Primary mucoepidermoid carcinoma of the pleura. A clinicopathologic study of two cases.
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Two cases of primary mucoepidermoid carcinoma of the pleura are described. The patients are 2 men, 48 and 61 years old. Clinically, both men sought care because of chest pain in the right side and breathing difficulty. Neither of the patients had a history of head and neck tumor, and physical examination revealed that no tumor was present in the head and neck area. Radiographic studies in both men disclosed the presence of a pleural-based mass. Both men underwent surgical excision of the mass. Histologically, in both cases the pleura showed areas of fibrinous pleuritis with an underlying neoplastic cellular proliferation composed of cells with epidermoid features without keratinization and presence of mucocytes. Both tumors were classified as low-grade tumors. Both patients were alive and well 8 and 12 months after surgical resection. The cases herein presented highlight the importance of including other epithelial tumors in the differential diagnosis of pleural tumors. (+info)
Successful treatment of tracheal mucoepidermoid carcinoma using rigid bronchoscopy combined with conventional surgical resection.
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Mucoepidermoid carcinoma of the trachea is a rare tumor. This investigation reports on a case of a 67-year-old male with mucoepidermoid carcinoma in the lower 1/3 of the trachea. The patient presented with intermittent coughing and hemoptysis lasting for 1 month. The preoperative investigation revealed an intraluminal polypoid mass in the posterolateral trachea with 75% stenosis of the tracheal lumen. A rigid bronchoscope was used to evaluate the airway before surgery, and the tumor was mechanically resected using the tip of the rigid bronchoscope just before intubation. Finally, the tumor was completely removed, and the airway was successfully reconstructed. At 6 months after surgery with no adjuvant chemoradiotherapy, the patient was free of disease. (+info)
Biological behavior of mucoepidermoid carcinoma of the esophagus.
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Mucoepidermoid carcinoma of the esophagus (MEC) is uncommon and has not been fully investigated. The biological behavior and clinical aspects of MEC were studied. The clinical features of eight patients with MEC were compared with 51 cases of squamous cell carcinoma of the esophagus (SCC). Proliferating cell nuclear antigen (PCNA), p53, and carcinoembryonic antigen (CEA) were stained in the resected specimens by immunohistochemistry. Seven out of 8 cases (87.5%) had stage III by TNM classification. Four cases died of widespread metastases and 2 cases died of local recurrence within 2 years after the surgery. Neither chemotherapy and radiotherapy were effective against MEC. Overall median survival periods were 10.8 months for MEC and 32.1 months for SCC (P<0.05). When patients in stage III alone were compared, MEC tended to have a worse prognosis than SCC (P=0.058). Immunohistochemical studies revealed that the positive rates of PCNA and CEA were significantly higher in MEC than in SCC (P<0.05), while there was no significant difference in p53 positive rate. Esophageal MEC had an aggressive biological nature and was resistant to adjuvant therapies. The poor prognosis of esophageal MEC may be caused by high proliferative and metastatic potential. (+info)
p63 expression in sclerosing mucoepidermoid carcinomas with eosinophilia arising in the thyroid.
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Primary sclerosing mucoepidermoid carcinomas with eosinophilia (SMECE) of the thyroid gland are rare tumors that can present diagnostic difficulties to the pathologist due to the unusual histologic features. Furthermore, the etiology of these tumors has been debated in the literature, with some authors believing that the tumors arise from remnants of the ultimobranchial body (UBB, solid cell nests) and others proposing that they arise from follicular epithelial cells. Because SMECE often occur in glands with chronic lymphocytic thyroiditis and UBB hyperplasia, and do not stain like follicular or parafollicular cells, it is likely that the tumors do arise from UBB/solid cell nests. In this study, we provide additional evidence for this relationship, by demonstrating that SMECE stain strongly positive for p63, which is a new marker for UBB/solid cell nests. (+info)
Cigarette smoke induces MUC5AC mucin overproduction via tumor necrosis factor-alpha-converting enzyme in human airway epithelial (NCI-H292) cells.
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Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death in the U.S. Because cigarette smoking is so importantly implicated in the pathogenesis of COPD and because mucus hypersecretion plays such an important role in COPD, understanding of the mechanisms of smoking-induced mucus hypersecretion could lead to new therapies for COPD. Cigarette smoke causes mucin overproduction via EGF receptor (EGFR) in airway epithelial cells, but the cellular mechanism remains unknown. Airway epithelial cells contain EGFR proligands on their surfaces, which can be cleaved by metalloprotease and subsequently bind to EGFR resulting in mucin production. We hypothesize that TNF-alpha-converting enzyme (TACE) is activated by cigarette smoke, resulting in increased shedding of EGFR proligand, leading to EGFR phosphorylation and mucin induction in human airway epithelial (NCI-H292) cells. Here we show that cigarette smoke increases MUC5AC production in NCI-H292 cells, an effect that is prevented by an EGFR-neutralizing antibody and by specific knockdown of transforming growth factor-alpha (TGF-alpha) using small interfering RNA (siRNA) for TGF-alpha, implicating TGF-alpha-dependent EGFR activation in the responses. Cigarette smoke increases TGF-alpha shedding, EGFR phosphorylation, and mucin production, which are prevented by metalloprotease inhibitors (GM-6001 and TNF-alpha protease inhibitor-1) and by specific knockdown of TACE with TACE siRNA, implicating TACE in smoking-induced responses. Furthermore, pretreatment with antioxidants prevents smoking-induced TGF-alpha shedding and mucin production, suggesting that reactive oxygen species is involved in TACE activation. These results implicate TACE in smoking-induced mucin overproduction via the TACE-proligand-EGFR signal pathway in NCI-H292 cells. (+info)
A study of MECT1-MAML2 in mucoepidermoid carcinoma and Warthin's tumor of salivary glands.
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The t(11;19)(q21;p13) chromosomal translocation has been described in two distinct types of salivary gland neoplasms: mucoepidermoid carcinoma (MEC) and Warthin's tumor (WT). Since this translocation has been recently shown to generate a MECT1-MAML2 fusion gene, we evaluated 10 primary MEC and seven primary WT to further define the molecular association of these two entities using cytogenetic, as well as in situ hybridization (ISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses directed against the fusion gene. A karyotype was established in all neoplasms except for two MEC cases. Of the eight karyotyped MECs, five showed the t(11;19)(q21;p13), two had a normal karyotype, and one case presented a -Y and +X. Three of the WT revealed a normal karyotype and four had several abnormalities which did not involve chromosomes 11 and 19. ISH analysis performed in cytogenetic suspension and/or in tumor paraffin sections demonstrated MAML2 rearrangement in 7 of 10 cases of MEC: all five cases with t(11;19), one case with normal karyotype, and one unkaryotyped case. RT-PCR analysis confirmed the expression of the MECT1-MAML2 gene in all MEC cases that were positive by ISH analysis. Neither the t(11;19) nor MECT1-MAML2 was detected in any case of WT, nor in control samples from polymorphous low-grade adenocarcinoma, acinic cell carcinoma, or normal parotid gland tissue. We have demonstrated that ISH and RT-PCR are sensitive methods for detecting MECT1-MAML2 in MEC. In contrast, we did not detect the t(11;19) nor MECT1-MAML2 expression in seven cases of WT. (+info)
Exaggerated IL-8 and IL-6 responses to TNF-alpha by parainfluenza virus type 4-infected NCI-H292 cells.
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Respiratory viruses induce and potentiate airway inflammation, which is related to the induction of proinflammatory mediators such as interleukin (IL)-8 and IL-6. Here we report on mechanisms implicated in IL-8 and IL-6 production by airway epithelium-like NCI-H292 cells exposed to parainfluenza virus type 4a (PIV-4). PIV-4 readily infected NCI-H292 cells as reflected by intracellular PIV-4 antigen expression. PIV-4 infection triggered a biphasic IL-8 and IL-6 mRNA response. Transient transfection with truncated and mutated promoter constructs identified NF-kappaB and activator protein (AP)-1, and CCAAT-enhancer binding protein (C/EBP) as the relevant transcription factors for PIV-4-induced IL-8 and IL-6 gene transcription, respectively. An increase of DNA-binding activities for NF-kappaB and C/EBP paralleled the induction of the first and second IL-8 and IL-6 mRNA peaks, whereas the onset of AP-1 paralleled the first IL-8 mRNA peak only. The second mRNA peak, apparently dependent on viral replication, coincided also with a marked reduction of IL-8 and IL-6 mRNA degradation. Importantly, cells at the time of the reduced mRNA degradation displayed an exaggerated IL-8 and IL-6 protein production to a secondary stimulus, as exemplified by steeper dose-response curves to TNF-alpha. Thus PIV-4 infection enhances epithelial IL-8 and IL-6 production by transcriptional and posttranscriptional mechanisms. The previously unrecognized phase of reduced IL-8 and IL-6 mRNA degradation and the concurrent amplified epithelial IL-8 and IL-6 responses may play an important role in virus-induced potentiation of airway inflammation. (+info)
Mucoepidermoid carcinoma of the thymus: a case report.
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Mucoepidermoid carcinoma of the thymus is an extremely rare malignant mediastinal neoplasm, and to our knowledge, only 13 cases have been reported. We report a case of mucoepidermoid carcinoma of the thymus that was seen in a 53-yr-old man with right chest pain. Chest CT scan showed a huge, cystic mass having a focal solid portion with direct invasion of the adjacent anterior chest wall and pericardium in the anterior mediastinum. Mucoepidermoid carcinoma of the thymus should be included in the differential diagnosis for masses of the anterior mediastinum associated with extensive cystic changes, although the carcinoma is exceedingly rare. (+info)