The complexity and heterogeneity of tumours have hindered efforts to identify commonalities among different cancers. Furthermore, because we have limited information on the prevalence and nature of ubiquitous molecular events that occur in neoplasms, it is unfeasible to implement molecular-targeted cancer screening and prevention. Here, we found that the FEAT protein is overexpressed in most human cancers, but weakly expressed in normal tissues including the testis, brain, and liver. Transgenic mice that ectopically expressed FEAT in the thymus, spleen, liver, and lung spontaneously developed invasive malignant lymphoma (48%, 19/40) and lung-metastasizing liver cancer (hepatocellular carcinoma) (35%, 14/40) that models human hepatocarcinogenesis, indicating the FEAT protein potently drives tumorigenesis in vivo. Gene expression profiling suggested that FEAT drives receptor tyrosine kinase and hedgehog signalling pathways. These findings demonstrate that integrated efforts to identify FEAT-like ubiquitous oncoproteins are useful and may provide promising approaches for cost-effective cancer screening and prevention.
The photoluminescence decay in amorphous semiconductors is described by power law t −δ at long times. The power-law decay of photoluminescence at long times is commonly observed but recent experiments have revealed that the exponent, δ ∼ 1.2 − 1.3, is smaller than the value 1.5 predicted from a geminate recombination model assuming normal diffusion. Transient currents observed in the time-of-flight experiments are highly dispersive characterized by the disorder parameter α smaller than 1. Geminate recombination rate should be influenced by the dispersive transport of charge carriers. In this paper we derive the simple relation, δ = 1 + α/2. Not only the exponent but also the amplitude of the decay calculated in this study is consistent with measured photoluminescence in a-Si:H.
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