Ricerc@Sapienza

One of the major limits of chemotherapy is depending on the ability of the cancer cells
to elude and adapt to dierent drugs. Recently, we demonstrated how the activation of the M2
muscarinic receptor could impair neuroblastoma cell proliferation. In the present paper, we investigate
the possible eects mediated by the preferential M2 receptor agonist arecaidine propargyl ester (APE)
on drug resistance in two neuroblastoma cell lines, SK-N-BE and SK-N-BE(2C), a sub-clone presenting

The role of muscarinic receptors has been largely documented over the past few decades. Recently we demonstrated that the activation of M2 muscarinic receptors arrested cell proliferation and induced apoptosis in glioblastoma and in other tumour types. This paper aims to evaluate the expression of the M2 muscarinic receptor subtypes in different neuroblastoma cell lines and its role in the control of cell proliferation and survival. Neuroblastoma is the most common solid extracranial tumour, appearing during childhood and displaying a differentiated clinical behaviour.

The mouse neuroblastoma N18TG2 clone is unable to differentiate and is defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone.

Background: Molecular mechanisms of interaction between cells and extremely low frequency magnetic fields (ELF-MFs) still represent a matter of scientific debate. In this paper, to identify the possible primary source of oxidative stress induced by ELF-MF in SH-SY5Y human neuroblastoma cells, we estimated the induced electric field and current density at the cell level. Methods: We followed a computational multiscale approach, estimating the local electric field and current density from the whole sample down to the single cell level.

Chimeric antigen receptor (CAR) T-cell therapy has been shown to be dramatically effective in the treatment of B-cell malignancies. However, there are still substantial obstacles to overcome, before similar responses can be achieved in patients with solid tumors. We evaluated both in vitro and in a preclinical murine model the efficacy of different 2nd and 3rd generation CAR constructs targeting GD2, a disial-ganglioside expressed on the surface of neuroblastoma (NB) tumor cells.