Application of an L-shaped anterolateral thigh flap in reconstruction after hemiglossectomy.

OBJECTIVE: Tongue defect reconstruction is one of the key components of tongue cancer surgery. In this study, we used an L-shaped flap design adopted as a simple and efficient method to repair tongue defects after hemiglossectomy. Furthermore, we evaluated and contrasted the clinical effects of two methods, the L-shaped and traditional methods. STUDY DESIGN: Fifteen patients in the L-shaped group and 20 patients in the traditional group were evaluated and compared in terms of postoperative complications, dysphagia, language function and appearance satisfaction. RESULTS: The results (Table 1) showed that there were 2 cases of donor area invalid traumas, and 2 patients had scar hyperplasia in the traditional group. The degree of global and functional dysphagia of the L-shaped group (2.60 ± 0.29 and 11.47 ± 1.38) was lower than that of the traditional group (3.55 ± 0.29 and 15.75 ± 1.22) (P < 0.05). In the language evaluation, the traditional group (3.20 ± 0.26) had lower scores than the L-shaped group (4.13 ± 0.30) (P < 0.05). CONCLUSION: The L-shaped ALTP flap is a simple and efficient modification of ALTP, that can be used for half-tongue repair after radical operations for tongue cancer. It has better performance in the recovery of dysphagia and language function than the traditional ALTP flap.

Tumor necrosis factor receptor-associated factor 6 mediated the promotion of salivary adenoid cystic carcinoma progression through Smad-p38-JNK signaling pathway induced by TGF-ß.

BACKGROUND: Tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) has been proved to play an important role in tumorigenesis, invasion, and metastasis. However, its precise role salivary adenoid cystic carcinoma (SACC) has not been determined. The aim of this study was to explore the role of TRAF6 in SACC including invasion and metastasis of SACC cells. MATERIALS AND METHODS: Immunohistochemistry and quantitative real-time PCR were performed in SACC tissues paired with their adjacent normal tissues to analyze the expression of TRAF6. Downstream proteins expression was explored when TRAF6 was knockdown by siRNA. RESULTS: The results show that TRAF6 is upregulated in SACC samples, especially in SACC with metastasis, which is closely correlated with an aggressive phenotype (P = .0073) and shorter life survival span (P = .0061) in SACC patients. Knockdown of TRAF6 can attenuate the promotion effect of SACC cell invasion induced by TGF-ß. Western blot results also showed that silencing TRAF6 expression can inhibit the activation of SMAD2, SMAD3, ERK, p38, and JNK induced by TGF-ß in SACC cells. CONCLUSION: These data suggested that TRAF6 regulates TGF-ß-mediated SACC progression through SMAD2/3-ERK-p38-JNK cascades.

Endoscopic-Assisted Resection of Benign Tumors of the Accessory Parotid Gland.

PURPOSE: Modified endoscopically assisted resection of benign tumors in the accessory parotid gland region (APGR) has been reported, and the surgery confers a potential risk of injury to the great auricular nerve. This clinical research study provides an updated approach for the resection of benign tumors of the APGR. PATIENTS AND METHODS: Thirteen cases diagnosed with primary benign tumors in the APGR were treated by endoscopically assisted resection through a margin of the tragus, and its feasibility was evaluated. RESULTS: All tumors were completely resected. The procedures lasted 45 to 70 minutes (mean, 54 minutes). None of the endoscopically assisted surgeries proceeded to open surgery. The patients were followed for 3 to 14 months, without postoperative complications, including pain, facial or auricular nerve weakness, salivary fistula, infection, tumor recurrence, Frey syndrome, or depression deformity. The scars were concealed and esthetically satisfactory. CONCLUSION: Endoscopically assisted resection of benign tumors through a margin of the tragus in the APGR is a safe technique that achieves excellent esthetic and functional results.

The application of a carbon dioxide laser in the treatment of superficial oral mucosal lesions.

To evaluate the safety and advantages of using carbon dioxide (CO2) laser in the treatment of oral mucosal lesion, including vascular malformations, precancerous lesions, and verrucous nevus, a retrospective analysis was conducted for 73 patients with oral mucosal lesions who received CO2 laser treatment during June 2012 to December 2013, including 25 patients with vascular malformations, 22 patients with oral leukoplakia, 18 patients with oral mucosal lichen planus, and 8 patients with oral mucosal and labial mucosal verrucous nevus. The lesions ranged from 0.8 × 0.8  cm to 4 × 3  cm. Twenty patients with lesions removed using the traditional scalpel, assisted with an electric knife, were the control group. The operative time was from 3 to 10 minutes, with an average of 5.5 minutes; the average amount of intraoperative bleeding was 5  mL. None of the 73 patients had postoperative infections, and all wounds healed well after the surgery. The patients were followed up for 1 year. Two patients with oral leukoplakia showed recurrence after the surgery, and a reoperation achieved satisfactory treatment effects. The operative time of the control group was in the range of 4 to 15 minutes, with an average of 9.5 minutes, and the average amount of intraoperative bleeding was 10  mL. None of the 20 patients had postoperative infections, and the wounds also showed healing well after the surgery. The application of CO2 laser in the treatment of oral mucosal lesions has the advantages of reduced bleeding, a clear view during surgery, and a shorter operative time.

Minimally invasive selective neck dissection: a prospective study of endoscopically assisted dissection via a small submandibular approach in cT(1-2_N(0) oral squamous cell carcinoma.

BACKGROUND: Selective neck dissection (SND) in clinical N0 (cN0) cases of oral squamous cell carcinoma (SCC) has been performed by surgeons using a retroauricular or modified facelift approach with robotic or endoscopic assistance. However, these procedures provide cosmetic satisfaction at the cost of possible maximal invasiveness. In this prospective study, we introduced and evaluated the feasibility as well as surgical invasiveness and cosmetic outcome of endoscopically-assisted SND via a small submandibular approach. METHODS: Forty-four patients with cT1-2N0 oral SCC (OSCC) were randomly divided into two groups of endoscopically-assisted SND and conventional SND. Perioperative and postoperative outcomes of patients were evaluated, including the length of the incision, operating time for neck dissection, estimated blood loss during the operation, amount and duration of drainage, total hospitalization period, total number of lymph nodes retrieved, satisfaction scores based on the cosmetic results, perioperative local complications, shoulder syndrome, and follow-up information. RESULTS: The mean operation time in the endoscopically-assisted group (126.04 ± 12.67 min) was longer than that in the conventional group (75.67 ± 16.67 min). However, the mean length of the incision was 4.33 ± 0.76 cm in the endoscopically-assisted SND group, and the amount and duration of drainage, total hospital stay, postoperative shoulder pain score, and cosmetic outcomes were superior in the endoscopically-assisted SND group. Additionally, the retrieved lymph nodes and complications were comparable. CONCLUSIONS: Endoscopically-assisted SND via a small submandibular approach had a longer operation time than the conventional approach. However, endoscopically-assisted SND was feasible and reliable while providing minimal invasiveness and satisfactory appearance.

RECK overexpression reduces invasive ability in ameloblastoma cells.

BACKGROUND: Ameloblastoma is a frequent odontogenic neoplasm characterized by local invasiveness and high risk of recurrence. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a tumor suppressor that inhibits metastasis and angiogenesis. The aim of this study was to investigate effects of RECK overexpression on invasive potential in ameloblastoma cells. METHODS: Lentiviral vectors containing human RECK gene were created and subsequently stably transfected into immortalized ameloblastoma cell line hTERT(+) -AM. Functional characteristics of hTERT(+) -AM cells with stable RECK overexpression included proliferation, migration, invasion, and regulation of matrix metalloproteinases (MMP)-2, MMP-9 measured by zymography or commercially available assays. RESULTS: The stable and higher expression of RECK mRNA and protein (P < 0.01) was detected in RECK-transfected hTERT(+) -AM cells. RECK overexpression caused a decrease in migration and invasion (P < 0.01) for hTERT(+) -AM cells and a decrease in activity of MMP-2, MMP-9 (P < 0.01). Proliferation was not affected by RECK overexpression (P > 0.05). CONCLUSIONS: Overexpression of RECK gene significantly inhibited cell invasive ability of hTERT(+) -AM cells, suggesting RECK may be a new target for ameloblastoma treatment.

Identification and validation of methylated differentially expressed miRNAs and immune infiltrate profile in EBV-associated gastric cancer.

BACKGROUND: The recent discovery of cancer/tissue specificity of miRNA has indicated its great potential as a therapeutic target. In Epstein-Barr virus-associated gastric cancer (EBVaGC), host genes are affected by extensive DNA methylation, including miRNAs. However, the role of methylated miRNA in the development of EBVaGC and immune cell infiltration has largely remained elusive. RESULTS: After crossmatching the DNA methylation and expression profile of miRNA and mRNA in the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas Research Network (TCGA), we discovered that miR-129-2-3p was significantly suppressed due to hypermethylation on its enhancer in EBVaGC. The differentially expressed genes (DEGs) added up to 30, among which AKAP12 and LARP6 were predicted to be the target genes of miR-129-2-3p and negatively correlated with patients' survival. Accordingly, miR-129-2-3p was significantly down-regulated in tumor samples in 26 (65%) out of 40 cases in our cohort (P < 0.0001). The proliferation, migration and invasion functions of GC cells were significantly promoted when transfected with miR-129-2-3p inhibitor and suppressed when transfected with mimics or treated with 5-aza-2'-deoxycytidine. Moreover, a comprehensive regulation network was established by combining the putative transcription factors, miRNA-mRNA and protein-protein interaction (PPI) analysis. Pathway enrichment analysis showed that cytokine activity, especially CCL20, was the most prominent biological process in EBVaGC development. Immune cell infiltration analysis demonstrated CD4+ T cell, macrophage and dendritic cell infiltrates were significantly enriched for the prognostic-indicated hub genes. CONCLUSION: This study has provided a comprehensive analysis of differentially expressed miRNAs and mRNAs associated with genome-wide DNA methylation by integrating multi-source data including transcriptome, methylome and clinical data from GEO and TCGA, QPCR of tumor samples and cell function assays. It also gives a hint on the relationships between methylated miRNA, DEGs and the immune infiltration. Further experimental and clinical investigations are warranted to explore the underlying mechanism and validate our findings.

SIRT6-PARP1 is involved in HMGB1 polyADP-ribosylation and acetylation and promotes chemotherapy-induced autophagy in leukemia.

High mobility group box protein 1 (HMGB1) is an evolutionarily conserved non-histone chromatin-binding protein. In a previous study, we showed that treating leukemic cells with chemotherapeutic drugs leads to the translocation of HMGB1, which is involved in autophagy and ultimately promotes chemoresistance in leukemia. However, the underlying translocation mechanism of HMGB1 in chemotherapy-induced autophagy remains unclear. In this study, we showed that knockdown of SIRT6 or PARP1 gene expression significantly inhibited HMGB1 cytoplasmic translocation and autophagy. Meanwhile, we found that SIRT6, an important upstream protein of PARP1, associated with PARP1, leading to the stimulation of polyADP-ribose polymerase activity. We further demonstrated that SIRT6 and PARP1 activation were required for chemotherapy-induced ADP-ribosylation of HMGB1 in leukemic cells and then influenced the acetylation of HMGB1, finally promoting the autophagy of leukemic cells mediated by HMGB1 translocation. These findings provide new insights into the mechanism of chemotherapeutic drug resistance. Targeting the HMGB1 translocation may overcome autophagy-related chemoresistance in leukemia.

Postoperative immune response and surgical stress in selective neck dissection: Comparison between endoscopically assisted dissection and open techniques in cT1-2N0 oral squamous cell carcinoma.

BACKGROUND: Endoscopically assisted selective neck dissection (SND) has recently been applied in clinical N0 cases of oral squamous cell carcinoma (OSCC). However, nothing is known of the immune response after surgery. METHODS: A total of 60 patients with cT1-2N0 OSCC randomly underwent endoscopically assisted SND and open operations. The serum levels of IL-6, IL-8, IL-10, IL-1b, TNF-a, CRP, cortisol, ACTH, and growth hormone were analyzed before the start of the surgery (T0) and at 2 (T1), 6 (T2), 24 (T3), and 72 h (T4) after surgery. RESULTS: A total of 31 patients were randomized for endoscopic SND, whereas 29 underwent open procedures. The release of IL-6, IL-10 and CRP was significantly lower in the endoscopic group than in the open surgery group (p < 0.05), and cortisol levels were also lower in the endoscopic group (p < 0.05). CONCLUSIONS: Endoscopic SND could effectively provide lower inflammatory responses and surgical stress, reducing peri-operative trauma and accelerating recovery.

Endoscopically-assisted operations in the treatment of odontogenic peripheral osteomyelitis of the posterior mandible.

The aim of this study was to evaluate the possibility of using an endoscope in the treatment of five patients with odontogenic peripheral osteomyelitis of the posterior mandible diagnosed between March 2012 and September 2014. After imaging and general preoperative examination, the patients had endoscopically-assisted curettage and sequestrectomy. The data collected included the duration of the operation, complications, and patients' degree of satisfaction. The mean duration of the operation through an intraoral incision, was 46 (range 40-60) minutes. Patients were followed up at 1 week, 3 months, and 6 months, with no signs of recurrence. One patient reported postoperative swelling in the mandibular angle but this settled. The incision was minimal and left no postoperative scar on the face. All the patients recovered free of complications and were satisfied with the results of the operation. Because of the minimally-invasive intraoral incision, endoscopically-assisted treatment of odontogenic peripheral osteomyelitis of the posterior mandible can maintain external facial integrity without surgical scars.

Mitochondrial fission determines cisplatin sensitivity in tongue squamous cell carcinoma through the BRCA1-miR-593-5p-MFF axis.

Cisplatin has been widely employed as a cornerstone chemotherapy treatment for a wide spectrum of solid neoplasms; increasing tumor responsiveness to cisplatin has been a topic of interest for the past 30 years. Strong evidence has indicated that mitochondrial fission participates in the regulation of apoptosis in many diseases; however, whether mitochondrial fission regulates cisplatin sensitivity remains poorly understood. Here, we show that MFF mediated mitochondrial fission and apoptosis in tongue squamous cell carcinoma (TSCC) cells after cisplatin treatment and that miR-593-5p was downregulated in this process. miR-593-5p attenuated mitochondrial fission and cisplatin sensitivity by targeting the 3' untranslated region sequence of MFF and inhibiting its translation. In exploring the underlying mechanism of miR-593-5p downregulation, we observed that BRCA1 transactivated miR-593-5p expression and attenuated cisplatin sensitivity in vitro. The BRCA1-miR-593-5p-MFF axis also affected cisplatin sensitivity in vivo. Importantly, in a retrospective analysis of multiple centers, we further found that the BRCA1-miR-593-5p-MFF axis was significantly associated with cisplatin sensitivity and the survival of patients with TSCC. Together, our data reveal a model for mitochondrial fission regulation at the transcriptional and post-transcriptional levels; we also reveal a new pathway for BRCA1 in determining cisplatin sensitivity through the mitochondrial fission program.