Chemocauterization of Congenital Fistula from the Accessory Parotid Gland

Congenital sialo-cutaneous fistula arising from the accessory parotid gland is extremely rare. Although the fistula tract can be successfully excised after making a skin incision along the skin tension line around the fistula opening, a facial scar inevitably remains. We here report a case of sialo-cutaneous fistula that was treated with chemocauterization with trichloroacetic acid (TCA). TCA cauterization is an easy and effective option for the treatment of congenital fistula from an accessory parotid gland, especially from the aesthetic point of view

Follicular Thyroid Carcinoma Presenting as Bilateral Cheek Masses

Mandibular metastasis of thyroid carcinoma is extremely rare. We present the case of a 46-year-old woman who had bilateral huge cheek masses that had grown rapidly over several years. Intra-oral mucosal tissue biopsy and imaging work-up including computed tomography scan and magnetic resonance imaging were performed and the initial diagnosis was presumed to be central giant cell granuloma. Incidentally detected thyroid lesions were studied with ultra-sonography guided fine needle aspiration and diagnosed as simple benign nodules. Due to continuous oral bleeding and the locally destructive feature of the lesions, we decided to excise the mass surgically. To avoid functional deficit, a stepwise approach was performed: Firstly, the larger left mass was excised and the mandible was reconstructed with a fibular free flap. The final pathologic diagnosis was follicular thyroid cancer. Postoperative I-131 thyroid scan and whole body positron-emissions-tomography were performed. Right side mass was revealed as a thyroid malignancy. Multiple bony metastases were detected. Since further radioactive iodine therapy was required, additional total thyroidectomy and right side mandibulectomy with fibular free flap reconstruction was performed. The patient also underwent high dose radioactive iodine therapy and palliative extra-beam radiotherapy for the metastatic lumbar lesion. Follicular thyroid carcinoma should be considered as a differential diagnosis for mandibular mass lesions

Clinical Manifestations of Recurrent Parotid Pleomorphic Adenoma

Objectives. This study was undertaken to confirm the clinical characteristics of recurrent pleomorphic adenoma (RPA), and to identify those factors that affect the development of malignant transformation (MT) from RPA. Methods. The medical records of 270 patients, who were operated upon for parotid PA, were retrospectively reviewed. The pathologic specimens of a selected series of 23 patients were reviewed for histologic subtype and microscopic multi-nodularity. Results. Mean age of initial operation in RPA without MT (RPA(-MT)) group was significantly lower than that of primary PA group. Mean age of the revision operation in RPA with MT (RPA(+MT)) group was significantly greater than that of RPA(-MT) group. Mean interval from operation to recurrence shortened after each revision operation. The risk of MT and additional recurrence increased significantly with recurrence. In RPA(-MT) group tumor recurrence occurred in 21.4% of patients despite a clear resection margin. Conclusion. The risk factors for MT may be an age of over 45 yr and multiple recurrences. However, younger patients are more at risk of recurrence. A clear resection margin cannot guarantee a cure in RPA, and it seems that parotid pleomorphic adenomas slowly gain malignant characteristics after repeated recurrences.SUH MW, 2005, KOREAN J HEAD NECK O, V21, P146HANNA EY, 2005, CUMMINGS OTOLARYNGOL, P1348Ghosh S, 2003, CLIN OTOLARYNGOL, V28, P262Glas AS, 2002, CANCER, V94, P2211, DOI 10.1002/cncr.10445Glas AS, 2001, HEAD NECK-J SCI SPEC, V23, P311BRADLEY PJ, 2001, CURR OPIN OTOLARYNGO, V9, P100Carew JF, 1999, OTOLARYNG HEAD NECK, V121, P539Junquera L, 1999, HEAD NECK-J SCI SPEC, V21, P652Hancock BD, 1999, ANN ROY COLL SURG, V81, P299Bankamp DG, 1999, LARYNGO RHINO OTOL, V78, P77Hoorweg JJ, 1998, EUR J SURG ONCOL, V24, P452Henriksson G, 1998, CANCER, V82, P617Laskawi R, 1998, BRIT J ORAL MAX SURG, V36, P48Klijanienko J, 1997, HEAD NECK-J SCI SPEC, V19, P629Leverstein H, 1997, EUR ARCH OTO-RHINO-L, V254, P313SunardhiWidyaputra S, 1995, PATHOL RES PRACT, V191, P1186PHILLIPS PP, 1995, ANN OTO RHINOL LARYN, V104, P100BUCHMAN C, 1994, LARYNGOSCOPE, V104, P1231NATVIG K, 1994, HEAD NECK-J SCI SPEC, V16, P213JACKSON SR, 1993, J LARYNGOL OTOL, V107, P546MCGREGOR AD, 1988, BRIT J PLAST SURG, V41, P177FEE WE, 1978, LARYNGOSCOPE, V88, P265SEIFERT G, 1976, HNO, V24, P415NAEIM F, 1976, ARCH PATHOL LAB MED, V100, P271FRAZELL EL, 1954, CANCER, V7, P637

5-lipoxygenase mediates docosahexaenoyl ethanolamide and N-arachidonoyl-L-alanine-induced reactive oxygen species production and inhibition of proliferation of head and neck squamous cell carcinoma cells

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Abstract Background Endocannabinoids have recently drawn attention as promising anti-cancer agents. We previously observed that anandamide (AEA), one of the representative endocannabinoids, effectively inhibited the proliferation of head and neck squamous cell carcinoma (HNSCC) cell lines in a receptor-independent manner. In this study, using HNSCC cell lines, we examined the anti-cancer effects and the mechanisms of action of docosahexaenoyl ethanolamide (DHEA) and N-arachidonoyl-L-alanine (NALA), which are polyunsaturated fatty acid (PUFA)-based ethanolamides like AEA. Methods and Results DHEA and NALA were found to effectively inhibit HNSCC cell proliferation. These anti-proliferative effects seemed to be mediated in a cannabinoid receptor-independent manner, since the antagonist of cannabinoid receptor-1 (CB1) and vanilloid receptor-1 (VR1), two endocannabinoid receptors, did not reverse the ability of DHEA and NALA to induce cell death. Instead, we observed an increase in reactive oxygen species (ROS) production and a decrease of phosphorylated Akt as a result of DHEA and NALA treatment. Antioxidants efficiently reversed the inhibition of cell proliferation and the decrease of phosphorylated Akt induced by DHEA and NALA; inhibition of 5-lipoxygenase (5-LO), which is expected to be involved in DHEA- and NALA-degradation pathway, also partially blocked the ability of DHEA and NALA to inhibit cell proliferation and phosphorylated Akt. Interestingly, ROS production as a result of DHEA and NALA treatment was decreased by inhibition of 5-LO. Conclusions From these findings, we suggest that ROS production induced by the 5-LO pathway mediates the anti-cancer effects of DHEA and NALA on HNSCC cells. Finally, our findings suggest the possibility of a new cancer-specific therapeutic strategy, which utilizes 5-LO activity rather than inhibiting it

Gastric Choristoma of the Oropharynx

Heterotopic gastric mucosa tissue is also called gastric choristoma, and this type of lesion can be found anywhere in the alimentary tract. However, gastric choristoma in the pharynx is very rare; only 10 cases of pharyngeal gastric choristoma have been reported in the English medical literature. A 32-yr-old woman was referred to our institution for the evaluation of a large mass that originated from the posterior wall of the oropharynx. The mass did not cause any symptoms except for the occasional sensation of a foreign body. Gadolinium-enhanced T1 weighted imaging showed a 5 cm-sized mass with central enhancement and hypointense portions, yet the radiological diagnosis was not clear. Transoral mass excision was performed with using electrocautery for making the diagnosis and for treating the mass. The microscopic analysis revealed gastric choristoma

Induction chemotherapy in head and neck squamous cell carcinoma of the paranasal sinus and nasal cavity: A role in organ preservation

Background/Aims: The role of induction chemotherapy (IC) for eyeball preservation has not been established in head and neck squamous cell carcinoma (HNSCC) of the paranasal sinus and nasal cavity (PNSNC). Periorbital involvement frequently leads to eyeball exenteration with a margin of safety. We evaluated the treatment outcomes, including survival and eyeball preservation, of patients who received IC for HNSCC of the PNSNC. Methods: We reviewed 21 patients diagnosed with HNSCC of the PNSNC who were treated with IC. We analyzed response, eyeball preservation rate, and overall survival. Results: Tumors were located in the paranasal sinus (n = 14) or nasal cavity (n = 7). Most patients had stage T4a (n = 10) or T4b (n = 7) disease. More than half of the patients received a chemotherapy regimen of docetaxel, fluorouracil, and cisplatin (n = 11). Thirteen patients (61.9%) achieved a partial response after IC and 15 patients (71.4%) achieved T down-staging. Among 17 patients with stage T4 disease, which confers a high risk of orbital exenteration, 14 (82.4%) achieved preservation of the involved eye. The 3-year overall survival (OS) rate of patients who achieved a partial response to IC was 84.6%. The 3-year OS rate of patients with stable disease or disease progression after IC was 25.0% (p = 0.038). Conclusions: IC could be considered for down-staging patients with advanced T-stage disease. It could also be a reasonable option for eyeball preservation in locally advanced HNSCC of the PNSNC.

Endoscopic management of recurrent tracheoesophageal fistula with trichloroacetic acid chemocauterization: a preliminary report

PURPOSE: Open repair with a second thoracotomy is technically challenging and has a high risk of complications for the treatment of a recurrent tracheoesophageal fistula (RTEF). Therefore, less invasive endoscopic techniques have been developed. Here, we report on the chemocauterization with trichloroacetic acid (TCA) technique for endoscopic management of RTEF. METHODS: Three patients who had an open repair with thoracotomy for congenital tracheoesophageal fistula and were diagnosed with RTEF were included in this study. Rigid ventilating bronchoscopy with telescopic magnification was used to evaluate and manage the RTEF. After identification of the fistula opening, a 50% TCA-soaked small cotton ball was applied in the opening 3 times during each session. RESULTS: The mean number of procedures was 3.3, and the fistulae were closed in all cases. Closure of the fistula was confirmed by esophagogram and/or bronchoscopy. There were no postoperative complications. CONCLUSION: The results of this study showed that chemocauterization with TCA can be safe and effective for the management of RTEF

Laser-assisted endoscopic submucosal medial arytenoidectomy (LESMA)

Various surgical techniques have been proposed for the management of patients with bilateral vocal fold paralysis (VFP) or posterior glottic stenosis (PGS), which make use of external and endoscopic approaches. The purpose of these surgical treatments is to restore an adequate airway without disturbing voice quality and swallowing. It has been known that medial arytenoidectomy and cordotomy using laser, which partially resects the medial portion of the arytenoids, can preserve the airway and voice quality without damage on the membranous vocal fold.1 However, laser arytenoidectomy and cordotomy may result in granulation or scar tissue formation after surgery, which could fail to restore the adequate airway. Submucous medial arytenoidectomy can prevent granulation tissue formation, thus accelerating healing processes and improving treatment outcomes. We herein describe our experiences in the management of bilateral VFP and PGS by combining posterior transverse partial cordotomy, as described by Dennis and Kashima,2 with modified method of submucosal medial arytenoidectomy, as described by Crumley

Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line

Glucocorticoids (GCs) modulate the synthesis of many pro-inflammatory cytokines and influence multiple transduction pathways. GCs negatively or positively influence the transcription factors of their target genes. All of these transcription signals are closely connected to cancer survival or death. We investigated the action of dexamethasone (DEX) on head and neck cancer cell lines. When SNU-1041 and SNU-1076 were treated with DEX, the cell lines showed different patterns of responses. DEX inhibition of cell growth depended on concentration in SNU-1041, but not in SNU-1076. Furthermore, DEX Suppressed Vascular endothelial growth factor (VEGF) secretion from SNU-1041, but not from SNU-1076. We explored the mechanism that explains these distinct differences. After DEX treatment, the differences of NF-kappa B (p65), glucocorticoid receptor and p-AKT were not observed between the cell lines. However, phospho-signal transducer and activator of transcription 3 (STAT3) decreased in SNU-1041 only. Moreover, STAT3 inhibition using si-RNA Suppressed VEGF secretion. When STAT3 was overexpressed after DEX treatment, the level of VEGF in the culture media was restored. Taken together, we suggest that p-STAT3 can be a mediating factor which regulates VEGF secretion in the DEX treatment. Because the relationship between the three Molecules DEX, STAT3 and VEGF is scarcely known, our findings clarified one of the signaling pathways of DEX, which is often used in clinical conditions.Shim SH, 2009, INT J MOL MED, V23, P805, DOI 10.3892/ijmm_00000196Matthews L, 2009, ENDOCRINOLOGY, V150, P75, DOI 10.1210/en.2008-0196Wilson C, 2008, BRIT J CANCER, V99, P2054, DOI 10.1038/sj.bjc.6604804Egberts JH, 2008, CANCER BIOL THER, V7, P1044Chen Z, 2008, MED RES REV, V28, P185, DOI 10.1002/med.20101Sommer P, 2007, ONCOGENE, V26, P7111, DOI 10.1038/sj.onc.1210524Yemelyanov A, 2007, ONCOGENE, V26, P1885, DOI 10.1038/sj.onc.1209991Yano A, 2006, CLIN CANCER RES, V12, P3003, DOI 10.1158/1078-0432.CCR-05-2085Xie TX, 2006, CANCER RES, V66, P3188, DOI 10.1158/0008-5472.CAN-05-2674Xu Q, 2005, ONCOGENE, V24, P5552, DOI 10.1038/sj.onc.1208719Jung JE, 2005, FASEB J, V19, P1296, DOI 10.1096/fj.04-3099fjeSchmidt S, 2004, CELL DEATH DIFFER, V11, pS45, DOI 10.1038/sj.cdd.4401456Yu H, 2004, NAT REV CANCER, V4, P97, DOI 10.1038/nrc1275NECELA BM, 2004, P AM THORAC SOC, V1, P239Wang Z, 2003, J BIOL CHEM, V278, P50897, DOI 10.1074/jbc.M310297200Herr I, 2003, CANCER RES, V63, P3112Niu GL, 2002, ONCOGENE, V21, P2000, DOI 10.1038/sj/onc/1205260Planey SL, 2000, BIOCHEM BIOPH RES CO, V279, P307Kofler R, 2000, HISTOCHEM CELL BIOL, V114, P1Evans-Storms RB, 2000, ENDOCRINOLOGY, V141, P1854FOLKMAN J, 1995, NAT MED, V1, P27FIDLER IJ, 1994, CELL, V79, P185SANCHEZ I, 1993, CELL GROWTH DIFFER, V4, P215BURNSTEIN KL, 1991, STEROIDS, V56, P52HARMON JM, 1979, J CELL PHYSIOL, V98, P267