscopes revealed the anatomy of the cysts as consisting of a squamous epithelial wall richly expressing E-cadherin and CDX2.
In a prospective study, we found that analysis of cysts by nCLE identified mucinous cysts with greater accuracy than measurement of CEA and cytology analysis.
The fact that most CFTR-positive ADPKD cysts also express NKCC1 suggests that transepithelial Cl(-) secretion in ADPKD involves molecular mechanisms similar to secretory epithelia.
We found that a weak or absence of expression of claudin 3 and claudin 4 in surface OSE changed to typical cell-border localisation in OSE of inclusion cysts in the normal ovarian stroma.
We found that a weak or absence of expression of claudin 3 and claudin 4 in surface OSE changed to typical cell-border localisation in OSE of inclusion cysts in the normal ovarian stroma.