Background
Sialadenoma papilliferum (SP) is an extremely rare benign neoplasm of salivary glands. To explore and define the clinicopathological features of SP, we retrospectively analyzed 89 cases previously reported and five new cases.
Methods
The clinical features, histopathology, immunohistochemistry and molecular analysis of our cases were further performed and the related literatures were reviewed and analyzed.
Results
Combining 89 cases from the literature with our cases, the hard palate was the most common locations for SP. However, two of our cases were rarely located in the esophageal mucosa. Among all cases, the male gender was more affected, with the average age and median age of 61.8 and 62 years, respectively. Conventional histomorphologically, SP was characterized by complex papillary structures with a biphasic growth pattern of exophytic squamous component and endophytic glandular component. The glandular structures were lined by a double layer of epithelium composed of flattened or cuboidal basal cells and a cuboidal or columnar luminal cells formed papillary infoldings into the ductal lumina. Immunohistochemically, the luminal epithelial configurations showed strong expression of CK7 along the luminal cell membrane, while the basal myoepithelia displayed strong nuclear p63 expression. In both the glandular and squamous tumour components showed BRAF V600E-positive immunostaining and BRAF V600E mutation.
Conclusion
For the first time, we have comprehensively aggregated and analyzed 90 cases sialadenoma papilliferum from almost all previous publications, and further explored the clinicopathological features of SP; concordantly, this study demonstrated that SP shows a papillomatous growth pattern with exophytic and endophytic proliferation of ductal epithelium composed of double-layered cells harboring BRAF V600E mutation. Additionly, adequate treatment for SP is surgical excision, with a favorable prognosis in patients.
BackgroundIn most documented literature, metanephric adenoma (MA) is described as a benign tumour. Nevertheless, the nature of MA remains unclear and the clinical criteria of different MA subtypes are not well established. In the present study, we investigated the clinicopathological characteristics of MA, especially those of the uncommon histological subtypes.MethodsA cohort study was performed on 18 patients with pathologically proven MA in our institute from January 2004 to June 2014. The patients’ clinicopathological and radiological data were retrospectively analysed and evaluated with an emphasis on the corresponding subtypes.ResultsThe patient population had a female: male ratio of 1:1 and mean age of 50 years (range, 18–66 years). The mean tumour size was 3.9 cm (range, 1.4–9.0 cm). There were no pathognomonic radiological features that posed a challenge for a preoperative diagnosis of MA. Fourteen patients underwent radical nephrectomy, and the other four underwent partial nephrectomy. Three histological subtypes were observed: classic MA (n = 10), malignant MA (n = 2), and composite MA with coexistence of different malignant components (n = 6). Despite the presence of atypical histological features and malignant components among the patients, only one patient developed distant metastasis (median postoperative follow-up, 56 months; range, 30–86 months).ConclusionsMAs are a heterogeneous group of neoplasms with different biological characteristics. The correct identification of this entity and its subtypes would facilitate stratification of optimal management protocols and accurate assessment of the prognosis.
SET domain bifurcated 1 (SETDB1) is a histone H3 lysine 9 methyltransferase that is highly expressed in various tumor types, including breast cancer. However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explore the role of SETDB1 in breast cancer cells. SETDB1 downregulation in BT549 and MDA-MB-231 cells reduced cell proliferation, whereas upregulation in MCF7 and T47D cells enhanced proliferation. Depletion of SETDB1 suppressed cell migration and invasion in vitro and reduced lung metastasis in vivo. By contrast, SETDB1 overexpression enhanced cell migration and invasiveness. Notably, SETDB1 overexpression appeared to induce epithelial-mesenchymal transition (EMT) in MCF7 cells. Mechanistic investigations indicated that SETDB1 acts as an EMT inducer by binding directly to the promoter of the transcription factor Snail. Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer.
Our results demonstrated that LAMP2 expression levels correlated with tumor histological differentiation and TNM stages. High expression of LAMP2 predicts poor prognosis in patients with ESCC.
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