Epigenetic mechanisms in virus-induced tumorigenesis

About 15–20% of human cancers worldwide have viral etiology. Emerging data clearly indicate that several human DNA and RNA viruses, such as human papillomavirus, Epstein–Barr virus, Kaposi’s sarcoma-associated herpesvirus, hepatitis B virus, hepatitis C virus, and human T-cell lymphotropic virus, contribute to cancer development. Human tumor-associated viruses have evolved multiple molecular mechanisms to disrupt specific cellular pathways to facilitate aberrant replication. Although oncogenic viruses belong to different families, their strategies in human cancer development show many similarities and involve viral-encoded oncoproteins targeting the key cellular proteins that regulate cell growth. Recent studies show that virus and host interactions also occur at the epigenetic level. In this review, we summarize the published information related to the interactions between viral proteins and epigenetic machinery which lead to alterations in the epigenetic landscape of the cell contributing to carcinogenesis

Molecular pathways leading to loss of skeletal muscle mass in cancer cachexia can findings from animal models be translated to humans?

Background: Cachexia is a multi-factorial, systemic syndrome that especially affects patients with cancer of the gastrointestinal tract, and leads to reduced treatment response, survival and quality of life. The most important clinical feature of cachexia is the excessive wasting of skeletal muscle mass. Currently, an effective treatment is still lacking and the search for therapeutic targets continues. Even though a substantial number of animal studies have contributed to a better understanding of the underlying mechanisms of the loss of skeletal muscle mass, subsequent clinical trials of potential new drugs have not yet yielded any effective treatment for cancer cachexia. Therefore, we questioned to which degree findings from animal studies can be translated to humans in clinical practice and research. Discussion: A substantial amount of animal studies on the molecular mechanisms of muscle wasting in cancer cachexia has been conducted in recent years. This extensive review of the literature showed that most of their observations could not be consistently reproduced in studies on human skeletal muscle samples. However, studies on human material are scarce and limited in patient numbers and homogeneity. Therefore, their results have to be interpreted critically. Summary: More research is needed on human tissue samples to clarify the signaling pathways that lead to skeletal muscle loss, and to confirm pre-selected drug targets from animal models in clinical trials. In addition, improved diagnostic tools and standardized clinical criteria for cancer cachexia are needed to conduct standardized, randomized controlled trials of potential drug candidates in the future

Key concepts behind forming-free resistive switching incorporated with rectifying transport properties

This work reports the effect of Ti diffusion on the bipolar resistive switching in Au/BiFeO(3)/Pt/Ti capacitor-like structures. Polycrystalline BiFeO(3) thin films are deposited by pulsed laser deposition at different temperatures on Pt/Ti/SiO(2)/Si substrates. From the energy filtered transmission electron microscopy and Rutherford backscattering spectrometry it is observed that Ti diffusion occurs if the deposition temperature is above 600°C. The current-voltage (I–V) curves indicate that resistive switching can only be achieved in Au/BiFeO(3)/Pt/Ti capacitor-like structures where this Ti diffusion occurs. The effect of Ti diffusion is confirmed by the BiFeO(3) thin films deposited on Pt/sapphire and Pt/Ti/sapphire substrates. The resistive switching needs no electroforming process, and is incorporated with rectifying properties which is potentially useful to suppress the sneak current in a crossbar architecture. Those specific features open a promising alternative concept for nonvolatile memory devices as well as for other memristive devices like synapses in neuromorphic circuits