Monosomy 13 in metaphase spreads is a predictor of poor long-term outcome after bortezomib plus dexamethasone treatment for relapsed/refractory multiple myeloma

We retrospectively investigated the prognostic impact of high-risk cytogenetic abnormalities (CAs) on the outcome of treatment with bortezomib plus dexamethasone (BD) in 43 relapsed/refractory (Rel/Ref) multiple myeloma patients. Fluorescence in situ hybridization (FISH) analysis identified del(13q) in 25 patients, t(4;14) in 14, t(14;16) in 4, 1q21 abnormality in 12 and del(17p) in 2, while G-banding also detected chromosome 13 monosomy (-13) in metaphase spreads from 7 patients. Eighteen of 25 patients with FISH-detected chromosome 13 abnormalities also exhibited other abnormalities. Median observation period was 510 days, and median overall survival (OS) and progression-free survival (PFS) were 912 days and 162 days, respectively. Detection of del(13q), t(4;14), t(14;16) or 1q21 abnormalities by FISH and co-occurrence of chromosome 13 abnormality with other abnormalities were not associated with poorer outcomes. In contrast, detection of -13 by G-banding in metaphase spreads showed significant association with shorter OS, although the overall response rate and PFS were not inferior to those for patients without -13 detected by G-banding. BD therapy may be a potent weapon for overcoming most classical high-risk CAs, while the detection of -13 in metaphase spreads may serve as a predictor of highly progressive disease, even when treated with BD.     

Effects of metal cation doping in CeO2 support on catalytic methane steam reforming at low temperature in an electric field

Catalytic methane steam reforming was conducted at low temperature using a Pd catalyst supported on Ce_1−xM_xO₂ (x = 0 or 0.1, M = Ca, Ba, La, Y or Al) oxides with or without an electric field (EF). The effects of the catalyst support on catalytic activity and surface proton hopping were investigated. Results show that Pd/Al-CeO₂ (Pd/Ce_0.9Al_0.1O₂) showed higher activity than Pd/CeO₂ with EF, although their activity was identical without EF. Thermogravimetry revealed a larger amount of H₂O adsorbed onto Pd/Al-CeO₂ than onto Pd/CeO₂, so Al doping to CeO₂ contributes to greater H₂O adsorption. Furthermore, electrochemical conduction measurements of Pd/Al-CeO₂ revealed a larger contribution of surface proton hopping than that for Pd/CeO₂. This promotes the surface proton conductivity and catalytic activity during EF application.

Temperature dependence of electron/ion conductivity of Pd/CeO₂ and Pd/Al-CeO₂ under wet conditions with application of an electric field.     

Epithelioid myoepithelioma of the hard palate

Background

Myoepithelioma, a generally benign tumor comprised of myoepithelial cells, is an uncommon salivary gland tumor. Among four morphologic variants of myoepithelioma, epithelioid type has not been reported in the oral and maxillofacial region.

Case report

A 61-year-old man first noticed the mass 3 years previously. The oral examination revealed a firm, non-tender, and well-circumscribed mass in the middle of the hard palate. A magnetic resonance imaging scan showed a well-circumscribed mass with low signal intensity (T₁-weighted image) or increased signal intensity (T₂-weighted image).

Discussion

Immunohistochemically, the tumor cells in the present case reacted to the epithelial (CK HMW and CAM5.2) and the mesenchymal (vimentin) markers. However, myoepithelial markers (S-100 protein, α-smooth muscle actin, glial fibrillary acidic protein, and calponin), except p63, were not expressed in the tumor cells. These results indicated that the epithelial myoepithelioma cells differentiated into epithelial cells rather than myoepithelial cells. We believe that epithelioid myoepithelioma of the palate is a distinctive subtype of myoepithelioma that should be included in the differential diagnosis of tumors of the palate.     

G protein‐coupled receptor 30 contributes to improved remyelination after cuprizone‐induced demyelination

Estrogen exerts neuroprotective and promyelinating actions. The therapeutic effect has been shown in animal models of multiple sclerosis, in which the myelin sheath is specifically destroyed in the central nervous system. However, it remains unproven whether estrogen is directly involved in remyelination via the myelin producing cells, oligodendrocytes, or which estrogen receptors are involved. In this study, we found that the membrane‐associated estrogen receptor, the G protein‐coupled receptor 30 (GPR30), also known as GPER, was expressed in oligodendrocytes in rat spinal cord and corpus callosum. Moreover, GPR30 was expressed throughout oligodendrocyte differentiation and promyelinating stages in primary oligodendrocyte cultures derived from rat spinal cords and brains. To evaluate the role of signaling via GPR30 in promyelination, a specific agonist for GPR30, G1, was administered to a rat model of demyelination induced by cuprizone treatment. Histological examination of the corpus callosum with oligodendrocyte differentiation stage‐specific markers showed that G1 enhanced oligodendrocyte maturation in corpus callosum of cuprizone‐treated animals. It also enhanced oligodendrocyte ensheathment of dorsal root ganglion (DRG) neurons in co‐culture and myelination in cuprizone‐treated animals. This study is the first evidence that GPR30 signaling promotes remyelination by oligodendrocytes after demyelination. GPR30 ligands may provide a novel therapy for the treatment of multiple sclerosis. © 2012 Wiley Periodicals, Inc.