[Clinicopathological features and prognosis of malignant peripheral nerve sheath tumor: a retrospective study of 140 cases].

Objective: To investigate the clinicopathological features and prognosis of malignant peripheral nerve sheath tumors (MPNST). Methods: We retrospectively reviewed the clinical data of MPNST patients who were treated at Cancer Institute & Hospital, Chinese Academy of Medical Science from January 1999 to January 2016. A total of 140 patients with 66 male and 74 female with MPNST were enrolled in the study. The median age was 40 at the time of diagnosis. Survival analysis were estimated by Kaplan-Meier method and Log rank test. Multivariate analysis were estimated by Cox proportional hazards regression model. Results: The median follow-up time was 43.0 months. The 3- and 5-year overall survival (OS) rates were 56.4% and 48.6%, respectively. The 3-year local recurrence (LR) rate and distant metastasis (DM) rates were 42.9% and 49.3%, respectively. Univariate analysis showed that the tumor location, AJCC stage, S-100, radiotherapy and margin status affected 5-year OS rate (all P<0.05). The tumor location, AJCC stage, S-100, Ki-67 staining, margin status, radiotherapy and chemotherapy affected 3-year LR rate (all P<0.05). The tumor location, AJCC stage, S-100, Ki-67 staining and margin status affected 3-year DM rate (all P<0.05). Multivariate analysis showed that the tumor location, AJCC stage, S-100 were independent factors for 5-year OS rate (all P<0.05). The tumor location, Ki-67 staining and chemotherapy were independent factors for LR (all P<0.05) while the AJCC stage, margin status and Ki-67 staining were independent factors for DM (all P<0.05). Conclusions: MPSNT is an aggressive tumor with poor prognosis. Multiple factors were identified in this study. Patients with the tumor located at head and neck, advanced AJCC stage and negative S-100 usually have a low 5-year overall survival rate. Patients with the tumor located at head and neck, Ki-67 staining ≥ 20% and without chemotherapy had a higher tendency of local recurrence. Poor prognosis factors for DM were advanced AJCC stage, positive margin and Ki-67 staining ≥ 20%.

Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1, by Z.-B. Zhong, Y.-J. Wu, J.-N. Luo, X.-N. Hu, Z.-N. Yuan, G. Li, Y.-W. Wang, G.-D. Yao, X.-F. Ge, published in Eur Rev Med Pharmacol Sci 2019; 23(24): 10867-10873-DOI: 10.26355/eurrev_201912_19790-PMID: 31858555" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19790.

Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

OBJECTIVE: Recently, long non- coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in the development of thyroid cancer (TC), and to explore the underlying mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, transwell assay and wound healing assay were conducted. QRT-PCR and Western blot assay were used to explore the underlying mechanism. Furthermore, the function of DLX6-AS1 was identified in vivo. RESULTS: DLX6-AS1 expression level in TC tissues was significantly higher than that of the corresponding normal tissues. Moreover, TC cell migration and invasion were markedly inhibited after DLX6-AS1 was knocked down in vitro. The mRNA and protein expressions of UPF1 were both remarkably up-regulated after knockdown of DLX6-AS1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo. CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC.

Has_circ_0008274 promotes cell proliferation and invasion involving AMPK/mTOR signaling pathway in papillary thyroid carcinoma.

OBJECTIVE: Circular RNAs (circRNAs) have been known as important regulators in tumorigenesis. Whether circRNAs are involved in papillary thyroid carcinoma (PTC) requires to be determined. In the present study, we aimed to investigate the expression and function of has_circ_0008274 in PTC. PATIENTS AND METHODS: Tissue expression of has_circ_0008274 was evaluated in Gene Expression Omnibus datasets (GSE93522). Real-time PCR assays were used to detect the expression of has_circ_0008274 in human PTC tissues and cell lines. The correlation of has_circ_0008274 expression with clinicopathological factors was statistically analyzed. The MTT assay, colony formation assay, transwell assays were performed to analyze and compare cell viability and invasion. Western blot analysis was used to quantify the expression of AMPK/mTOR signaling pathway proteins. RESULTS: We found that has_circ_0008274 was significantly upregulated in PTC tissues, and the level of has_circ_0008274 was negatively associated with TNM stage and lymph node metastasis. Loss-of-function assay indicated that knockdown of has_circ_0008274 suppressed PTC cells proliferation and invasion in vitro. Mechanistically, has_circ_0008274 could inhibit the activation of AMPK/mTOR signaling pathway, which was demonstrated by measuring the expression levels of p-AMPK and p-mTOR. CONCLUSIONS: These results demonstrate that increased has_circ_0008274 expression modulates has_circ_0008274 to enhance PTC cells proliferation and invasion. Has_circ_0008274/ AMPK/mTOR axis may be a novel therapeutic candidate target in PTC treatment.

[Determination of micro Pb in preserved egg by flame atomic absorption spectrometry].

The method for the determination of micro Pb in preserved egg by flame atomic absorption spectrometry was studied in this paper. These samples are treated with ammonium persulfate, it is not necessary to preconcentrate the lead by extraction, the method is sensitive, easy to operate and has good precision and accuracy. The detection limit was 0.016 microgram.mL-1, the relative standard deviation of Pb was 3.2%, and the rates of recovery were 94.0%-98.0%.

[Study on the levels of immunoglobulin in gingival cervicular fluid.].

The levels of IgG,IgA in gingival cervicular fluid (GCF) and serum were measured by immunodiffusion method.GCF was collected in improved and graduated capillaries from 50 healthy persons and 32 adult periodontitis patients (AP).The result showed that the level of IgG in GCF of healthy persons was 1.96g/L and the ratio of IgG in GCF to that in serum was 19%.The level of IGA in GCF of healthy persons was not available.In AP,the levels of IgG,IgA in GCF were 7.2g/L,0.83g/L and the ration of IgG and IgA in GCF to those in serum were 71%,61% respectively.Rank correlation between Ig and clinic index in AP showed thant only the level of IgG in GCF had positive correlation with GI.This study reported for the first time the level of IgG in GCF of healthy persons and suggested that the level of IgG in GCF had positive correlation with degree of inflammation in gingiva.

Fc(alpha) receptor I (CD89) on neutrophils in periodontal lesions.

AIMS: In this study, we have examined the occurrence of FcalphaRI-bearing cells in gingival tissue, gingival fluid and blood, in search for possible roles of IgA and FcalphaRI in periodontal lesions. METHODS: Gingival biopsies from inflamed and healthy sites were obtained from patients with chronic marginal periodontitis. Sections of inflamed gingiva were examined by immunofluorescence techniques and compared to sections from healthy sites. Smears were made from blood and gingival crevicular fluid and similarly studied. RESULTS: Dense infiltrates of neutrophils with strong expression of FcalphaRI (and FcgammaRIII) were found in connective tissue and epithelium of the apical part of periodontal pockets from diseased sites. In contrast, only few such cells were found in healthy gingiva from the same patients. Neutrophils in gingival fluid, tissue and blood expressed FcalphaRI with similar intensity, whereas the expression of FcgammaRIII was significantly decreased in gingival crevicular fluid. Considerable numbers of bacteria from gingival plaque were found to be covered by IgA. CONCLUSION: It is suggested that FcalphaRI on neutrophils may play an important rôle in elimination of IgA-opsonized bacteria, both in periodontal tissue and the adjacent pockets.

Reduced numbers of Langerhans cells and increased HLA-DR expression in keratinocytes in the oral gingival epithelium of HIV-infected patients with periodontitis.

BACKGROUND: HIV-seropositive (HIV+) patients become increasingly susceptible to periodontal diseases as HIV infection proceeds. We have previously shown that HIV+ patients with chronic marginal periodontitis (CMP) have remarkably increased numbers of gingival plasma cells in the connective tissue underlying the oral gingival epithelium, but depressed specific serum IgG levels towards periodontopathogenic bacteria. Langerhans cells (LC) and keratinocytes (KC) are antigen-presenting cells that are important in promoting immune responses. METHOD: In this study we examined, by means of immunofluorescence, the distribution and numbers of LC and activated KC in biopsies taken from inflamed periodontal sites in HIV+ and HIV patients with CMP. RESULTS: In the pocket epithelium in both patient groups, basal layer KC expressed HLA-DR molecules. In the oral gingival epithelium of HIV+ patients, basal layer KC also expressed HLA-DR molecules and numbers of LC were decreased as compared with HIV persons. CONCLUSION: The findings suggest that the oral gingiva in HIV+ patients may be affected by inflammation.

Soluble Fc gamma receptors in periodontal lesions.

Soluble Fc gamma-binding components were detected in gingival fluid from periodontal lesions by incubation with biotinylated human Fc gamma fragments. Fc gamma III receptor was identified by incubation of gingival fluid with monoclonal antibody. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western transfer showed that most of the Fc gamma-binding components had minimal mobility in a 4-15% gradient gel under nonreducing conditions. Under reducing conditions, the main band of Fc gamma-binding components in gingival fluid migrated corresponding to protein A of 49 kDa. The pattern of Fc gamma-binding components was similar in serum and gingival fluid except for the observation in gingival fluid of Fc gamma-binding components migrating like standard proteins of 19 to 20 kDa, a size that corresponds to the polypeptide part of Fc gamma II receptor and Fc gamma III receptor.

Increased levels of soluble Fc gamma receptor III in gingival fluid from periodontal lesions.

Enzyme-linked immunosorbent assay was used for determination of the concentration of soluble Fc gamma receptor III (Fc gamma RIII) in 40 samples of gingival fluid obtained from periodontal pockets in 30 patients with periodontitis. The assay was based on a monoclonal immobilized antibody binding Fc gamma RIII and a polyclonal Fc gamma RIII rabbit antibody for its quantification. The results indicate a substantially increased concentration of soluble Fc gamma RIII in gingival fluid as compared to the serum level. This increased concentration of soluble Fc gamma RIII may interfere with phagocytosis and immune homeostasis in the periodontal lesions.

Topical distribution of Fc gammaRI, Fc gammaRII and Fc gammaRIII in inflamed human gingiva.

The topical distribution of Fc gamma receptor types I, II and III (Fc gammaRI-III) was analyzed by means of immunohistochemistry in human gingival tissue obtained from 12 patients with chronic periodontitis. CD68+ macrophages expressing all three classes of Fc gammaR were found throughout the whole gingival connective tissue (CT), whereas dense infiltrates of polymorphonuclear granulocytes (identified by staining for neutrophil elastase) with strong staining for Fc gammaRIII and Fc gammaRII were found subjacent to the apical part of the pocket epithelium (PE) and in the PE itself. CD19+ B lymphocytes with variable staining intensity for Fc gammaRII were observed in clusters subjacent to the PE and extending into the central part of the CT. Only a few scattered CD3+ T lymphocytes stained for Fc gammaRIII. Some spindle-shaped cells (CD68-, therefore non-macrophages) and apparently non-cellular fibrous tissue elements stained for Fc gammaRI and Fc gammaRII. In the epithelium, Fc gammaRII+ dendritic cells were frequently observed in the entire oral gingival epithelium and in the coronal part of the PE. Occasionally, some keratinocytes which stained for Fc gammaRII and Fc gammaRIII were found. The observations indicate that Fc gammaR of the various classes are amply expressed on numerous cell types in inflamed gingival tissue. The specific distribution pattern detected suggests that Fc gammaRs may play a role in the mediation of chronic inflammation in the periodontal lesion.