An Endoscopic Endonasal Nasopharyngectomy with Posterolateral Extension

xlomafota13 shared this article with you from Inoreader An Endoscopic Endonasal Nasopharyngectomy with Posterolateral Extension Via Journal of Neurological Surgery Part B: Skull Base J Neurol Surg B Skull Base DOI: 10.1055/s-0041-1735557 Background Invasion depth influences the choice for extirpation of nasopharyngeal malignancies. This study aims to validate the feasibility of endoscopic endonasal resection of lesions with a posterolateral invasion. As a secondary goal, the study intends to propose a classification system of endoscopic endonasal nasopharyngectomy determined by the depth of posterolateral invasion. Methods Eight cadaveric specimens (16 sides) underwent progressive nasopharyngectomy using an endoscopic endonasal approach. Resection of the torus tubarius, Eustachian tube (ET), medial pterygoid plate and muscle, lateral nasal wall, and lateral pterygoid plate and muscle were sequentially performed to expose the fossa of Rosenmüller, petroclival region, parapharyngeal space (PPS), and jugular foramen, respectively. Results Technical feasibility of endonasal nasopharyngectomy toward a posterolateral direction was validated in all 16 sides. Nasopharyngectomy was classified into four types as follows: (1) type 1: resection restricted to the posterior or superior nasopharynx; (2) type 2: resection includes the torus tubarius which is suitable for lesions extended into the petroclival region; (3) type 3: resection includes the distal cartilaginous ET, medial pterygoid plate, and muscle, often required for lesions extending laterally into the PPS; And (4) type 4: resection includes the lateral nasal wall, pterygoid plates and muscles, and all the cartilaginous ET. This extensive resection is required for lesions involving the carotid artery or extending to the jugular foramen region. Conclusion Selected lesions with posterolateral invasion into the PPS or jugular foramen is amenable to a resection via expanded endonasal approach. Classification of nasopharyngectomy based on tumor depth of posterolateral invasion helps to plan a surgical approach. [...] Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany Article in Thieme eJournals: Table of contents  |  Abstract  |  Full text View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Treatment Modality and Second Primary Tumors of the Head and Neck

xlomafota13 shared this article with you from Inoreader Treatment Modality and Second Primary Tumors of the Head and Neck Via O.R.L. Journal for oto-rhino-laryngology and its borderlands Introduction: Second primary tumors (SPTs) in head and neck cancer are thought to occur from premalignant lesions that are present at the time of the primary tumor diagnosis. The association of the modality used to treat the primary lesion with SPT occurrence is not clear. Objective: The aim of the study was to assess the incidence of SPTs in patients with head and neck malignancies, according to treatment modality. Methods: We conducted a retrospective cohort study. All patients who were treated at Soroka Medical Cente r between 2000 and 2013 for a head and neck squamous cell carcinoma were assessed. Data analysis included tumor site of the primary and second primary and treatment modality of the primary tumor. In addition, demographics as well as habits were recorded as well. Results: Of the 184 patients included in the cohort, SPT developed in 31 patients (17%) with a median time to diagnosis of 4.3 years. Smoking was reported in 74% of those with SPT and 78% of those without. The most common site for SPT was the lungs, with 13 cases, 42% of the total SPTs. Among patients who developed an SPT, for 12 of those with an index tumor in the oral cavity or oro-hypopharynx, 8 (67%) developed an SPT in the same location; for 18 of those with an index tumor in the larynx, 11 (61%) developed a SPT in the lungs and bronchi (p = 0.001). On multivariate analysis, the treatment modality used was not found to be associated with the occurrence of SPTs and the radiotherapy showed no protecti ve or harmful effect (HR 0.64 p = 0.24). Conclusion: Treatment modality used for head and neck cancer does not seem to be associated with the occurrence of SPTs. ORL View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Superior Semicircular Canal Dehiscence Revision Surgery Outcomes: A Single Institution's Experience

xlomafota13 shared this article with you from Inoreader Superior Semicircular Canal Dehiscence Revision Surgery Outcomes: A Single Institution's Experience Via leak of cerebrospinal fluid World Neurosurg. 2021 Sep 25:S1878-8750(21)01426-1. doi: 10.1016/j.wneu.2021.09.083. Online ahead of print. ABSTRACT BACKGROUND: Superior semicircular canal dehiscence (SSCD) is an abnormality of the otic capsule which normally overlies the superior semicircular canal. Surgical management is indicated in patients with persistent and debilitating symptoms. Given the complexity of the disease, there are patients who experience less favorable surgical outcomes and require revision surgery. The purpose of this study was to report to the rate of postoperative symptomatic improvement in patients who required revision surgery. METHODS: A retrospective analysis of patients undergoing SSCD surgical repair at a single institution was performed. Information on patient demographics, primary and secondary surgical approaches, surgical outcomes, and follow-up length was collected. RESULTS: 17 patients underwent 20 revision surgeries. There were eleven (65%) females and six (35%) males. Mean age of the cohorts was 50 years (range 30-68 years), and mean follow-up length was 6.8 months (range 0.1-31.1 months). Cerebrospinal fluid (CSF) leak was noted in 67% of cases. The greatest postoperative symptomatic resolution was reported in oscillopsia (100%), headache (100%), and internal sound amplification (71%), while the least postoperative symptomatic resolution was reported in tinnitus (42%), aural fullness (40%), and dizziness (29%). CONCLUSION: Revision surgery can provide symptomatic improvement in select SSCD patients; however, patients should be cautioned about the possibility of less favorable outcomes than in index surgery. Revision surgeries are associated with a considerably higher rate of perioperative CSF leak. PMID:34583007 | DOI:10.1016/j.wneu.2021.09.083 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The potential of using artificial intelligence to improve skin cancer diagnoses in Hawai‘i’s multiethnic population

xlomafota13 shared this article with you from Inoreader The potential of using artificial intelligence to improve skin cancer diagnoses in Hawai'i's multiethnic population Via Melanoma Research - Published Ahead-of-Print Skin cancer remains the most commonly diagnosed cancer in the USA with more than 1 million new cases each year. Melanomas account for about 1% of all skin cancers and most skin cancer deaths. Multiethnic individuals whose skin is pigmented underestimate their risk for skin cancers and melanomas and may delay seeking a diagnosis. The use of artificial intelligence may help improve the diagnostic precision of dermatologists/physicians to identify malignant lesions. To validate our artificial intelligence's efficiency in distinguishing between images, we utilized 50 images obtained from our International Skin Imaging Collaboration dataset (n = 25) and pathologically confirmed lesions (n = 25). We compared the ability of our artificial intelligence to visually diagnose these 50 skin cancer lesions with a panel of three dermatologists. The artificial intelligence model better differentiated between melanoma vs. nonmelanoma with an area under the curve of 0.948. The three-panel member dermatologists correctly diagnosed a similar number of images (n = 35) as the artificial intelligence program (n = 34). Fleiss' kappa (ĸ) score for the raters and artificial intelligence indicated fair (0.247) agreement. However, the combined result of the dermatologists panel with the artificial i ntelligence assessments correctly identified 100% of the images from the test data set. Our artificial intelligence platform was able to utilize visual images to discriminate melanoma from nonmelanoma, using de-identified images. The combined results of the artificial intelligence with those of the dermatologists support the use of artificial intelligence as an efficient lesion assessment strategy to reduce time and expense in diagnoses to reduce delays in treatment. Received 1 March 2021 Accepted 6 August 2021 Correspondence to Mark Lee Willingham Jr., MS, Department of Sociology, Community Health Educator, University of Hawai'i Cancer Center, 701 Ilalo St., Suite #414, Honolulu, HI 96813, Hawai'i, USA, Tel: 1 808 441 8186; fax: 1 808 586 3052; e-mail: Mlw237@hawaii.edu Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Risk factors in pediatric melanoma: a retrospective study of 39 cases

xlomafota13 shared this article with you from Inoreader Risk factors in pediatric melanoma: a retrospective study of 39 cases Via Melanoma Research - Published Ahead-of-Print Pediatric melanoma is a rare form of the tumor whose epidemiology is widely increasing thanks to the improvement of dermoscopic and anatomopathologic diagnostic techniques. Although it is a tumor of considerable interest in adults, little has been described about the pediatric field. The objective of our study was then to ident ify the possible risk factors for the development of melanoma in the pediatric population. We performed a retrospective study conducted in the Melanoma and Skin Cancer Unit and Unit of Dermatology (Livorno, Italy). We analyzed a population of 38 children under 21 years with a diagnosis of melanoma. This population was compared with a control population of 114 children followed up in our dermatologic clinic. From our combined univariate-multivariate statistics analysis, the number of nevi [regression coefficient (RC) of 1.04 and odds ratio (OR) of 2.8 confidence interval (Cl, 1.2–6.6)], and family history of melanoma [RC of 1.99 and OR of 7.3 (Cl, 2.3–22.7)] emerged as possible risk factors for the development of melanoma. The identification of these elements would allow the physician to carry out a more targeted preliminary assessment of the patient, potentially decisive in cases of diagnostic doubt of the lesion. Our study also lays the foundations for identifying those child ren who, despite not having received a diagnosis of melanoma on histologic examination, should be considered as patients susceptible to a focused follow-up, because of the presence of the risk factors that emerged from our research. Received 16 June 2021 Accepted 3 August 2021 Correspondence to Giovanni Bagnoni, MD, Melanoma and Skin Cancer Unit AVNO (Area Vasta Nord Ovest) and Unit of Dermatology, Specialist Surgery Area, Department Of General Surgery, Livorno Hospital, Viale Vittorio Alfieri 36, Livorno, LI 57124, Italy, Tel: +39 0586 223243; e-mail: giovanni.bagnoni@uslnordovest.toscana.it Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

AREL1 E3 ubiquitin ligase inhibits TNF-induced necroptosis via the ubiquitination of MTX2

xlomafota13 shared this article with you from Inoreader AREL1 E3 ubiquitin ligase inhibits TNF-induced necroptosis via the ubiquitination of MTX2 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1195. doi: 10.3892/etm.2021.10629. Epub 2021 Aug 20. ABSTRACT Previously, we reported on a novel anti-apoptotic E3 ubiquitin ligase, apoptosis-resistant E3 ubiquitin protein ligase 1 (AREL1), that ubiquitinates inhibitors of apoptosis proteins antagonists. The present study demonstrated that AREL1 ubiquitinated Metaxin 2 (MTX2), which was involved in TNF-induced necroptosis. MTX2 has been identified as a protein that belongs to the Metaxin family. It interacts with another Metaxin protein, Metaxin 1 (MTX1), which is localized in the outer membrane of mitochondria, and is involved in TNF-induced necroptosis. This study found that AREL1 interacted with MTX2, but not MTX1, while the amino-terminal domain of MTX2 interacted with MTX1, AREL1 interacted with the carboxyl-terminal domain of MTX2. Furthermore, AREL1 expression led to a decrease in the protein expression of MTX2, but not MTX1. However, a mutant form of AREL1, AREL1C790A, which is deficient for E3 activity, did not cause MTX2 degradation. Moreover, the protein levels of MTX2 were increased by AREL1 knockdown. Therefore, these results implied that AREL1 ubiquitinates and promotes the degradation of MTX2. The expression of MTX2, together with MTX1, enhanced TNF-induced necroptosis. However, AREL1 inhibited necroptosis even in cells expressing Metaxin proteins. Therefore, these results suggested that the inhibition of AREL1-dependent ubiquitination of MTX2 could be beneficial to sensitize tumor cells to TNF-induced necroptosis. PMID:34584540 | PMC:PMC8422393 | DOI:10.3892/etm.2021.10629 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

hsa-miR-15b-5p regulates the proliferation and apoptosis of human vascular smooth muscle cells by targeting the ACSS2/PTGS2 axis

xlomafota13 shared this article with you from Inoreader hsa-miR-15b-5p regulates the proliferation and apoptosis of human vascular smooth muscle cells by targeting the ACSS2/PTGS2 axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1208. doi: 10.3892/etm.2021.10642. Epub 2021 Aug 24. ABSTRACT A previous bioinformatic analysis from our group predicted that the interaction of microRNA (miRNA/miR)-15b with the acyl-CoA synthetase short chain family member 2 (ACSS2) gene was important for the development of abdominal aortic aneurysm (AAA). Apoptosis of aortic vascular smooth muscle cells (VSMCs) is a pathological feature of AAA. The present study aimed to explain the roles of miR-15b/ACSS2 in AAA by exploring their effects on the proliferation and apoptosis of aortic VSMCs. Human aortic VSMCs (T/G HA-VSMC cell line) were divided into six groups and were transfected with miR-15b-5p mimics, mimic negative control (NC), miR-15b-5p inhibitors, inhibitor NC, miR-15b-5p mimics+pcDNA3.1 and miR-15b-5p mimics+ACSS2-overexpessing vector. CCK-8 assay was used to determine cell proliferation. Annexin V-FITC/PI staining and flow cytometry assays were used to measure cell apoptosis. Dual-luciferase reporter assays were used to confirm the targeted relationship between miR-15b-5p and ACSS2. Reverse transcription-quantitative PCR and/or western blotting were used to examine the expression levels of miR-15b-5p, ACSS2 and prostaglandin-endoperoxide synthase 2 (PTGS2). Following transfection of T/G HA-VSMCs with mimics and inhibitors to respectively upregulate and downregulate miR-15b-5p, the results demonstrated that overexpression of miR-15b-5p inhibited cell proliferation and promoted cell apoptosis; silencing of miR-15b-5p obtained the opposite results. ACSS2 may be a direct target of miR-15b-5p, since the luciferase activity of a ACSS2 wild-type vector, but not that of a ACSS2 mutant reporter, was significantly inhibited by miR-15b-5p mimics compared with controls. Additionally, the expression levels of ACSS2 and its downstream gene PTGS2 were significantly reduced or increased following transfection with miR-15b-5p mimics or in hibitors, respectively. Furthermore, overexpression of ACSS2 reversed the antiproliferative and proapoptotic effects of miR-15b-5p mimics by blocking the production of PTGS2 protein. In conclusion, miR-15b-5p may promote the apoptosis and inhibit the proliferation of aortic VSMCs via targeting the ACSS2/PTGS2 axis. The present study provided preliminary evidence indicating that the miR-15b-5p/ACSS2/PTGS2 axis may be a potential target for the treatment of AAA. PMID:34584553 | PMC:PMC8422401 | DOI:10.3892/etm.2021.10642 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Podofilox suppresses gastric cancer cell proliferation by regulating cell cycle arrest and the c-Myc/ATG10 axis

xlomafota13 shared this article with you from Inoreader Podofilox suppresses gastric cancer cell proliferation by regulating cell cycle arrest and the c-Myc/ATG10 axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1203. doi: 10.3892/etm.2021.10637. Epub 2021 Aug 23. ABSTRACT Gastric cancer (GC) is a malignancy for which effective therapeutic drugs are limited. Podofilox exhibits antitumor effects in various types of cancer; however, whether it may inhibit GC growth remains unknown. The aim of the present study was to investigate the role of podofilox in GC. Cell Counting Kit-8, colony formation and cell cycle assays were used to detect the role of podofilox on cellular proliferation and the cell cycle, respectively. A microarray was used to detect the transcriptional changes induced by podofilox in GC cells. The results of the present study demonstrated that podofilox inhibited GC cell proliferation and colony formation. The half maximal inhibitory concentration of podofilox in AGS and HGC-27 cells was 2.327 and 1.981 nM, respectively. In addition, treatment with podofilox induced G0/G1 cell cyc le arrest. Molecular analysis based on microarray data demonstrated that podofilox altered the expression levels of genes involved in the cell cycle, c-Myc and p53 signaling. Autophagy-related 10 (ATG10), which was highly expressed in GC tissues, was also downregulated by podofilox, as demonstrated by the results of the microarray analysis and immunoblotting. To determine the involvement of ATG10 in GC, ATG10 was knocked down in GC cells by small interfering RNA, which suppressed the proliferation and colony formation of GC cells compared with those observed in the control-transfected cells. Taken together, the results of the present study suggested that podofilox may inhibit GC cell proliferation by preventing the cell cycle progression and regulating the c-Myc/ATG10 signaling pathway. PMID:34584548 | PMC:PMC8422391 | DOI:10.3892/etm.2021.10637 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

CXCR4 protects bone marrow-derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway

xlomafota13 shared this article with you from Inoreader CXCR4 protects bone marrow-derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1200. doi: 10.3892/etm.2021.10634. Epub 2021 Aug 23. ABSTRACT The present study aimed to investigate the regulatory mechanism of chemokine (C-X-C motif) receptor 4 (CXCR4) on endothelial progenitor cells (EPCs) through the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway under hypoxic conditions. Mononuclear cells were isolated from the bone marrow (BM) of young Sprague-Dawley (SD) rats. Bone marrow-derived endothelial progenitor cells (BM-EPCs) were characterized by using Dil-labeled acetylated low-density lipoprotein (Dil-ac-LDL) and fluorescein isothiocyanate-labeled UEA (FITC-UEA-1). Phenotype identification of BM-EPCs was based on red cytoplasm and green cytomembrane. Flow cytometry was employed to examine the markers CD14, CD34, and KDR. Expression level of the EPC-specific surface marker CD14 was found to be negative, while the expression level of CD34 and KDR was positive. In addition, CXCR4 was stably overexpressed in BM-EPCs after transfection with adenovirus-CXCR4. Cell proliferation, migration and apoptosis abilities were measured through the application of CCK-8, followed by Transwell and flow cytometry assays. The expression level of CXCR4, PI3K and Akt was determined by reverse transcription-quantitative PCR and western blotting assays. Functional experiments demonstrated that hypoxia inhibited BM-EPC proliferation and migration, while accelerating BM-EPC apoptosis. Additionally, CXCR4 was found to promote proliferation and migration, and suppress apoptosis in BM-EPCs with or without hypoxia treatment. Evidence also demonstrated that CXCR4 markedly upregulated the expression levels of PI3K and Akt. Furthermore, PI3K inhibitor (LY294002) and CXCR4 inhibitor (AMD3100) effectively inhibited the proliferation, migration and resistance to apoptosis of CXCR4-mediated BM-EPCs under hypoxic conditions. PMID:34584545 | PMC:PMC8422402 | DOI:10.3892/etm.2021.10634 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Gain of TPPP as a predictor of progression in patients with bladder cancer

xlomafota13 shared this article with you from Inoreader Gain of TPPP as a predictor of progression in patients with bladder cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1204. doi: 10.3892/etm.2021.10638. Epub 2021 Aug 24. ABSTRACT The present study investigated the role of tubulin polymerization promoting protein (TPPP) in the regulation of bladder cancer (BC) cell proliferation and migration, in addition to the association between TPPP gene copy number amplification and clinicopathological characteristics of BC. TPPP gene amplification was measured in human BC epithelial cells and samples obtained from 52 patients with BC via fluorescence in situ hybridization. TPPP gain was defined as mean TPPP copy number >2.2 per nucleus (cutoff). The neutrophil-to-lymphocyte ratio (NLR) was also obtained from the preoperative data of the patients. For in vitro assays, BC cell lines were transfected with either TPPP small interfering RNAs or scrambled control, following which cell proliferation and migration were determined using Cell Counting Kit-8 and Transwell migra tion assays, respectively. The percentage of cells with TPPP copy number amplification in the four BC epithelial cell lines (MGH-U1, -U1R, -U3, -U4) examined (86.0-100.0%) was found to be higher compared with that in the normal human uroepithelial cell lines (3.0 and 9.0%). Patients were divided into one- (1.9%), two- (55.8%), three- (7.7%), four- (26.9%) and five-copy (7.7%) types. Results calculated using Fisher's exact test indicated that the gain of TPPP in patients with BC associated significantly with age (P<0.05), advanced histological grade (P<0.001), tumor stage (P<0.05), histological type (P<0.001) and NLR (P<0.05). In MGH-U1R and MGH-U4 cells, cell proliferation and migration were revealed to be significantly lower following TPPP knockdown compared with those in cells transfected with the scrambled control. In conclusion, findings from the present study suggest that TPPP is important for cell proliferation, cell migration and BC progression, such that TPPP copy number assessment would be advised for preoperative urine cytology for urothelial neoplasia diagnosis. PMID:34584549 | PMC:PMC8422379 | DOI:10.3892/etm.2021.10638 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.