Erratum: Dihydroartemisinin inhibits the Raf/ERK/MEK and PI3K/AKT pathways in glioma cells.

[This corrects the article DOI: 10.3892/ol.2015.

An allele of rs619586 polymorphism in MALAT1 alters the invasiveness of meningioma via modulating the expression of collagen type V alpha (COL5A1).

The rs619586 polymorphism has been shown to alter the expression of MALAT1, which act as a competing endogenous RNA (ceRNA) against miR-145. And miR-145 was found to target COL5A1, the interaction between which was shown to be involved in the pathogenesis of invasive meningioma. In this study, we aimed to explore the effect of rs619586 polymorphism and its underlying molecular mechanism in invasive meningioma.

Dihydroartemisinin inhibits the Raf/ERK/MEK and PI3K/AKT pathways in glioma cells.

It has previously been reported that dihydroartemisinin (DHA) is an effective novel anticancer compound in a number of types of tumor cells. Previous studies have demonstrated the anticancer activity of DHA in gioma cells. However, its underlining mechanism remains unclear.

The expression of ATF3, MMP-2 and maspin in tissue chip of glioma.

This paper tested and analyzed the expression of ATF3 (activating transcription factor), MMP-2 (matrix metalloprotease) and maspin in tissue chip of glioma and its correlation with glioma advancement. Based on immunohistochemical staining, this paper selected 100 patients with glioma and 13 healthy persons to test the relative expression of ATF3, MMP-2 and maspin. The result witnessed 72.

Decreased FOXD3 Expression Is Associated with Poor Prognosis in Patients with High-Grade Gliomas.

Background: The transcription factor forkhead box D3 (FOXD3) plays important roles in the development of neural crest and has been shown to suppress the development of various cancers. However, the expression and its potential biological roles of FOXD3 in high-grade gliomas (HGGs) remain unknown.

Methods: The mRNA and protein expression levels of FOXD3 were examined using real-time quantitative PCR and western blotting in 23 HGG and 13 normal brain samples, respectively.

Activating transcription factor 3 is overexpressed in human glioma and its knockdown in glioblastoma cells causes growth inhibition both in vitro and in vivo.

Glioblastomas are highly malignant gliomas that are extremely invasive with high rates of recurrence and mortality. It has been reported that activating transcription factor 3 (ATF3) is expressed in elevated levels in multiple malignant tumors. The purpose of this study was to investigate the function of ATF3 in the development of glioma and its clinical significance.

Clinical research for curing ankylosing spondylitis through combining etanercept, thalidomide and sulfasalazine.

This article is to explore the curative effect of treating ankylosing spondylitis (AS) through combining etanercept, thalidomide and sulfasalazine. Sixty-two patients with AS were divided into 3 groups: experimental group Ais treated by etanercept+ thalidomide + sulfasalazine for 1 year (n=22); control group B was treated with etanercept; control group C was treated with thalidomide + sulfasalazine for 1 year (n=20). In 1st, 3rd, 6th, 12th month after the treatment, ASAS20 and ASAS50 were obtained through Bath ankylosing spondylitis disease activity index (BASDAI), Bath ankylosing spondylitis functional index (BASFI), erythrocyte sedimentation rate (ESR), C react protein (CRP) and then curative effect was analyzed.