Topic: temozolomide

Diaphanous-related formin (DIAPH) 3 is a key regulator of fundamental processes such as division, adhesion, motility and polarity. Diaph3 is exclusively expressed in neural progenitors in the developing mouse brain and its deficiency causes aberrant cell division and aneuploidy, resulting in the loss of neural progenitor cells. Errors in mitosis often lead to mitotic catastrophe and subsequent cell death, impeding the proliferation of aneuploid cells. Nevertheless, aneuploidy is a hallmark of highly proliferative cancer cells and is generally associated with poor prognosis and therapeutic resi

Gliomas, the heterogeneous primary brain tumors lacking efficient treatment, interact with their tumor microenvironment (TME) and the central nervous system (CNS) resident cells to support their own survival and growth. Deeper knowledge on these interactions is needed to improve treatment, and therefore glioma models incorporating components of human TME are of great interest. The aim of this work was to develop a three-dimensional (3D) in vitro coculture model for assessing physical and functional neuro-glioma interactions. For that, human glioblastoma cell line LN229/GFP-derived spheroids we

Glioblastoma (GBM) tumors rely on neovascularization, driven by specific tumor signals that stimulate endothelial cell (EC) proliferation, migration, and differentiation. Moreover, extracellular vesicles (EVs) has emerged as a key mediator in tumor angiogenesis. This in vitro study assesses glioblastoma-derived EVs' (GD-EV) potential in endothelial cell remodelling (ECR). Glioblastoma cell (U87 MG) conditioned media, treated with the chemotherapeutic drug, Temozolomide (TMZ), EV inhibitor (GW4869), or TMZ+EV inhibitor, were incubated with endothelial cells, HUVEC. Dose-& time-dependent stu

Glioblastoma multiforme (GBM) is a highly therapy-resistant primary brain tumor, especially due to the presence of Glioblastoma Stem Cells (GSCs). In fact, GBM treatment imposes a combination of brain surgery, radiotherapy and chemotherapy with Temozolomide (TMZ) but still fails to completely abolish the tumor. Given this, exploring differentiation induction in GSCs emerges as a promising strategy for GBM treatment. Accordingly, we aimed to investigate the mechanisms that regulate stemness maintenance and differentiation in GBM using Whole-Cell Patch Clamp, Western Blot, Immunofluorescence and

Chemotherapy with Temozolomide (TMZ) is a mainstay for the treatment of primary brain tumors (glioblastomas; GBM). However, drug efficacy is reduced through a profound ability of GBM cells for DNA-repair and by the blood tumor barrier (BTB), which restricts intratumoral TMZ accumulation. Coherently, GBM almost invariably relapse with fatal outcome. We here show that GBM associated myeloid cells (GAM) simultaneously induce chemoresistance on the genetic and the vascular level by activating GP130 receptor signaling, which can be addressed therapeutically. After performing transcriptomic screens