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

Carcinosarcomas, also known as true malignant mixed tumors, are rare tumors of the salivary gland and are composed of both malignant epithelial and malignant mesenchymal elements. They may occur in pre-existing pleomorphic adenomas or arise de novo. Here we report the first case of carcinosarcoma of the parotid gland composed of mucoepidermoid carcinoma and osteosarcoma. The tumor had originated from the parotid gland and extended into the parapharyngeal space. To the best of our knowledge, there have been no reports on mucoepidermoid carcinoma mixed with osteosarcoma ex pleomorphic adenoma in the parotid gland.
Adenoma, Pleomorphic ; Carcinoma, Mucoepidermoid ; Carcinosarcoma ; Mixed Tumor, Malignant ; Osteosarcoma ; Parotid Gland ; Salivary Glands

OBJECTIVETo explore the diagnostic value of MYB protein expression for adenoid cystic carcinoma and its differential diagnosis from other salivary gland tumors, and to further investigate the status of MYB gene copy number.

METHODSMYB expression was studied by immunohistochemistry in 34 adenoid cystic carcinomas, 55 non-adenoid cystic carcinomas (other salivary gland tumors) including 10 pleomorphic adenomas, 10 basal cell adenomas, 10 epithelial-myoepithelial carcinomas, 9 basal cell adenocarcinomas, 8 mucoepidermoid carcinomas, 4 carcinoma in pleomorphic adenomas, and 4 polymorphous low-grade adenocarcinoma. MYB gene copy number status was detected by FISH in MYB protein-positive cases.

RESULTS82.4% (28/34) of adenoid cystic carcinomas were MYB protein-positive, compared with 9.1% (5/55) of non-adenoid cystic carcinomas, and the difference between the two groups was statistically significant (P < 0.01). 2/18 of adenoid cystic carcinomas had duplication of MYB gene by FISH, and all non-adenoid cystic carcinomas were negative although the difference was not statistically significant (P = 0.435).

CONCLUSIONSMYB protein expression is a useful diagnostic marker for adenoid cystic carcinomas in its separation from other salivary gland tumors. In addition, duplication of MYB gene is no a major mechanism for the MYB protein overexpression.

Adenoma ; Adenoma, Pleomorphic ; Biomarkers, Tumor ; genetics ; metabolism ; Carcinoma, Adenoid Cystic ; diagnosis ; genetics ; metabolism ; Carcinoma, Mucoepidermoid ; Diagnosis, Differential ; Gene Dosage ; Humans ; Immunohistochemistry ; Proteomics ; Proto-Oncogene Proteins c-myb ; genetics ; metabolism ; Salivary Gland Neoplasms

OBJECTIVETo study the clinicopathologic characteristics of primary salivary gland-type lung carcinomas, and the immunophenotypic value of TTF-1, Napsin A and Ki-67 in their differential diagnosis.

METHODSTotally 48 special type lung cancer surgical removal specimens were collected in China-Japan Friendship Hospital during September 2009 to December 2014. A panel of immunohistochemical markers (TTF-1, Napsin A, Ki-67, CK5/6, CK7 and p63) were conducted on these specimens.

RESULTSThe 48 cases of special type lung cancer included 25 cases of primary salivary gland-type lung carcinoma (18 cases of adenoid cystic carcinoma and 7 cases of mucoepidermoid carcinoma), 5 cases pulmonary adenocarcinoma with mucoepidermoid carcinoma-like or adenoid cystic carcinoma-like structure, and 18 cases of pulmonary adenosquamous carcinoma. Compared with pulmonary adenocarcinoma with mucoepidermoid carcinoma-like or adenoid cystic carcinoma-like structure and pulmonary adenosquamous carcinoma, primary salivary gland-type lung carcinomas have special characteristics in median age, sex, location, tumor size, LN involvement and pleura invasion, with negative TTF-1 and Napsin A expression as well as lower Ki-67 index detected by immunohistochemistry. Primary salivary gland-type lung carcinomas usually have an indolent behavior.

CONCLUSIONSPrimary salivary gland-type lung carcinomas are low-aggressive entities. The origins of primary salivary gland-type lung carcinomas were different from that of pulmonary adenocarcinoma with mucoepidermoid carcinoma-like or adenoid cystic carcinoma-like structure and pulmonary adenosquamous carcinoma. Negative TTF-1 and Napsin A expression as well as Ki-67 index lower than 20% have special value for primary salivary gland-type lung carcinomas in their differential diagnosis.

Adenocarcinoma ; diagnosis ; Aspartic Acid Endopeptidases ; metabolism ; Biomarkers, Tumor ; metabolism ; Carcinoma, Adenoid Cystic ; diagnosis ; Carcinoma, Mucoepidermoid ; diagnosis ; China ; DNA-Binding Proteins ; metabolism ; Humans ; Immunohistochemistry ; Ki-67 Antigen ; metabolism ; Lung Neoplasms ; diagnosis ; Transcription Factors

Malignant salivary gland tumors only represent 0.08% of all childhood tumors and mucoepidermoid carcinoma (MEC) is the most common histologic type. Although there are many reports describing second malignant neoplasm (SMN) in patients treated for childhood cancer, salivary gland tumors rarely appears. In Korea, there has been no report about MEC that developed in children as a SMN. We report a MEC in a 4 years and 8 months old female child that developed after completing treatment for yolk sac tumor of lower abdomen. The primary tumor presented with metastasis at the time of diagnosis, and therefore, the child underwent high-dose chemotherapy with autologous peripheral blood stem cell transplantation along with surgery and radiotherapy. Three years and five months after completing treatment, MEC developed in her submandibular gland. She was treated with surgery and radiotherapy and is in disease free state for 5 months at the time of this writing.
Abdomen ; Carcinoma, Mucoepidermoid ; Child ; Diagnosis ; Drug Therapy ; Endodermal Sinus Tumor ; Female ; Humans ; Korea ; Neoplasm Metastasis ; Peripheral Blood Stem Cell Transplantation ; Radiotherapy ; Salivary Gland Neoplasms ; Salivary Glands ; Submandibular Gland ; Writing

Mucoepidermoid carcinoma is a malignant epithelial tumour of glandular tissue, usually of the major salivary glands. However it can present in the minor salivary glands, especially in the soft palate. We report the case of a 72-year-old Malay female after presentation with sore throat, fever and odynophagia, was diagnosed with mucoepidermoid carcinoma of the soft palate.
Mucoepidermoid Tumor ; Salivary Gland Neoplasms ; Salivary Glands, Minor

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

The present study was conducted to investigate the effects of gossypol acetic acid (GAA) on the proliferation of human mucoepidermoid carcinoma cell line MEC-1 in vitro and its possible molecular mechanisms of DNA double-strand breaks (DSB). MTT assay was performed to test the inhibition of proliferation of MEC-1 cells by GAA. DSB and γH2AX foci formation induced by GAA were detected by neutral comet assay and immunostaining. GAA (5-40 μmol/L) inhibited the growth of MEC-1 cells in a dose- and time-dependent manner. One of the indexes of comet assay, percentage of head DNA was decreased, however other indexes, including tail length, percentage of tail DNA, tail moment (TM) and Olive tail moment (OTM) were increased when treated with 2.5- 40 μmol/L GAA for 24 h or 20 μmol/L GAA for 3-48 h, compared with those in control. The percentage of γH2AX-positive cells was also increased when MEC-1 was treated with 2.5-20 μmol/L GAA for 24 h or 20 μmol/L GAA for 3-48 h, compared with that in control. All these results show that GAA inhibits the proliferation of MEC-1, and DSB maybe one of the mechanisms of inhibitory effect of GAA on the growth of tumor cells.
Antineoplastic Agents, Phytogenic ; pharmacology ; Carcinoma, Mucoepidermoid ; genetics ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA Breaks, Double-Stranded ; drug effects ; Gossypol ; analogs & derivatives ; pharmacology ; Humans ; Parotid Neoplasms ; genetics ; pathology

Mucoepidermoid carcinoma generally arises from salivary glands and represents 5~10% of all salivary tumors. Arising within the jaws as primary central bony lesions, central mucoepidermoid carcinomas are extremely rare, accounting for only 2~3% of all mucoepidermoid tumors. Central mucoepidermoid carcinoma of the mandible was first reported in 1939 and since then approximately 100 cases have been documented in the literature. Several hypotheses have been proposed to explain the pathogenesis of intraosseous salivary tumors. The most likely source of most intraosseous tumors is odontogenic epithelium. Waldron and Mustoe suggested that central mucoepidermoid carcinoma be included in primary intraosseous carcinoma of the jaw. We report here on a case of central mucoepidermoid carcinoma affecting the mandible and discuss the clinical, radiographic, and histological findings.]]>
Accounting ; Carcinoma, Mucoepidermoid ; Epithelium ; Jaw ; Mandible ; Mucoepidermoid Tumor ; Salivary Gland Neoplasms ; Salivary Glands

BACKGROUND: The protein expression profile of clear cell type mucoepidermoid carcinoma (MEC) is not well known. METHODS: We examined a case of clear cell type MEC by immunohistochemical (IHC) array using 59 antibodies against oncoproteins, proliferation-related proteins, apoptosis-related proteins, growth factor-related proteins, angiogenesis-related proteins, and matrix proteins. RESULTS: MEC tumor cells showed 40 to 60% more expression of BCL-2 and cyclin-dependent kinase 4 than normal gingival tissue, and 20-40% more expression of BCL-2-associated agonist of cell death, deleted in malignant brain tumors 1, E-cadherin, eIF5A, hypoxia-inducible factor, vimentin, and Wnt-1. Expression of other proteins, including p53, epidermal growth factor receptor, proliferating cell nuclear antigen, survivin, carcinoembryonic antigen, beta-catenin, poly-ADP ribose-polymerase, etc. were relatively weak in MEC tumor cells. CONCLUSIONS: The IHC array for our MEC contained strong oncogenic signals involving Wnt-1/adenomatous polyposis coli, tumor necrosis factor a/signal transducer and activator of transcription 3/BCL-2, and pAKT pathways, signals that could result in the prolonged survival of clear tumor cells.
Antibodies ; beta Catenin ; Brain Neoplasms ; Cadherins ; Carcinoembryonic Antigen ; Carcinoma, Mucoepidermoid ; Cell Death ; Cyclin-Dependent Kinase 4 ; Immunohistochemistry ; Oncogene Proteins ; Oncogenes ; Proliferating Cell Nuclear Antigen ; Proteins ; Receptor, Epidermal Growth Factor ; Transducers ; Tumor Necrosis Factor-alpha ; Vimentin