Valproic acid treatment of glioblastoma multiforme in a child

Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

“…When VPA was given as maintenance therapy for childhood malignant glioma after postoperative combined chemotherapy and irradiation, about 10% of these patients were maintained in continuous complete remission and an equal number of patients showed at least partial responses ). An additional pediatric patient with glioblastoma multiforme responded to VPA after showing progressive disease shortly after having received combined chemotherapy and irradiation as well as topotecane (Witt et al, 2004). Another pediatric patient suffering from a relapsed supratentorial primitive neuroectodermal tumour while receiving chemotherapy (CCNU, VCR and cisplatinum) after total resection and irradiation showed conspicuous signs of glial differentiation induction and a nonmalignant morphology on histological examination.…”

The MEK-1/ERKs signalling pathway is differentially involved in the self-renewal of early and late avian erythroid progenitor cells

“…Work of others addressing the role of the ERK/MAPK signalling pathway in murine and human erythroid progenitors yielded conflicting findings (Nagata et al, 1998;Matsuzaki et al, 2000;Witt et al, 2000;von Lindern et al, 2001). In these cells, activation of MEK-1 as detected by ERK/MAPK phosphorylation was induced by erythropoietin (Epo) and the c-Kit ligand stem cell factor (SCF).…”

“…A few interesting leads (including the role of the PI3K pathway) were not further pursued in the present work. Instead we focused on the Ras/MEK-1/ERK-MAPK pathway since conflicting results exist with respect to its role in erythropoiesis (Nagata et al, 1998;Matsuzaki et al, 2000;Witt et al, 2000;von Lindern et al, 2001) and since it was the only self-renewal-specific pathway identified.…”

“…In different culture models of erythroid progenitor, conflicting results have been obtained with respect to the role of the ERK/MAPK pathway (Nagata et al, 1998;Matsuzaki et al, 2000;Witt et al, 2000;von Lindern et al, 2001). Notably, this pathway seemed to be fully dispensable for the EpoR/c-kitdriven renewal of primary mammalian erythroid progenitors (Von Lindern et al, 2001).…”

Autocrine transforming growth factor-β regulation of hematopoiesis: many outcomes that depend on the context

“…The ability of these chemicals to induce changes in gene expression is mediated in part by changes in signal transduction pathways. Butyrate caused sustained activation of JAK/STAT signaling in murine erythroleukemia cells, moreover, erythodifferentiation of K562 cells by HU and butyrate involved the phosphorylation of p38 and dephosphorylation of ERK and JNK MAPKs (Witt et al, 2000;Park et al, 2001). Smad activation is also involved in the regulation of HU-and butyrate-induced erythroid differentiation of K562 cells.…”