20 results on '"Carcinoma, Mucoepidermoid drug therapy"'
Search Results
2. [Long-term follow-up of a multimodally managed pulmonary mucoepidermoid carcinoma in a cat].
- Author
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Lamolet R, Manassero M, Reyes-Gomez E, and Béguin J
- Subjects
- Animals, Antineoplastic Agents therapeutic use, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid pathology, Carcinoma, Mucoepidermoid surgery, Cat Diseases pathology, Cats, Female, Follow-Up Studies, Lung pathology, Lung surgery, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Lung Neoplasms surgery, Treatment Outcome, Carcinoma, Mucoepidermoid veterinary, Cat Diseases drug therapy, Cat Diseases surgery, Combined Modality Therapy veterinary, Lung Neoplasms veterinary, Mitoxantrone therapeutic use
- Abstract
Introduction: The present case describes the treatment of a mucoepidermoid carcinoma in a 13-year-old female sterilized European domestic cat, using lung lobectomy and -accompanying mitoxantrone chemotherapy. Six, 14, 19 and 27 months after the initial treatment tomodensitometric and radiographic examinations showed no abnormalities. However, the cat had to be euthanized 27 months after the lung lobectomy due to a soft tissue sarcoma in the interscapular area.
- Published
- 2021
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3. Challenges in diagnosis of pulmonary mucoepidermoid carcinoma: A case report.
- Author
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Zhou X, Zhang M, Yan X, Zhong Y, Li S, Liu J, Peng L, and Gan X
- Subjects
- Adult, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Bronchoscopy, Carcinoma, Mucoepidermoid drug therapy, Female, Humans, Lung Neoplasms drug therapy, Carcinoma, Mucoepidermoid diagnosis, Carcinoma, Mucoepidermoid pathology, Lung Neoplasms diagnosis, Lung Neoplasms pathology
- Abstract
Rationale: Pulmonary mucoepidermoid carcinomas (PMECs) of the lung are rare malignant tumors. Despite progresses in examinations, the tumor represents a diagnostic challenge for pathologists and clinical physicians. Here, we present a patient who was eventually diagnosed with PMEC by the bronchoscopic examinations conducted three times., Patient Concerns: We present the case of a 41-year-old female who was initially diagnosed with pulmonary pleomorphic adenoma (PPA) with a 68 × 82 mm mass and nodules in her lung and eventually diagnosed with PMEC., Diagnoses: Based on histopathology, immunohistology, and imaging studies, the patient was diagnosed with PMEC (pT4N2M1)., Interventions: The patient received first-line systemic chemotherapy regime (gemcitabine combined with carboplatin)., Outcomes: The patient received 2 cycles of chemotherapy. Based on the response evaluation criteria in solid tumor, she achieved partial response, and the mass was distinctly decreased from 68 × 22 mm to 41 × 17 mm., Lessons: This case presents a rare PMEC overlapping with PPA, based on histological findings, suggesting that besides imaging studies and laboratory examinations, multiple biopsies and ThinPrep cytology tests are necessary to obtain an accurate diagnosis. The patient showed positive response to chemotherapy.
- Published
- 2019
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4. Mycoplasma hyorhinis reduces sensitivity of human lung carcinoma cells to Nutlin-3 and promotes their malignant phenotype.
- Author
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Boyarskikh UA, Shadrina AS, Smetanina MA, Tsepilov YA, Oscorbin IP, Kozlov VV, Kel AE, and Filipenko ML
- Subjects
- Adult, Aged, Aged, 80 and over, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid genetics, Carcinoma, Mucoepidermoid metabolism, Carcinoma, Mucoepidermoid microbiology, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Carcinoma, Non-Small-Cell Lung metabolism, Carcinoma, Non-Small-Cell Lung microbiology, Cell Line, Tumor, Drug Resistance, Neoplasm, Female, Gene Expression drug effects, Humans, Lung Neoplasms genetics, Lung Neoplasms metabolism, Male, Middle Aged, Mycoplasma Infections metabolism, Mycoplasma Infections microbiology, Signal Transduction, Transcriptome, Young Adult, Imidazoles pharmacology, Lung Neoplasms drug therapy, Lung Neoplasms microbiology, Mycoplasma Infections physiopathology, Mycoplasma hyorhinis physiology, Piperazines pharmacology
- Abstract
Purpose: MDM2 inhibitors are promising anticancer agents that induce cell cycle arrest and tumor cells death via p53 reactivation. We examined the influence of Mycoplasma hyorhinis infection on sensitivity of human lung carcinoma cells NCI-H292 to MDM2 inhibitor Nutlin-3. In order to unveil possible mechanisms underlying the revealed effect, we investigated gene expression changes and signal transduction networks activated in NCI-H292 cells in response to mycoplasma infection., Methods: Sensitivity of NCI-Н292 cells to Nutlin-3 was estimated by resazurin-based cell viability assay. Genome-wide transcriptional profiles of NCI-H292 and NCI-Н292
Myc.h cell lines were determined using Illumina Human HT-12 v3 Expression BeadChip. Search for key transcription factors and key node molecules was performed using the geneXplain platform. Ability for anchorage-independent growth was tested by soft agar colony formation assay., Results: NCI-Н292Myc.h cells were shown to be 1.5- and 5.2-fold more resistant to killing by Nutlin-3 at concentrations of 15 and 30 µM than uninfected NCI-Н292 cells (P < 0.05 and P < 0.001, respectively). Transcriptome analysis revealed differential expression of multiple genes involved in cancer progression and metastasis as well as epithelial-mesenchymal transition (EMT). Moreover, we have shown experimentally that NCI-Н292Myc.h cells were more capable of growing and dividing without binding to a substrate. The most likely mechanism explaining the observed changes was found to be TLR4- and IL-1b-mediated activation of NF-κB pathway., Conclusions: Our results provide evidence that mycoplasma infection is an important factor modulating the effect of MDM2 inhibitors on cancer cells and is able to induce EMT-related changes.- Published
- 2018
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5. Poly-L-Arginine Induces Apoptosis of NCI-H292 Cells via ERK1/2 Signaling Pathway.
- Author
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Wang YN, Zhang LL, Fan XY, Wu SS, and Zhang SQ
- Subjects
- Alveolar Epithelial Cells drug effects, Alveolar Epithelial Cells enzymology, Alveolar Epithelial Cells metabolism, Carcinoma, Mucoepidermoid enzymology, Carcinoma, Mucoepidermoid metabolism, Carcinoma, Mucoepidermoid pathology, Caspase 3 metabolism, Cell Line, Tumor, Dose-Response Relationship, Drug, Humans, Lung Neoplasms enzymology, Lung Neoplasms metabolism, Lung Neoplasms pathology, Mitogen-Activated Protein Kinase 1 antagonists & inhibitors, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 antagonists & inhibitors, Mitogen-Activated Protein Kinase 3 metabolism, Phosphorylation, Proto-Oncogene Proteins c-bcl-2 metabolism, Apoptosis drug effects, Carcinoma, Mucoepidermoid drug therapy, Lung Neoplasms drug therapy, MAP Kinase Signaling System drug effects, Peptides pharmacology
- Abstract
Cationic protein is a cytotoxic protein secreted by eosinophils and takes part in the damage of airway epithelium in asthma. Poly-L-arginine (PLA), a synthetic cationic protein, is widely used to mimic the biological function of the natural cationic protein in vitro. Previous studies demonstrated the damage of the airway epithelial cells by cationic protein, but the molecular mechanism is unclear. The purpose of this study aimed at exploring whether PLA could induce apoptosis of human airway epithelial cells (NCI-H292) and the underlying mechanism. Methods . The morphology of apoptotic cells was observed by transmission electron microscopy. The rate of apoptosis was analyzed by flow cytometry (FCM). The expressions of the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), Bcl-2/Bax, and cleaved caspase-3 were assessed by western blot. Results . PLA can induce apoptosis in NCI-H292 cells in a concentration-dependent manner. Moreover, the phosphorylation of the ERK1/2 and the unbalance of Bcl2/Bax, as well as the activation of caspase-3, were involved in the PLA-induced apoptosis. Conclusions . PLA can induce the apoptosis in NCI-H292 cells, and this process at least involved the ERK1/2 and mitochondrial pathway. The results could have some indications in revealing the apoptotic damage of the airway epithelial cells. Besides, inhibition of cationic protein-induced apoptotic death in airway epithelial cells could be considered as a potential target of anti-injury or antiremodeling in asthmatics.
- Published
- 2018
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6. Clinicopathological characteristics and molecular analysis of primary pulmonary mucoepidermoid carcinoma: Case report and literature review.
- Author
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Li X, Guo Z, Liu J, Wei S, Ren D, Chen G, Xu S, and Chen J
- Subjects
- Aged, Carboplatin administration & dosage, Carcinoma, Mucoepidermoid pathology, Carcinoma, Mucoepidermoid surgery, Disease-Free Survival, Humans, Lung Neoplasms pathology, Lung Neoplasms surgery, Male, Neoplasm Recurrence, Local pathology, Neoplasm Recurrence, Local surgery, Paclitaxel administration & dosage, Treatment Outcome, Carcinoma, Mucoepidermoid drug therapy, Lung Neoplasms drug therapy, Neoplasm Recurrence, Local drug therapy
- Abstract
Primary pulmonary mucoepidermoid carcinoma (PMEC) is extremely rare. Herein, we report a case of a 71-year-old male patient with high-grade PMEC involving the right upper lobe that was successfully resected via lobectomy. As a result of invasion into the pleural and paratracheal lymph nodes, four cycles of adjuvant chemotherapy with paclitaxel and carboplatin were administered. There were no signs of relapse during 10 months of follow-up. Furthermore, we reviewed the literature and summarized the surgical approaches, prognostic factors, and underlying genetic mechanisms of PMEC, which will benefit clinical treatment., (© 2017 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.)
- Published
- 2018
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7. Clinical trial of nintedanib in patients with recurrent or metastatic salivary gland cancer of the head and neck: A multicenter phase 2 study (Korean Cancer Study Group HN14-01).
- Author
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Kim Y, Lee SJ, Lee JY, Lee SH, Sun JM, Park K, An HJ, Cho JY, Kang EJ, Lee HY, Kim J, Keam B, Kim HR, Lee KE, Choi MY, Lee KH, and Ahn MJ
- Subjects
- Adenocarcinoma secondary, Adult, Aged, Bone Neoplasms drug therapy, Bone Neoplasms secondary, Carcinoma, Adenoid Cystic secondary, Carcinoma, Mucoepidermoid secondary, Early Termination of Clinical Trials, Female, Head and Neck Neoplasms drug therapy, Head and Neck Neoplasms pathology, Humans, Liver Neoplasms drug therapy, Liver Neoplasms secondary, Lung Neoplasms secondary, Male, Middle Aged, Neoplasm Recurrence, Local pathology, Palliative Care, Pleural Neoplasms drug therapy, Pleural Neoplasms secondary, Republic of Korea, Salivary Gland Neoplasms pathology, Treatment Failure, Adenocarcinoma drug therapy, Antineoplastic Agents therapeutic use, Carcinoma, Adenoid Cystic drug therapy, Carcinoma, Mucoepidermoid drug therapy, Indoles therapeutic use, Lung Neoplasms drug therapy, Neoplasm Recurrence, Local drug therapy, Salivary Gland Neoplasms drug therapy
- Abstract
Background: Salivary gland cancers (SGCs) are uncommon and account for less than 5% of all head and neck cancers, but they are histologically heterogeneous. No specific therapy, including targeted agents, has consistently improved clinical outcomes in recurrent/metastatic SGC. Recent studies suggest that vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) play important roles in SGC. Nintedanib is a potent small-molecule, triple-receptor tyrosine kinase inhibitor (VEGFR1, VEGFR2, and VEGFR3; fibroblast growth factor receptor 1 [FGFR1], FGFR2, and FGFR3; and PDGFRα and PDGFRß). This study sought to determine the antitumor activity of nintedanib in patients with recurrent or metastatic SGC., Methods: This open-label, multicenter, phase 2, single-arm study was conducted at 11 hospitals in South Korea. Patients with pathologically confirmed recurrent and/or metastatic SGC for whom at least 1 line of systemic chemotherapy had failed were enrolled. Nintedanib was given orally at 200 mg twice a day until disease progression or unacceptable toxicity. The primary endpoint was the response rate. The secondary endpoints were progression-free survival, overall survival, toxicity, and the disease-control rate. The Simon 2-stage minimax design was used., Results: The median age of the patients was 54 years, 60% were female, and 95% had an Eastern Cooperative Oncology Group performance status of 0 or 1. The majority of the patients had adenoid cystic carcinoma (65%), and 40% received at least 2 prior rounds of chemotherapy. After 20 patients were enrolled, the study was stopped because no responders were observed at stage I. There were no partial responses, but the disease-control rate was 75% (15 of 20). The median duration of stable disease was 8.2 months (range, 1.76-12.36 months). At the time of the data cutoff, with a median follow-up of 9.5 months, the median overall survival had not been reached, and the progression-free survival rate at 6 months was 60% (95% confidence interval, 0.34-0.79). Grade 3 adverse events included liver enzyme elevation (25%) and nausea/vomiting (5%). Four patients who required a dose reduction because of a grade 3 liver enzyme elevation showed no further grade 3 events., Conclusions: Single-agent nintedanib did not yield a partial response but did achieve a 75% disease-control rate with long-term stabilization in SGC patients. Because of the high rate and long duration of disease control with a good safety profile, further investigation is warranted. Cancer 2017;123:1958-1964. © 2017 American Cancer Society., (© 2017 American Cancer Society.)
- Published
- 2017
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8. Pathological complete response to gefitinib in a 10-year-old boy with EGFR-negative pulmonary mucoepidermoid carcinoma: a case report and literature review.
- Author
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Li S, Zhang Z, Tang H, He Z, Gao Y, Ma W, Chang Y, Wei B, Ma J, Liu K, Ma Z, and Wang Q
- Subjects
- Carcinoma, Mucoepidermoid diagnostic imaging, Carcinoma, Mucoepidermoid surgery, Child, DNA-Binding Proteins genetics, ErbB Receptors antagonists & inhibitors, Gefitinib, Humans, Lung Neoplasms pathology, Lung Neoplasms surgery, Male, Mutation, Neoadjuvant Therapy methods, Neoplasm Staging, Oncogene Proteins, Fusion genetics, Protein Kinase Inhibitors therapeutic use, Quinazolines administration & dosage, Tomography, X-Ray Computed methods, Transcription Factors, Treatment Outcome, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid genetics, ErbB Receptors genetics, Lung Neoplasms drug therapy, Quinazolines pharmacology
- Abstract
Background and Aims: Pulmonary Mucoepidermoid carcinoma (MEC) accounts for 0.1-0.2% of all lung cancer. It occurred in the 3-78 years old, and 50% patients younger than 30. MEC has no standard treatment, but recently reports indicated MEC without epidermal growth factor receptor (EGFR) mutations sensitive to gefitinib., Objectives: To explore a new standard treatment strategy for MEC, after reviewed literature related to MEC, we used Gefitinib to treatment a patient with EGFR-negative MEC, and observe its effects., Methods: 10-year-old boy was diagnosed with low-grade MEC by bronchial lung biopsy, EGFR gene mutation test was negative. Gefitinib was administered as neoadjuvant therapy at 125 mg daily., Results: The patient underwent right middle lobe, lower lobe resection and mediastinal lymph node dissection. After surgery, the patient had gained weight (5 kg) after 18 days of gefitinib therapy. A CT scan of the chest 1 month after surgical resection showed no recurrence, and followed for 22 months after treatment without tumour recurrence, suggesting that the patient was completely cured., Conclusion: Gefitinib has potential to become a standard treatment for pulmonary MEC patients, including pediatric patients. However, the mechanisms need further investigation., (© 2015 John Wiley & Sons Ltd.)
- Published
- 2017
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9. Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of replicative senescence.
- Author
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Marino Gammazza A, Campanella C, Barone R, Caruso Bavisotto C, Gorska M, Wozniak M, Carini F, Cappello F, D'Anneo A, Lauricella M, Zummo G, Conway de Macario E, Macario AJ, and Di Felice V
- Subjects
- Acetylation, Apoptosis drug effects, Carcinoma, Mucoepidermoid genetics, Carcinoma, Mucoepidermoid metabolism, Carcinoma, Mucoepidermoid pathology, Cell Line, Tumor, Cell Survival drug effects, Chaperonin 60 genetics, Chaperonins metabolism, Cyclin-Dependent Kinase Inhibitor p21 metabolism, Dose-Response Relationship, Drug, G2 Phase Cell Cycle Checkpoints drug effects, Histones metabolism, Humans, Lung Neoplasms genetics, Lung Neoplasms metabolism, Lung Neoplasms pathology, Mitochondrial Proteins genetics, Protein Binding, Proteolysis, Signal Transduction drug effects, Ubiquitination, Antibiotics, Antineoplastic pharmacology, Carcinoma, Mucoepidermoid drug therapy, Cell Proliferation drug effects, Cellular Senescence drug effects, Chaperonin 60 metabolism, Doxorubicin pharmacology, Lung Neoplasms drug therapy, Mitochondrial Proteins metabolism, Protein Processing, Post-Translational drug effects, Tumor Suppressor Protein p53 metabolism
- Abstract
The chaperone Hsp60 is pro-carcinogenic in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not yet known whether doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of Hsp60. We found a doxorubicin dose-dependent viability reduction in a human lung mucoepidermoid cell line that was paralleled by the appearance of cell senescence markers. Concomitantly, intracellular Hsp60 levels decreased while its acetylation levels increased. The data suggest that Hsp60 acetylation interferes with the formation of the Hsp60/p53 complex and/or promote its dissociation, both causing an increase in the levels of free p53, which can then activate the p53-dependent pathway toward cell senescence. On the other hand, acetylated Hsp60 is ubiquitinated and degraded and, thus, the anti-apoptotic effect of the chaperonin is abolished with subsequent tumor cell death. Our findings could help in the elucidation of the molecular mechanisms by which doxorubicin counteracts carcinogenesis and, consequently, it would open new roads for the development of cancer treatment protocols targeting Hsp60., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2017
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10. A case of pulmonary mucoepidermoid carcinoma responding to carboplatin and paclitaxel.
- Author
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Sonobe S, Inoue K, Tachibana S, Shiojiri M, Maeda T, Nakanishi N, Moritaka T, Ikura Y, and Kawaguchi T
- Subjects
- Bronchial Neoplasms pathology, Carboplatin administration & dosage, Carcinoma, Mucoepidermoid secondary, Disease-Free Survival, Humans, Lung Neoplasms secondary, Male, Middle Aged, Paclitaxel administration & dosage, Tracheal Neoplasms pathology, Treatment Outcome, Antineoplastic Agents therapeutic use, Bronchial Neoplasms drug therapy, Carcinoma, Mucoepidermoid drug therapy, Lung Neoplasms drug therapy, Tracheal Neoplasms drug therapy
- Abstract
A 59-year-old man was admitted to our hospital with dyspnea and cough. A large polypoid tumor was observed in the lower trachea and bronchoscopic polypectomy was performed using a snare to relieve symptoms. The tumor was diagnosed as a high grade mucoepidermoid carcinoma mainly by the histology of piecemeal specimens obtained by bronchoscopic resection. The primary lesion involved the trachea and the main bronchus, and there were multiple metastases in the lung. The patient was treated with the combination of carboplatin and paclitaxel. After four cycles of chemotherapy, the tumors were significantly reduced. He remains well without evidence of tumor progression for 25 months. This case suggests that the combination chemotherapy of carboplatin and paclitaxel can be an option for treatment of pulmonary mucoepidermoid carcinoma.
- Published
- 2014
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11. Erlotinib in metastatic bronchopulmonary mucoepidermoid carcinoma.
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Lee KW, Chan AB, Lo AW, and Lam KC
- Subjects
- Adult, Carcinoma, Mucoepidermoid secondary, Carcinoma, Mucoepidermoid surgery, Erlotinib Hydrochloride, Humans, Lung Neoplasms secondary, Male, Mediastinal Neoplasms surgery, Pleural Neoplasms drug therapy, Pleural Neoplasms secondary, Protein Kinase Inhibitors adverse effects, Quinazolines adverse effects, Splenic Neoplasms drug therapy, Splenic Neoplasms secondary, Carcinoma, Mucoepidermoid drug therapy, Lung Neoplasms drug therapy, Mediastinal Neoplasms pathology, Protein Kinase Inhibitors therapeutic use, Quinazolines therapeutic use
- Published
- 2011
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12. B-cell lymphoma-2 over-expression protects δ-elemene-induced apoptosis in human lung carcinoma mucoepidermoid cells via a nuclear factor kappa B-related pathway.
- Author
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Xie CY, Yang W, Ying J, Ni QC, Pan XD, Dong JH, Li K, and Wang XS
- Subjects
- Antineoplastic Agents, Phytogenic pharmacology, Antineoplastic Agents, Phytogenic therapeutic use, Carcinoma, Mucoepidermoid drug therapy, Cell Line, Tumor, DNA Fragmentation, Drugs, Chinese Herbal pharmacology, Drugs, Chinese Herbal therapeutic use, Flow Cytometry, Humans, Lung Neoplasms drug therapy, Nitric Oxide Synthase Type II metabolism, Phytotherapy, Sesquiterpenes therapeutic use, Signal Transduction drug effects, bcl-X Protein metabolism, p38 Mitogen-Activated Protein Kinases metabolism, Apoptosis drug effects, Carcinoma, Mucoepidermoid metabolism, Curcuma chemistry, Lung Neoplasms metabolism, NF-kappa B metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Sesquiterpenes pharmacology
- Abstract
δ-Elemene, an antitumor component, is a chemical compound isolated from Curcuma wenyujin, a Chinese traditional herb. We examined whether δ-elemene could affect apoptosis in human lung carcinoma mucoepidermoid NCI-H292 cells, and test whether and how the over-expression of B-cell lymphoma-2 (Bcl-2) and B-cell lymphoma extra large (Bcl-xL) could off-set the effect of δ-elemene on cell growth. The result demonstrated that δ-elemene significantly induced apoptosis of NCI-H292, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, DNA fragmentation measurement, Annexin V (AnV) binding of externalized phosphatidylserine and the mitochondrial probe JC-1 using flow cytometry. Treatment of NCI-H292 with δ-elemene increased both p38 mitogen-activated protein kinase (MAPK) and inducible nitric oxide synthese (iNOS) levels, suggesting these two molecules maybe relate to the apoptotic effect of δ-elemene. The cells with Bcl-2 or Bcl-xL over-expression showed an elevation of nuclear factor kappa B (NF-kappa B) activity, accompanying a significant reduction of δ-elemene-induced apoptosis. Furthermore, inhibition of NF-kappa B by IkBαSR, which is a powerful inhibitor of NF-kappa B, restored the ability of δ-elemene to induce apoptosis in the cells transfected with Bcl-2. These data strongly indicated that the apoptotic effect of δ-elemene on NCI-H292 was closely associated with the activity of NF-kappa B, which was up-regulated by Bcl-2 and Bcl-xL. In conclusion, δ-elemene induced apoptosis in NCI-H292 cells. The apoptotic effect of δ-elemene could be significantly offset by over-expression of either Bcl-2 or Bcl-xL. Bcl-2 and Bcl-xL were able to increase the activity of NF-kappa B, which was a known anti-apoptotic molecule in human lung cancer cells.
- Published
- 2011
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13. Cavitary mucoepidermoid carcinoma of lung with metastases in skeletal muscles as presenting features: a case report and review of the literature.
- Author
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Singh A, Pandey KC, and Pant NK
- Subjects
- Antineoplastic Combined Chemotherapy Protocols therapeutic use, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid pathology, Humans, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Male, Middle Aged, Muscle Neoplasms pathology, Tomography, X-Ray Computed, Carcinoma, Mucoepidermoid diagnosis, Lung Neoplasms diagnosis, Muscle Neoplasms secondary, Muscle, Skeletal pathology
- Abstract
Mucoepidermoid carcinomas (MECs) of lung are rare neoplasms originating in bronchial submucosal glands and comprising 0.1-0.2% of primary lung cancers. MECs, the most common malignancy in salivary glands, were earlier thought to occur only in salivary glands. Later studies showed that they can arise as a primary in bronchus, esophagus, lacrimal glands, pancreas, thymus and thyroid gland. Initially described as a benign adenoma, it is now considered to be a malignant epithelial tumor. There have been reports of metastases to regional lymph nodes, other parts of the lung and distant organs. Cavitary lesion in MEC of lung is rare. Here, we report a case of MEC of lung with metastases to skeletal muscles of thigh and arm. To the best of our knowledge, this is the only case of MEC of lung presenting with such unusual pattern of metastasis as presenting feature with almost no symptoms of primary lesion.
- Published
- 2010
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14. Mucoepidermoid carcinoma of the lung, response to EGFR inhibitors, EGFR and K-RAS mutations, and differential diagnosis.
- Author
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Rossi G, Sartori G, Cavazza A, and Tamberi S
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- Aged, Carcinoma, Mucoepidermoid diagnosis, Diagnosis, Differential, Epithelium metabolism, Female, Humans, Keratins metabolism, Lung Neoplasms diagnosis, Mucin 5AC metabolism, Mucins metabolism, Mutation, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid genetics, ErbB Receptors antagonists & inhibitors, ErbB Receptors genetics, Genes, ras, Lung Neoplasms drug therapy, Lung Neoplasms genetics
- Abstract
Mucoepidermoid carcinoma (MEC) of the lung needs to be carefully distinguished from other lung tumors with similar features, particularly from adenosquamous carcinoma, this latter tumor frequently showing EGFR mutations. In contrast with the data reported by Han et al in the last July issue of Lung Cancer, neither EGFR nor K-RAS mutations were observed in MEC from caucasian patients.
- Published
- 2009
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15. [Clinical study of lung mucoepidermoid tumors].
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Gao Y, Chen SX, and Luo WJ
- Subjects
- Adolescent, Adult, Bronchoscopy, Carcinoma, Mucoepidermoid pathology, Carcinoma, Mucoepidermoid surgery, Female, Follow-Up Studies, Humans, Lung Neoplasms pathology, Lung Neoplasms surgery, Male, Middle Aged, Young Adult, Carcinoma, Mucoepidermoid drug therapy, Lung Neoplasms diagnosis
- Abstract
Objective: To investigate clinical and pathological characteristics of lung mucoepidermoid tumors and summarize methods for diagnosing and treating it., Methods: Records of a total of 2,751 consecutive patients with lung cancer were reviewed and 10 of whom with mucoepidermoid tumors were identified. Chest radiographs, computer tomographs, and bronchoscopes were performed to all of them. Eight of them underwent thoracotomy and some also received chemotherapy and/or radiotherapy. One patient received Chinese herb therapy only while another did not receive any therapy., Results: Pathological examination showed that the 10 patients had low-grade mucoepidermoid tumors. All patients were alive. Seven patients who received thoracotomy did not recur. One patient whose tumor was located in trachea recurred 5.2 years after the operation., Conclusion: Bronchoscope can play an important role in the process of diagnosis. Pathological staging is vital for prognosis. Lung mucoepidermoid tumors should be treated with complete surgical resection with lymph node sampling and dissection and close follow-up.
- Published
- 2008
16. Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells.
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Campanella C, Bucchieri F, Ardizzone NM, Marino Gammazza A, Montalbano A, Ribbene A, Di Felice V, Bellafiore M, David S, Rappa F, Marasà M, Peri G, Farina F, Czarnecka AM, Conway de Macario E, Macario AJ, Zummo G, and Cappello F
- Subjects
- Apoptosis drug effects, Blotting, Western, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid pathology, Cell Line, Tumor, Cell Survival drug effects, Comet Assay, DNA drug effects, DNA Damage, Formazans metabolism, Gene Expression drug effects, Humans, Hydrogen Peroxide pharmacology, Immunohistochemistry, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Tetrazolium Salts metabolism, Trypan Blue metabolism, Tumor Suppressor Protein p53 biosynthesis, Tumor Suppressor Protein p53 genetics, Carcinoma, Mucoepidermoid metabolism, Caspase 3 metabolism, Chaperonin 60 metabolism, Lung Neoplasms metabolism, Oxidative Stress
- Abstract
Hsp60, a mitochondrial chaperonin highly conserved during evolution, has been found elevated in the cytosol of cancer cells, both in vivo and in vitro, but its role in determining apoptosis during oxidative stress (OS) has not yet been fully elucidated. The aim of the present work was to study the effects of OS on Hsp60 levels and its interactions with procaspase- 3 (p-C3) and p53 in tumor cells. NCI-H292 (mucoepidermoid carcinoma) cells were exposed to various concentrations of hydrogen peroxide (H2O2) for 24 hours. Cell viability was determined by Trypan blue and MTT assays. DNA damage was assessed by the Comet assay, and apoptosis was measured by the AnnexinV cytofluorimetric test. Exposure to increasing concentrations of H2O2 resulted in a reduction of cell viability, DNA damage, and early apoptotic phenomena. Hsp60, p-C3, p53, and p21 were assessed by Western blotting and immunocytochemistry before and after OS. Hsp60 and p-C3 were present before and after OS induction. Immunoprecipitation experiments showed an Hsp60/p-C3 complex before OS that persisted after it, while an Hsp60/p53 complex was not detected in either condition. The presence of wild type (wt) p53 was confirmed by RT-PCR, and p21 detection suggested p53 activation after OS. We postulate that, although OS may induce early apoptosis in NCI-H292 cells, Hsp60 exerts an anti-apoptotic effect in these cells and, by extension, it may do so in other cancer cells.
- Published
- 2008
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17. Mucoepidermoid carcinoma of lung: potential target of EGFR-directed treatment.
- Author
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Han SW, Kim HP, Jeon YK, Oh DY, Lee SH, Kim DW, Im SA, Chung DH, Heo DS, Bang YJ, and Kim TY
- Subjects
- Adult, Antineoplastic Agents therapeutic use, Carcinoma, Mucoepidermoid genetics, Carcinoma, Mucoepidermoid metabolism, ErbB Receptors biosynthesis, ErbB Receptors genetics, Female, Gefitinib, Humans, Lung Neoplasms genetics, Lung Neoplasms metabolism, Male, Middle Aged, Mutation, Quinazolines therapeutic use, Carcinoma, Mucoepidermoid drug therapy, ErbB Receptors antagonists & inhibitors, Lung Neoplasms drug therapy, Protein Kinase Inhibitors therapeutic use
- Abstract
Mucoepidermoid carcinoma (MEC) of lung is a rare malignancy of lung which originates from minor salivary glands of tracheobronchial tree. EGFR targeted therapy by inhibition of EGFR activation with the specific tyrosine kinase inhibitors (TKIs) has shown meaningful anti-tumor activity in patients with EGFR TK mutation and/or amplification, or in patients with adenocarcinoma. In the present study, we find that MEC has EGFR mutation in 40% (2 out of 5) of cases, and all mutations are L858R mutation. In addition, we also observed that a MEC patient well-responded to EGFR TKI in the absence of EGFR mutation or amplification. These data indicate for the first time that MEC of lung is another potential target of EGFR inhibitor, and more extended clinical investigation is warranted.
- Published
- 2008
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18. The synthetic retinoid CD437 selectively induces apoptosis in human lung cancer cells while sparing normal human lung epithelial cells.
- Author
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Sun SY, Yue P, Chen X, Hong WK, and Lotan R
- Subjects
- Apoptosis genetics, Carcinoma, Large Cell drug therapy, Carcinoma, Large Cell metabolism, Carcinoma, Large Cell pathology, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid metabolism, Carcinoma, Mucoepidermoid pathology, Epithelial Cells cytology, Epithelial Cells drug effects, Epithelial Cells metabolism, Gene Expression Regulation, Gene Expression Regulation, Neoplastic, Humans, Lung cytology, Lung metabolism, Lung Neoplasms metabolism, Lung Neoplasms pathology, Proto-Oncogene Proteins c-bcl-2 biosynthesis, Proto-Oncogene Proteins c-bcl-2 genetics, Tumor Cells, Cultured, Tumor Suppressor Protein p53 physiology, bcl-X Protein, Antineoplastic Agents pharmacology, Apoptosis drug effects, Lung drug effects, Lung Neoplasms drug therapy, Retinoids pharmacology
- Abstract
The synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) induces apoptosis in a variety of cancer cells including lung cancer cells. Our previous studies have demonstrated that cancer cells with wild-type p53 are more sensitive to CD437 than those having mutant p53, although CD437 can induce both p53-dependent and -independent apoptosis. Because normal human lung epithelial cells have wild-type p53, the question arose as to whether they are also sensitive to CD437-induced apoptosis. To address this question, we compared and contrasted the effects of CD437 on apoptosis induction and the expression of several p53-regulated apoptosis-related genes between normal human lung epithelial cells and human lung cancer cells containing wild-type p53. CD437 induced apoptosis as evidenced by apoptotic morphological changes, increased DNA fragmentation, and activation of caspase cascades in two lung cancer cell lines but not in two normal human lung epithelial cells. CD437 selectively increased the p53 protein level and concomitantly induced the expression of several p53-regulated apoptosis-related genes including Bax, Fas, DR4, and DR5 only in the two lung cancer cell lines. Furthermore, the normal lung epithelial cells, which expressed constitutively higher levels of two antiapoptotic decoy receptors DcR1 and DcR2 than lung cancer cells, exhibited an increase in the expression of these receptors after CD437 treatment, whereas no increase was detected in lung cancer cells. These results predict a differential effect of CD437 on tumor and normal cells in vivo and strongly suggest that CD437 may be a useful agent for chemoprevention and/or treatment of human cancer, especially lung cancer.
- Published
- 2002
19. Simvastatin effects on a human lung carcinoma and cholesterol homeostasis of host and non-host mice.
- Author
-
Polo M and de Bravo MG
- Subjects
- Animals, Body Weight drug effects, Carcinoma, Mucoepidermoid metabolism, Enzyme Inhibitors pharmacology, Female, Humans, Lung Neoplasms metabolism, Mice, Mice, Nude, Microsomes, Liver enzymology, Neoplasm Transplantation, Anticholesteremic Agents pharmacology, Carcinoma, Mucoepidermoid drug therapy, Cholesterol metabolism, Hydroxymethylglutaryl CoA Reductases metabolism, Liver enzymology, Lung Neoplasms drug therapy, Simvastatin pharmacology
- Abstract
In order to investigate the effect of a competitive inhibitor of the HMG-CoA reductase on tumor growth and cholesterol homeostasis of host and non-host mice, we maintained a human lung mucoepidermoid carcinoma (HLMC) in nude mice, treating these animals with Simvastatin for 33 days. The drug increased the total activity of hepatic HMG-CoA reductase without affecting the cholesterolemia. Non-treated host animals presented lower serum, tissue and microsomal hepatic cholesterol than non-host animals. These differences disappeared when animals were treated with Simvastatin, though the induction of the reductase activity at mid-dark was higher in non-host than in host animals. Simvastatin produced no significant effects on both final tumor volume and body weight. Synthesis and cholesterol homeostasis restoration induced by liver and tumoral reductase would account for no effect on the HLMC growth after a long treatment with Simvastatin.
- Published
- 2001
- Full Text
- View/download PDF
20. Clinicopathologic study of mucoepidermoid carcinoma of the lung.
- Author
-
Shimizu J, Watanabe Y, Oda M, Morita K, Tsunezuka Y, and Nonomura A
- Subjects
- Adult, Aged, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Carcinoma, Mucoepidermoid drug therapy, Carcinoma, Mucoepidermoid surgery, Chemotherapy, Adjuvant, Female, Humans, Lung Neoplasms drug therapy, Lung Neoplasms surgery, Male, Middle Aged, Neoplasm Staging, Statistics, Nonparametric, Survival Rate, Carcinoma, Mucoepidermoid pathology, Lung Neoplasms pathology
- Abstract
Background: Mucoepidermoid carcinoma is a relatively uncommon form of lung cancer and has generally been viewed as a low grade malignant tumor. The present study was undertaken to establish a clinicopathological characterization of patients with this cancer who were treated surgically at Kanazawa University Hospital., Methods: Between 1973 and 1975, 10 patients with mucoepidermoid carcinoma were surgically treated in our department., Results: The 10-year survival rate after surgery for the central type of carcinoma was 67%, while the 4-year survival rate for the peripheral type was 25%. When the survival rates were analyzed in terms of Conlan's grades, grade 1 cases had a 10-year survival rate of 80%, while the 4-year survival rate for grade 2 and 3 cases was 20%. The four patients who survived 5 years or more following surgery all had a grade 1 central type tumor., Conclusions: These results suggest that mucoepidermoid carcinoma of the lung should not be viewed uniformly as a low grade malignant tumor, but that this tumor can sometimes be highly malignant with a poor prognosis. Since this tumor is often difficult to distinguish from adenosquamous carcinoma, and because accurate distinction between these two types of tumor seems to be essential for establishing a prognosis, there is an urgent need for a valid pathological method for differential diagnosis of mucoepidermoid carcinoma.
- Published
- 1998
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