Clinical diagnosis of skull base ORN was based on symptoms, computed tomography, or magnetic resonance imaging and endoscopy. The final confirmation was according to pathologic examination. Surgery had the best effect. Extensive ORN accompanied by radiation brain damage or cranial nerves damage had poor prognosis. Nasopharyngeal bleeding and exhaustion were the main causes of death.

Inhibitor of differentiation (Id)-1 and nuclear factor-kappa B (NF-κB) have been detected in many malignant tumors, and their presence has been correlated with the metastatic potential of these tumors. This study was undertaken to investigate the prognostic significance of the expression of Id-1 and the p65 subunit of NF-κB (NF-κB/p65) and the proteins' roles in the invasion process of nasopharyngeal carcinoma (NPC) cells. The messenger RNA (mRNA) and protein levels of Id-1 and NF-κB/p65 in normal nasopharyngeal epithelial cells and NPC cell lines were examined using reverse transcription-PCR and western blot analysis, whereas the mRNA and protein levels of Id-1 and NF-κB/p65 in clinical NPC specimens were determined by reverse transcription-PCR and immunohistochemistry. Short hairpin RNA (shRNA) was used to silence Id-1 and NF-κB/p65 to allow for the examination of matrix metalloproteinase (MMP)-9 expression and migratory capacity changes in CNE-2 cells. Multivariate Cox analysis revealed that elevated Id-1 expression was a significant independent predictor of the 5 year overall survival rate (hazards ratio = 16.720, P = 0.005). Furthermore, elevated expression of both Id-1 and NF-κB/p65 was associated with poor clinical survival (P = 0.049). Targeting Id-1 and NF-κB/p65 mRNA with shRNA in CNE-2 cells inhibited MMP-9 expression and decreased the migratory capacity of CNE-2 cells. In conclusion, Id-1 expression is a novel independent prognostic marker molecule that helps identify NPC patients with a poor prognosis. Additionally, combined analysis of Id-1 and NF-κB/p65 can be useful for identifying patients at risk for unfavorable clinical outcomes. Id-1 or/and NF-κB/p65 enhanced tumor cell migration, which is associated with the secretion of MMP-9.

Interferon-stimulated gene 15 (ISG15), the first identified ubiquitin-like protein, is known for its anti-viral capacity. However, its role in tumorigenesis remains controversial. Here, using RNA-seq profiling analysis, we identified ISG15 as a differentially expressed gene in nasopharyngeal carcinoma (NPC) and validated its overexpression in NPC samples and cells. High ISG15 levels in NPC tissues were correlated with more frequent local recurrence and shorter overall survival and disease-free survival. ISG15 overexpression promoted a cancer stem cell phenotype in NPC cells, including increased colony and tumorsphere formation abilities, pluripotency-associated genes expression, and in vivo tumorigenicity. By contrast, knockdown of ISG15 attenuated stemness characteristics in NPC cells. Furthermore, overexpression of ISG15 increased NPC cell resistance to radiation and cisplatin (DDP) treatment. Our study demonstrates a protumor role of ISG15, and suggests that ISG15 is a prognostic predictor and a potential therapeutic target for NPC.

Papillary thyroid carcinoma (PTC) is the one of the most common types of endocrine cancer and has a heterogeneous prognosis. Tumors from patients with poor prognosis may differentially express specific genes. Therefore, an analysis of The Cancer Genome Atlas (TCGA) database was performed and revealed that cytokine receptor-like factor 1 (CRLF1) may be a potential novel target for PTC treatment. The objective of the current study was to explore the expression of CRLF1 in PTC and to investigate the main functions and mechanisms of CRLF1 in PTC. PTC tissues exhibited higher CRLF1 expression at both the mRNA and protein levels than it did with normal thyroid tissues. High CRLF1 levels were associated with aggressive clinicopathological features and poor disease-free survival rates. By using loss-of-function and gain-of-function assays, we found that CRLF1 not only increased cell migration and invasion in vitro but also promoted tumor growth both in vitro and in vivo. In addition, CRLF1 induced epithelial–mesenchymal transitions. Overexpression of CRLF1 activated the ERK1/2 and AKT pathways. The oncogenic effects induced by CRLF1 were suppressed by treating the cells with the MEK inhibitor U0126 or the AKT inhibitor MK-2206. These results suggest that CRLF1 enhances cell proliferation and metastasis in PTC and thus may therefore be a potential therapeutic target for PTC.

Lipoxins are host anti-inflammatory molecules that play a vital role in restoring tissue homeostasis. The efficacy of lipoxins and their analog epilipoxins in treating inflammation and its associated diseases has been well documented. Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL) are two well-known inflammation related diseases caused by Kaposi's sarcoma-associated herpesvirus (KSHV). Controlling inflammation is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evaluating the therapeutic potential of using lipoxins. This study documents how KSHV manipulates and downregulates the secretion of the anti-inflammatory lipoxin A4 in host cells and the viral factors involved in this process using Kaposi's sarcoma-associated herpesvirus (KSHV), also termed human herpesvirus 8 (HHV-8), is etiologically associated with Kaposi's sarcoma (KS) and B-cell lymphoproliferative primary effusion lymphoma (PEL). KS is a proliferative angiogenic tumor of endothelial cells characterized by vascular red/purplish lesions in the skin (1-3). PEL, also known as body cavity lymphoma, is a non-Hodgkin's lymphoma primarily present in the body cavity (4). KS and PEL are a significant cause of death in HIV patients. The presence of a suppressed host immune system along with KSHV-coded immunomodulatory proteins contributes to KSHV infection, and the lifelong KSHV latency establishment is the primary factor for pathogenesis (5, 6). KSHV utilizes its latency cluster containing ORF73 (latency-associated nuclear antigen 1 [LANA-1]), ORF72 (viral cyclin [vCyclin]), ORF71 (K13/ vFLIP), and ORFK12 (kaposins A, B, and C), as well as 12 distinct pre-microRNAs, to modulate the host immune system and maintain lifelong latency (7-9). KSHV also encodes several homologs of cytokines and chemokines to alter the immune response (6).KSHV induces several proinflammatory host molecules such as COX-2/PGE2, 5-lipoxygenase, and LTB4 to establish latency and aid in its pathogenesis (10)(11)(12)(13)(14). Beside upregulating proinflammatory pathways, KSHV also modulates the immune system by downregulating anti-inflammatory pathways (15). Since altering the host immune system is the hallmark of KSHV infection and pathogenesis, it is important to understand the relationship between the various components of the host immune system and KSHV to design better therapeutics.To date, there is no effective treatment for KS and PEL. Current treatment involves the use of chemotherapeutics that work by targeting DNA replication of all dividing cells. This approach has the following disadvantages: low efficacy, cytotoxic side effects, depletion of CD4, and risk of secondary malignancies. Above all, these anticancer drugs do not control viral replication and pathogenesis. Surgery is an expensive alternative effective for small size lesions the chance of disease relapse is high. Since KSHV in KS and PEL remains primarily in the latent form, antiviral drugs are not

PurposeThe present study was designed to retrospectively evaluate the prognostic value of the C-reactive protein/albumin (CRP/ALB) ratio in laryngeal squamous cell carcinoma (LSCC).MethodsOne hundred and twenty-nine newly diagnosed LSCC patients admitted between May 2006 and October 2011 were retrospectively reviewed. Their serum CRP and ALB were quantified preoperatively. The relationship between the CRP/ALB ratio and the clinicopathologic features was analyzed. Receiver operating characteristic curve was used to calculate the prognostic value of the CRP/ALB ratio. Then, the Cox proportional hazards model was used in univariate and multivariate analyses to identify significant prognostic factors associated with disease-free survival and overall survival.ResultsThe cutoff value for CRP/ALB ratio was 0.047. An elevated CRP/ALB ratio was significantly associated with nodal metastasis, late disease stage, and recurrence. Also, high values of CRP/ALB ratio were significant predictors for poor overall survival and disease-free survival on multivariate analysis.ConclusionPretreatment CRP/ALB ratio may be a significant prognostic marker in LSCC.

We present a joint experimental and theoretical study on double iron atom doped germanium clusters, Fe2Ge n –/0 (n = 3–12). The experimental photoelectron spectra of cluster anions are reasonably reproduced by theoretical simulations. The low-lying structures of the iron-doped semiconductor clusters are obtained by using an ab initio computation-based genetic-algorithm global optimization method. We find that the smaller-sized Fe2Ge n – (n = 3–8) clusters adopt bipyramid-based geometries, while the larger ones (n ≥ 9) adopt polyhedral cagelike structures with one interior Fe atom. Interestingly, starting from n = 8, the most stable anionic clusters Fe2Ge n – exhibit structures that are different from that of their neutral counterparts Fe2Ge n . Robust ferromagnetic interaction is found between the two doped iron atoms in the neutral clusters Fe2Ge n , while the total spin moment always remains at 4 μB for all the neutral double iron atom doped germanium clusters up to n = 12. This behavior is in stark contrast to the magnetic quenching behavior typically observed in germanium clusters doped with a single Fe atom.

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