Sung Il Cho

Granular Cell Tumor on Larynx

Granular cell tumors (GCTs) are uncommon neoplasm. They can originate in any part of the body. The most common sites of origin are in the head and neck, while the larynx is a relatively uncommon location. Patients affected with a laryngeal GCT typically present with persistent hoarseness, stridor, hemoptysis, dysphagia, and otalgia but, the tumor may be asymptomatic. Care must be taken to differentiate this lesion from others due to the presence of pseudo-epitheliomatous hyperplasia which overlies the GCT and may occasionally mimic squamous cell carcinoma. Therefore, a confirmative diagnosis should be made histopathologically and should be supported by immunohistochemical staining. These tumors are treated by complete surgical resection. Examining the complete removal of the tumor through securing a negative free margin is considered to be a consequential procedure. We experienced a 64-yr-old man with a laryngeal granular cell tumor involving the right true vocal cord. He was treated by surgical resection under a fine dissection laryngomicroscope. Here we present this case and a review of literature.

Role of autophagy in cisplatin-induced ototoxicity

OBJECTIVE Hearing loss is a major side effect of cisplatin chemotherapy. Although cell death in cisplatin-induced ototoxicity is primarily caused by apoptosis, the exact mechanism behind the ototoxic effects of cisplatin is not fully understood. Autophagy is generally known as a pro-survival mechanism that protects cells under starvation or stress conditions. However, recent research has reported that autophagy plays a functional role in cell death also. This study aimed to investigate the role of autophagy in cisplatin-induced ototoxicity in an auditory cell line. METHODS Cultured HEI-OC1 cells were exposed to 30 μM cisplatin for 48 h, and cell viability was tested using MTT assays. To evaluate whether autophagy serves to cell death after cisplatin exposure, western blotting and immunofluorescence staining for LC3-II were performed. Markers of two autophagy-related pathways, mTOR and class III PI3K, were also investigated. RESULTS The formation of the autophagic protein LC3-II in response to 30 μM cisplatin increased with time. The early upregulation of autophagy exerted cytoprotective activity via the class III PI3K pathway. But later increase in autophagy induced cell death by suppressing the mTOR pathway. CONCLUSION Our results prove that autophagy could induce cell death during cisplatin-induced ototoxicity, and modulating the autophagic pathway might be another strategy against cisplatin-induced ototoxicity.

Protective effect of silymarin against cisplatin-induced ototoxicity

OBJECTIVES Silymarin is a plant extract with strong antioxidant properties in addition to anti-inflammatory and anticarcinogenic actions. The aim of this study was to investigate the potential preventive effect of silymarin on cisplatin ototoxicity in an auditory cell line, HEI-OC1 cells. METHODS Cultured HEI-OC1 cells were exposed to cisplatin (30 μM) with or without pre-treatment with silymarin (50 μM). Cell viability was evaluated using MTT assay. Hoechst 33258 staining was used to identify cells undergoing apoptosis. Western blot analysis was done to evaluate whether silymarin inhibits cisplatin-induced caspase and PARP activation. Cell-cycle analysis was done by flow cytometry to investigate whether silymarin is capable of protecting cisplatin-induced cell cycle arrest. RESULTS Cell viability significantly increased in cells pretreated with silymarin compared with cells exposed to cisplatin alone. Pre-treatment of silymarin appeared to protect against cisplatin-induced apoptotic features on Hoechst 33258 staining. Cisplatin increased cleaved caspase-3 and PARP on Western blot analysis. However, pre-treatment with silymarin inhibited the expression of cleaved caspase-3 and PARP. Silymarin did attenuate cell cycle arrest and apoptosis in HEI-OC1 cells. CONCLUSIONS Our results demonstrate that silymarin treatment inhibited cisplatin-induced cytotoxicity in the auditory cell line, HEI-OC1. Silymarin may be a potential candidate drug to eliminate cisplatin induced ototoxicity.

Galectin-8 Expression in Laryngeal Squamous Cell Carcinoma

Objectives Despite the ongoing development of treatment protocols for laryngeal squamous cell carcinoma (LSCC), the patients suffering with this malady have shown only a modestly improved outcome. This poor outcome has been attributed to the lack of therapy thats individualized to the tumors biological properties. Various studies have showed that galectin-8 is widely expressed in tumor tissues as well as in normal tissues, and the level of the galectin-8 expression may correlate with the malignancy of human squamous cell carcinoma. The purpose of this study is to evaluate the expression of galectin-8 and to investigate its correlations with the primary stage, the nodal involvement, the clinical stage and the histologic grade of squamous cell carcinoma of the larynx. Methods The paraffin-embedded tissue specimens from 77 patients who were diagnosed as LSCC between 1993 and 2007 were immunohistochemically stained for galectin-8. Results Immunohistochemical analysis showed that a strong positive expression of galectin-8 was correlated with the T-stages, the nodal stages and the clinical stages. However, the histopathologic grades were not correlated with the galectin-8 expression in LSCC. Conclusion The expression of galectin-8 protein can be used as a prognostic factor for patients with LSCC.

Lipoblastoma arising from the submandibular region.

A lipoblastoma is a rare, benign tumor arising from embryonic white fat. The tumors occur primarily in infancy and early childhood and commonly arise from the limbs and the trunk, but neck involvement is extremely rare. Our case arose in a 22-month-old male presenting with a rapidly enlarging soft mass in the right submandibular area. Lipoblastoma was diagnosed by histologic evaluation, the mass was completely removed, and there was no recurrence at 1-year follow-up.

Protective effect of (-)-epigallocatechin-3-gallate against cisplatin-induced ototoxicity

Objective: Ototoxicity due to cisplatin therapy interferes with treatment and often forces a reduction in the dosage, duration and frequency of the cisplatin therapy. (-)-Epigallocatechin-3-gallate is known to have the highest antioxidant potency among all tea catechins. This study aimed to investigate the effect of (-)-epigallocatechin-3-gallate on cisplatin ototoxicity in an auditory cell line: House Ear Institute-Organ of Corti 1 cells. Methods: Cultured House Ear Institute-Organ of Corti 1 cells were exposed to cisplatin with or without pre-treatment with (-)-epigallocatechin-3-gallate. Cell viability was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst 33258 staining was used to identify cells undergoing apoptosis. Western blot analysis was conducted to determine whether (-)-epigallocatechin-3-gallate inhibited cisplatin-induced caspase activation. Intracellular reactive oxygen species production was examined to investigate whether (-)-epigallocatechin-3-gallate was capable of scavenging cisplatin-induced reactive oxygen species accumulation. Results: Cell viability significantly increased in cells pre-treated with (-)-epigallocatechin-3-gallate compared with cells exposed to cisplatin alone. Cisplatin increased cleaved caspase-3 on Western blot analysis; however, pre-treatment with (-)-epigallocatechin-3-gallate inhibited the expression of caspase-3. (-)-Epigallocatechin-3-gallate attenuated reactive oxygen species production and apoptosis in House Ear Institute-Organ of Corti 1 cells. Conclusion: (-)-Epigallocatechin-3-gallate protected against cisplatin cytotoxicity through anti-apoptotic and anti-oxidative effects. Therefore, (-)-epigallocatechin-3-gallate could play a preventive role in cisplatin-induced ototoxicity.

Comparative antibacterial activity of topical antiseptic eardrops against methicillin-resistant Staphylococcus aureus and quinolone-resistant Pseudomonas aeruginosa

OBJECTIVE Aural irrigation using antiseptic solutions can be an effective medical treatment of chronic suppurative otitis media (CSOM) owing to the increasing prevalence of antibiotic-resistant CSOM infections. In the present study, we compared the antimicrobial activities of 100% Burows solution, 50% Burows solution, 2% acetic acid, vinegar with water (1:1), and 4% boric acid solution against methicillin-resistant Staphylococcus aureus (MRSA), methicillin-susceptible S. aureus (MSSA), quinolone-resistant Pseudomonas aeruginosa (QRPA), and quinolone-susceptible P. aeruginosa (QSPA) in vitro. METHODS We examined the antimicrobial activities of five antiseptic solutions against MRSA, MSSA, QRPA, and QSPA. The antimicrobial activities of the solutions were calculated as a percentage of the surviving microorganisms by dividing the viable count in each antiseptic solution with that in control. The time (D10 value) required for each of the five solutions to inactivate 90% of the microorganism population was also investigated. RESULTS Burows solution exhibited the highest antimicrobial activity and the lowest D10 value against MRSA, MSSA, QRPA, and QSPA, followed by 2% acetic acid, vinegar with water (1:1), and 4% boric acid solution. CONCLUSION Our results indicate that Burows solution has the most potent activity against bacteria including antibiotic-resistant strains. Twofold dilution of the solution is recommended to avoid ototoxicity.

Nasal Hemangiopericytoma Causing Oncogenic Osteomalacia

Oncogenic osteomalacia is a rare cause that makes abnormalities of bone metabolism. Our case arose in a 47-year-old woman presenting a nasal mass associated with osteomalacia. We excised the mass carefully. After surgery, it was diagnosed as hemangiopericytoma and her symptoms related with osteomalacia were relieved and biochemical abnormalities were restored to normal range. We report and review a rare case of nasal hemangiopericytoma that caused osteomalacia.

An inflammatory myofibroblastic tumor of the nasal dorsum

Inflammatory myofibroblastic tumor of the nose is an uncommon benign proliferative lesion that clinically mimics a neoplastic process. Our case arose in a 4-year-old girl presenting with a mass in the nasal dorsum. The mass was completely excised without any difficulty under general anesthesia. This tumor is a localized and completely benign lesion. Surgical resection is proper management for this condition.

53BP1 contributes to regulation of autophagic clearance of mitochondria

Autophagy, the primary recycling pathway within cells, plays a critical role in mitochondrial quality control under normal growth conditions and in the cellular response to stress. Here we provide evidence that 53BP1, a DNA damage response protein, is involved in regulating mitochondrial clearance from the cell via a type of autophagy termed mitophagy. We found that when either human or mouse cells were 53BP1-deficient, there was an increase in mitochondrial abnormalities, as observed through staining intensity, aggregation, and increased mass. Moreover, a 53BP1-depleted cell population included an increased number of cells with a high mitochondrial membrane potential (ΔΨm) relative to controls, suggesting that the loss of 53BP1 prevents initiation of mitophagy thereby leading to the accumulation of damaged mitochondria. Indeed, both 53BP1 and the mitophagy-associated protein LC3 translocated to mitochondria in response to damage induced by the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP). The recruitment of parkin, an E3-ubiquitin ligase, to mitochondria in response to CCCP treatment was significantly decreased in 53BP1-deficient cells. And lastly, using p53-deficient H1299 cells, we confirmed that the role of 53BP1 in mitophagy is independent of p53. These data support a model in which 53BP1 plays an important role in modulating mitochondrial homeostasis and in the clearance of damaged mitochondria.