H epatocellular carcinoma (HCC) is one of the most common cancers in the world, especially in Asia and Africa. Infection by hepatitis B and C viruses, exposure to aflatoxin B 1 , and cirrhosis of any etiology are considered the major risk factors for the development of HCC. 1 The ability to diagnose and treat HCC is limited. To date, surgery is offered as the main treatment, but improved approaches to long-term survival are urgently needed. The poor prognosis of HCC is largely a result of high recurrence after surgery and of resistance to chemotherapy. Therefore, it is necessary to find new clues to understand hepatocarcinogenesis and to explore new targets for the diagnosis of HCC and the development of effective therapeutic strategies.TIP30, also called CC3 or HTIP2, is a putative tumor suppressor. It was initially identified by a differential display analysis of mRNA from the highly metastatic human variant small cell lung carcinoma (v-SCLC) versus less metastatic classic small cell lung carcinoma (c-SCLC) cell lines. 2 Its expression has been detected in many human normal tissues; however, in some tumor types such as melanoma, breast cancer, neuroblastoma, glioblastoma, colon cancer, and hepatocellular carcinoma, its expression was found to be decreased. [2][3][4][5][6] Studies of Tip30-deficient mice revealed a high incidence of hepatocellular carcinoma and other tumors with a relatively long latency. 6 Expression of TIP30 was reduced in about 33% of surgical specimens from HCC patients. Some of these carci-

Glial loss in the hippocampus has been suggested as a factor in the pathogenesis of stress-related brain disorders that are characterized by dysregulated glucocorticoid (GC) secretion. However, little is known about the regulation of astrocytic fate by GC. Here, we show that astrocytes derived from the rat hippocampus undergo growth inhibition and display moderate activation of caspase 3 after exposure to GC. Importantly, the latter event, observed both in situ and in primary astrocytic cultures is not followed by either early- or late-stage apoptosis, as monitored by stage I or stage II DNA fragmentation. Thus, unlike hippocampal granule neurons, astrocytes are resistant to GC-induced apoptosis; this resistance is due to lower production of reactive oxygen species (ROS) and a greater buffering capacity against the cytotoxic actions of ROS. We also show that GC influence hippocampal cell fate by inducing the expression of astrocyte-derived growth factors implicated in the control of neural precursor cell proliferation. Together, our results suggest that GC instigate a hitherto unknown dialog between astrocytes and neural progenitors, adding a new facet to understanding how GC influence the cytoarchitecture of the hippocampus.

Background: The intracellular signaling cascades through which corticosterone rapidly alters neuronal activity are poorly defined. Results: Corticosterone alters glutamatergic transmission by activating diverse GPCR-dependent signaling pathways. Conclusion: Corticosterone-induced changes in neuronal excitability are initiated at the plasma membrane. Significance: The sequential recruitment and integration of diverse signaling cascades by corticosterone adds to the understanding of how steroids rapidly alter neuronal function.