Comprehensive analysis of the REST transcription factor regulatory networks in IDH mutant and IDH wild-type glioma cell lines and tumors.

The RE1-silencing transcription factor (REST) acts either as a repressor or activator of transcription depending on the genomic and cellular context. REST is a key player in brain cell differentiation by inducing chromatin modifications, including DNA methylation, in a proximity of its binding sites. Its dysfunction may contribute to oncogenesis.

DMRTA2 supports glioma stem-cell mediated neovascularization in glioblastoma.

Glioblastoma (GBM) is the most common and lethal brain tumor in adults. Due to its fast proliferation, diffusive growth and therapy resistance survival times are less than two years for patients with IDH-wildtype GBM. GBM is noted for the considerable cellular heterogeneity, high stemness indices and abundance of the glioma stem-like cells known to support tumor progression, therapeutic resistance and recurrence.

Methylcellulose/agarose hydrogel loaded with short electrospun PLLA/laminin fibers as an injectable scaffold for tissue engineering/3D cell culture model for tumour therapies.

This research aimed at designing and fabricating a smart thermosensitive injectable methylcellulose/agarose hydrogel system loaded with short electrospun bioactive PLLA/laminin fibers as a scaffold for tissue engineering applications or 3D cell culture models. Considering ECM-mimicking morphology and chemical composition, such a scaffold is capable of ensuring a hospitable environment for cell adhesion, proliferation, and differentiation. Its viscoelastic properties are beneficial from the practical perspective of minimally invasive materials that are introduced to the body injection.

Exploring Novel Therapeutic Opportunities for Glioblastoma Using Patient-Derived Cell Cultures.

Glioblastomas (GBM) are the most common, primary brain tumors in adults. Despite advances in neurosurgery and radio- and chemotherapy, the median survival of GBM patients is 15 months. Recent large-scale genomic, transcriptomic and epigenetic analyses have shown the cellular and molecular heterogeneity of GBMs, which hampers the outcomes of standard therapies.

Regulatory networks driving expression of genes critical for glioblastoma are controlled by the transcription factor c-Jun and the pre-existing epigenetic modifications.

Background: Glioblastoma (GBM, WHO grade IV) is an aggressive, primary brain tumor. Despite extensive tumor resection followed by radio- and chemotherapy, life expectancy of GBM patients did not improve over decades. Several studies reported transcription deregulation in GBMs, but regulatory mechanisms driving overexpression of GBM-specific genes remain largely unknown.