Role of ALD Al2O3 Surface Passivation on the Performance of p-Type Cu2O Thin Film Transistors

High-performance p- type oxide thin film transistors (TFTs) have great potential for many semiconductor applications. However, these devices typically suffer from low hole mobility and high off-state currents. We fabricated p-type TFTs with a phase-pure polycrystalline Cu2O semiconductor channel grown by atomic layer deposition (ALD). The TFT switching characteristics were improved by applying a thin ALD Al2O3 passivation layer on the Cu2O channel, followed by vacuum annealing at 300 degrees C. Detailed characterization by transmission electron microscopy-energy dispersive X-ray analysis and X-ray photoelectron spectroscopy shows that the surface of Cu2O is reduced following Al2O3 deposition and indicates the formation of a 1-2 nm thick CuAlO2 interfacial layer. This, together with field-effect passivation caused by the high negative fixed charge of the ALD Al2O3, leads to an improvement in the TFT performance by reducing the density of deep trap states as well as by reducing the accumulation of electrons in the semiconducting layer in the device off-state.Peer reviewe

sFRP2 in the aged microenvironment drives melanoma metastasis and therapy resistance

Cancer is a disease of aging, and aged cancer patients have a poorer prognosis. This may be due to accumulated cellular damage, decreases in adaptive immunity, and chronic inflammation. However, the effects of the aged microenvironment on tumor progression have been largely unexplored. Since dermal fibroblasts can have profound impacts on melanoma progression(1–4) we examined whether age-related changes in dermal fibroblasts could drive melanoma metastasis and response to targeted therapy. We find that aged fibroblasts secrete a Wnt antagonist, sFRP2, which activates a multi-step signaling cascade in melanoma cells that results in a decrease in β-catenin and MITF, and ultimately the loss of a key redox effector, APE1. Loss of APE1 attenuates the response of melanoma cells to ROS-induced DNA damage, rendering them more resistant to targeted therapy (vemurafenib). Age-related increases in sFRP2 also augment both angiogenesis and metastasis of melanoma cells. These data provide an integrated view of how fibroblasts in the aged microenvironment contribute to tumor progression, offering new paradigms for the design of therapy for the elderly