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Objective: Virtual Reality (VR) has been demonstrated to be an effective option for integrating psychological interventions in different therapeutic settings. This randomized controlled interventional study aims to assess the effects of VR, compared to tablet controlled intervention, on anxiety, depression, pain, and short‐term psychophysical symptoms in advanced cancer patients assisted at home. Methods: Participants were provided with a VR headset or a tablet (TAB) for 4 days. On the first and last day, anxiety and depression were measured by Hospital Anxiety and Depression Scale and pain by Brief Pain Inventory. Before and after each VR and tablet session, symptoms were collected by the Edmonton Symptom Assessment Scale (ESAS). Results: Fifty‐three patients (27 VR vs. 26 TAB) completed the study. Anxiety significantly decreased in the VR group after the 4‐day intervention. The analysis of ESAS showed a significant improvement in pain (p = 0.013), tiredness (p < 0.001), and anxiety (p = 0.013) for TAB group, and a significant reduction in tiredness (p < 0.001) in the VR group. Conclusions: Technological and user‐friendly tools, such as VR and tablets, might be integrated with traditional psychological interventions to improve anxiety and cancer‐related short‐term symptoms. Further studies are needed to better consolidate the possible beneficial effects of VR. [ABSTRACT FROM AUTHOR]

Background Sorafenib is the standard treatment of advanced hepatocarcinoma ( HCC) in cirrhotic patients with preserved liver function. It shares many adverse effects with other tyrosine-kinase ( TK) inhibitors and antiangiogenic drugs. TK inhibitors could have a direct toxicity on CNS, both by interfering with TK-related pathways and by inhibiting angiogenesis. Aims The aim of this study was to investigate whether sorafenib administration can be associated to metabolic encephalopathy in patients with cirrhosis. Methods We retrospectively reviewed medical records of all cirrhotic patients treated with sorafenib for HCC afferent at our Department from January 2009 to December 2011. Results Among 62 patients, we identified 10 patients with clinically significant cognitive impairment. Seven of these were clearly diagnosed with overt hepatic encephalopathy ( HE), one with brain metastases and two with drug-related toxic-metabolic encephalopathy. These last two cases were characterized by severe cognitive impairment, mood alteration and memory deficit. Clinical exam, blood tests and brain CT excluded organic causes of encephalopathy and precipitating factors of HE. Sorafenib discontinuation was associated with complete reversal of the syndrome, which recurred on drug re-administration in one case. Conclusions Our study suggests that sorafenib may be a precipitating factor of metabolic encephalopathy in cirrhotic patients with advanced HCC. This neurological syndrome appears to be not responsive to the conventional treatment for HE, but it is fully reversible by drug discontinuation. It can be speculated that the potential direct neuronal action of sorafenib may represent a trigger for the onset of metabolic encephalopathy in a subset of cirrhotic patients. [ABSTRACT FROM AUTHOR]

Pantaleo M A, Astolfi A, Nannini M, Ceccarelli C, Formica S, Santini D, Heinrich M C, Corless C, Dei Tos A P, Paterini P, Catena F, Maleddu A, Saponara M, Di Battista M & Biasco G (2011) Histopathology 59, 1071-1080 Differential expression of neural markers in KIT and PDGFRA wild-type gastrointestinal stromal tumours Aims: To compare the genomic signatures of wild-type (WT) and mutated GISTs and the murine interstitial cells of Cajal (ICCs) to find markers of cell differentiation and other functions that may identify cells that give rise to WT tumours. Methods and results: We analysed the gene expression profiles of a total of 30 tumour samples (four WT GISTs and 26 mutated GISTs), selected the genes most differentially expressed ( P < 0.001:448 probe sets) and validated these results by quantitative polymerase chain reaction (PCR) and immunohistochemistry. In addition, we conducted a meta-analysis merging data from human GISTs with a genomic data set from murine ICCs. The gene expression profiles of WT and mutated GISTs differed profoundly, especially in the expression of those genes restricted primarily to neural tissues. We found that mature ICCs are more similar to mutated GISTs than WT GISTs. Conclusions: WT GISTs have different genomic profiles from both mutated GISTs and murine mature ICCs. Considering that IGF1R expression is common to both WT GISTs and putative precursor ICCs, this study suggests that WT GISTs may derive either from ICCs at a different step of differentiation or from a different cell of origin. [ABSTRACT FROM AUTHOR]

Inflammation promotes colorectal carcinogenesis. Tumour growth often generates a hypoxic environment in the inner tumour mass. We here report that, in colon cancer cells, the expression of the pro-inflammatory enzyme cyclooxygenase-2 (COX-2) associates with that of the hypoxia response gene carbonic anhydrase-IX (CA-IX). The COX-2 knockdown, achieved by the stable infection of a COX-2 specific short harpin RNA interference (shCOX-2), down-regulates CA-IX gene expression. In colorectal cancer (CRC) cells, PGE2, the main COX-2 gene products, promotes CA-IX gene expression by ERK1/2 activation. In normoxic environment, shCOX-2 infected/CA-IX siRNA transfected CRC cells show a reduced level of active metalloproteinase-2 (MMP-2) that associates with a decreased extracellular matrix invasion capacity. In presence of hypoxia, COX-2 gene expression and PGE2 production increase. The knockdown of COX-2/CA-IX blunts the survival capability of CRC cells in hypoxia. At a high cell density, a culture condition that creates a mild pericellular hypoxic environment, the expression of COX-2/CA-IX genes is increased and triggers the invasive potential of colon cancer cells. In human colon cancer tissues, COX-2/CA-IX protein expression levels, assessed by Western blot and immunohistochemistry, correlate each other and increase with tumour stage. In conclusion, these data indicate that COX-2/CA-IX interplay promotes the aggressive behaviour of CRC cells. [ABSTRACT FROM AUTHOR]

A letter to the editor "An immunohistochemical study of potential diagnostic and therapeutic biomarkers of wild type gastrointestinal stromal tumours" by N.A. Wong and others which appeared in the 2015 issue of the periodical is presented.