Humans ; Carcinoma, Mucoepidermoid/pathology* ; Breast/pathology*

Humans ; Carcinoma, Mucoepidermoid/pathology* ; Thyroid Neoplasms/pathology* ; Eosinophilia/pathology*

OBJECTIVE: To investigate the clinicopathological characteristics of micro and mini parotid gland tumors and to provide reference for their clinical diagnosis and treatment. METHODS: Patients with parotid gland tumors treated in the Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology from December 2012 to April 2020 were selected. Relevant clinical data of the patients with tumor diameter ≤20 mm detected by preoperative CT were collected to analyze the clinicopathological characteristics and prognosis of micro and mini parotid gland tumors. And the collected data were divided into two groups with diameter 11-20 mm and diameter ≤10 mm according to tumor diameter measured by preoperative CT. The clinicopathological differences between the two groups were statistically analyzed. RESULTS: A total of 2 067 patients with primary epithelial parotid gland tumors were collected, and 685 patients with tumor diameter ≤20 mm were examined by CT, accounting for 33.1%. The ratio of male to female patients with micro and mini parotid gland tumors was 1 ∶1.93, the average age was (45.3±13.8) years (12-83 years), and the median course of disease was 12 months (1 week to 30 years). Among them, 635 cases (92.7%) were benign tumors, 50 cases (7.3%) were malignant tumors, and the ratio of benign to malignant was 12.7 ∶1. The most common benign tumor was pleomorphic adenoma, and the most common malignant tumor was mucoepidermoid carcinoma. The micro and mini parotid gland tumors were divided into 11-20 mm group (n=611) and ≤10 mm group (n=74), the clinical characteristics comparison of the two groups of gender ratio, average age, course of di-sease had no statistical difference (P>0.05). In the 11-20 mm diameter group, the percentage of benign and malignant tumor was 92.8% (567/611) and 7.2% (44/611) respectively, and the ratio of benign to malignant tumors was 12.9 ∶1. In the ≤10 mm diameter group, the percentage of benign and malignant tumor was 91.9% (68/74) and 8.1% (6/74) respectively, and the ratio of benign to malignant tumors was 11.3 ∶1. There was no significant difference between the two groups (P>0.05). Fifty patients with malignant tumor were followed up for the median follow-up period of 39.5 months (1-91 months). Local recurrence occurred in 2 patients with one death. The overall 2-year survival rate was 93.7% and the 5-year survival rate was 89.3%. CONCLUSION The majority of micro and mini parotid gland tumors was benign lesion. There was a good prognosis for micro and mini parotid gland carcinoma. Early surgical treatment was recommended for micro and mini parotid gland tumors.
Adenoma, Pleomorphic/surgery* ; Adult ; Carcinoma, Mucoepidermoid/pathology* ; Female ; Humans ; Male ; Middle Aged ; Parotid Gland ; Parotid Neoplasms/surgery* ; Retrospective Studies

Carcinoma, Mucoepidermoid/surgery* ; Child ; Humans ; Lung/pathology* ; Lung Neoplasms/surgery*

Objective: To study the clinicopathologic and genetic features of papillary cystic low-grade mucoepidermoid carcinoma (LG-MEC) and cystadenoma. Methods: A retrospective review was performed on salivary gland tumor patients with papillary cystic architecture who presented to department of oral pathology, Peking University School and Hospital of Stomatology between January 2010 and June 2022. Among this cohort, there were 17 males and 17 females with a range age of 23-82 years [(55.6±14.6) years]. Diagnosis was confirmed by histological, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) analysis. Finally, 15 papillary cystic LG-MEC and 19 cystadenoma patients were included in the present study. All patients were followed clinically and radiologically, and the duration of follow-up ranged from 1 to 141 months. Results: All neoplasms showed papillary proliferation with multilocular or giant cystic tumors. Papillary cystic LG-MEC was characterized by epidermoid cells, intermediate cell and mucous cells with multiple lining-layers. Papillary cystic LG-MEC had mild cellular atypia and a pushing infiltration. Cystadenoma was characterized by cuboidal, columnar and ciliated pseudostratified columnar lining epithelium. Squamous metaplasia, mucinous metaplasia and acidophilic degeneration could also be observed focally in cystadenoma. For IHC staining, papillary cystic LG-MEC showed diffusely and strongly positive for mucin 4 (MUC4) (15/15) and mucin 5 Subtype AC (MUC5AC) (4/15) in the epidermoid cells, intermediate cell and mucous cells. The epidermoid cells and intermediate cells were diffusely positive for p40 and p63. The Ki-67 index was about 10%-15% in LG-MEC. As a contrast, p40 (17/19) and p63 (14/15) were only detected in the basal cells of cystadenoma. Cystadenoma showed focal MUC5AC (4/19)expression and MUC4 (19/19)diffuse expression. In addition, the Ki-67 index was 5%-10% in cystadenoma. The MAML2 gene translocation was detected in 11 LG-MEC patients, but none in cystadenoma. Conclusions: The differential diagnosis points between papillary cystic LG-MEC and cystadenoma included the specific epidermoid cells, intermediate cells and mucus cells in LG-MEC, cell atypia, the pushing-infiltration pattern, diffuse expression of p40 and p63 in the lining epithelium, and a MAML2 gene rearrangement. The molecular test of MAML2 should be recommended to reduce missed LG-MEC diagnoses.
Male ; Female ; Humans ; Carcinoma, Mucoepidermoid/pathology* ; In Situ Hybridization, Fluorescence ; Ki-67 Antigen/genetics* ; Biomarkers, Tumor/analysis* ; Salivary Gland Neoplasms/diagnosis* ; Transcription Factors/metabolism* ; Cystadenoma ; Metaplasia

OBJECTIVE: The maximum standardized uptake value (SUVmax) of pulmonary mucoepidermoid carcinoma (PMEC) in fluorine-18fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) was evaluated as a preoperative predictor of pathologic grade and survival rate. MATERIALS AND METHODS: Twenty-three patients who underwent preoperative PET/CT and complete resection for PMEC were enrolled. The optimal cut-off SUVmax for tumor grade was calculated as 6.5 by receiver operating characteristic curve. The patients were divided into a high SUV group (n = 7) and a low SUV group (n = 16). Clinicopathologic features were compared between the groups by chi2 test and overall survival was determined by Kaplan-Meier analysis. RESULTS: The mean SUVmax was 15.4 +/- 11.5 in the high SUV group and 3.9 +/- 1.3 in the low SUV group. All patients except one from the low SUV group had low grade tumors and all had no nodal metastasis. The sensitivity and specificity of SUVmax from PET/CT for predicting tumor grade was 85.7% and 93.8%, respectively. During the follow-up period (mean, 48.6 +/- 38.7 months), four patients from the high SUV group experienced cancer recurrence, and one died of cancer. In contrast, none of the low SUV group had recurrence or mortality. Five-year overall survival rate was significantly higher in the low SUV group (100% vs. 71.4%, p = 0.031). CONCLUSION: Pulmonary mucoepidermoid carcinoma patients with high SUVmax in PET/CT had higher tumor grade, more frequent lymph node metastasis and worse long-term outcome. Therefore, PMEC patients with high uptake on PET/CT imaging might require aggressive mediastinal lymph node dissection and adjuvant therapies.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Carcinoma, Mucoepidermoid/*pathology/radiography ; Female ; Fluorodeoxyglucose F18/metabolism ; Humans ; Kaplan-Meier Estimate ; Lung Neoplasms/*pathology/radiography ; Lymph Nodes/pathology/radiography ; Lymphatic Metastasis ; Male ; Mediastinum/radiography ; Middle Aged ; Neoplasm Grading ; Neoplasm Recurrence, Local/pathology/radiography ; Positron-Emission Tomography/*methods ; Prognosis ; ROC Curve ; Retrospective Studies ; Sensitivity and Specificity ; Survival Rate ; Tomography, X-Ray Computed/*methods ; Young Adult

Carcinoma, Mucoepidermoid ; complications ; metabolism ; pathology ; DNA-Binding Proteins ; metabolism ; Diagnosis, Differential ; Eosinophilia ; complications ; metabolism ; pathology ; Epithelial Cells ; pathology ; Female ; Hashimoto Disease ; metabolism ; pathology ; surgery ; Humans ; Keratin-19 ; metabolism ; Membrane Proteins ; metabolism ; Middle Aged ; Thyroid Gland ; metabolism ; pathology ; surgery ; Thyroid Nodule ; metabolism ; pathology ; surgery ; Transcription Factors ; beta Catenin ; metabolism

Carcinoma, Mucoepidermoid ; pathology ; Female ; Humans ; Parotid Neoplasms ; pathology ; Sclerosis ; Young Adult

Adamantinoma ; pathology ; Carcinoma, Mucoepidermoid ; diagnostic imaging ; drug therapy ; pathology ; surgery ; Diagnosis, Differential ; Humans ; Male ; Mandibular Neoplasms ; diagnostic imaging ; pathology ; surgery ; Middle Aged ; Tomography, X-Ray Computed

OBJECTIVETo study the role of Slit-Robo signaling in the proliferation of human mucoepidermoid carcinoma Mc3 cells.

METHODSWe measured the expressions of Slit2 and Robo1 proteins in human mucoepidermoid carcinoma Mc3 cells using immunohistochemistry and flow cytometry. To test the role of Slit-Robo signaling in the proliferation of the cells, we treated the cells with the monoclonal antibody R5 against Robo1 receptor extracellular domain and observed the changes in the cell proliferation by cell counting and colonogenic assay; the expression of proliferating cell nuclear antigen (PCNA) in the cells following the treatment was measured with flow cytometry.

RESULTSTreatment of Mc3 cells with the monoclonal antibody R5 caused significantly suppressed cell growth and proliferation and obviously lowered the expression of PCNA.

CONCLUSIONSlit-Robo signaling can suppress the proliferation of Mc3 cells possibly by up-regulating the expression of PCNA.

Carcinoma, Mucoepidermoid ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Nerve Tissue Proteins ; metabolism ; Proliferating Cell Nuclear Antigen ; metabolism ; Receptors, Immunologic ; metabolism ; Salivary Gland Neoplasms ; pathology ; Signal Transduction