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This paper describes for the first time, a high-speed and low-power III-V p-channel QWFET using a compressively strained InSb QW structure. The InSb p-channel QW device structure, grown using solid source MBE, demonstrates a high hole mobility of 1,230cm 2 /V-s. The shortest 40nm gate length (L G ) transistors achieve peak transconductance (G m ) of 510μS/μm and cut-off frequency (f T ) of 140GHz at supply voltage of 0.5V. These represent the highest G m and f T ever reported for III-V p-channel FETs. In addition, effective hole velocity of this device has been measured and compared to that of the standard strained Si p-channel MOSFET. IntroductionThe III-V compound semiconductor quantum-well field effect transistor (QWFET) is one of the most promising device candidates for future high-speed, low-power logic applications due to its high electron mobility. Recently, highperformance III-V n-channel QWFETs have been demonstrated [1][2][3][4]. However, for implementation of CMOS logic, there is a significant challenge of identifying high mobility III-V p-channel candidates [5]. In this work, we demonstrate for the first time a high-speed and low-power III-V p-channel QWFET using a compressively strained InSb QW structure, which achieves cut-off frequency (f T ) of 140GHz at transistor gate length (L G ) of 40nm and supply voltage (V CC ) of 0.5V. This represents the highest f T ever reported for III-V p-channel FETs.

Background Glioblastoma (GBM) is a highly aggressive brain tumor with rapid subclonal diversification, harboring molecular abnormalities that vary temporo-spatially, a contributor to therapy resistance. Fluorescence guided neurosurgical resection utilizes administration of 5-aminolevulinic acid (5ALA) generating individually fluorescent tumor cells within a background population of non-neoplastic cells in the invasive tumor region. The aim of the study was to specifically isolate and interrogate the invasive GBM cell population using a novel 5ALA based method. Methods We have isolated the critical invasive GBM cell population by developing 5ALA-based metabolic fluorescence activated cell sorting. This allows purification and study of invasive cells from GBM without an overwhelming background “normal brain” signal to confound data. The population was studied using RNAseq, rtPCR and immunohistochemistry, with gene targets functionally interrogated on proliferation and migration assays using siRNA knockdown and known drug inhibitors. Results RNAseq analysis identifies specific genes such as SERPINE1 which is highly expressed in invasive GBM cells but at low levels in the surrounding normal brain parenchyma. siRNA knockdown and pharmacological inhibition with specific inhibitors of SERPINE1 reduced the capacity of GBM cells to invade in an in vitro assay. Rodent xenografts of 5ALA positive cells were established and serially transplanted, confirming tumorigenicity of the fluorescent patient derived cells but not the 5ALA negative cells. Conclusions Identification of unique molecular features in the invasive GBM population offer hope for developing more efficacious targeted therapies compared to targeting the tumor core and for isolating tumor sub-populations based upon intrinsic metabolic properties.

Despite advances in surgery, radiation therapy, and chemotherapeutics, patients with malignant glioma have a dismal prognosis. The formations of aberrant tumour vasculature and glioma cell invasion are major obstacles for effective treatment. Angiogenesis is a key event in the progression of malignant gliomas, a process involving endothelial cell proliferation, migration, reorganization of extracellular matrix and tube formation. Such processes are regulated by the homeostatic balance between proangiogenic and antiangiogenic factors, most notably vascular endothelial growth factors (VEGFs) produced by glioma cells. Current strategies targeting VEGF-VEGF receptor signal transduction pathways, though effective in normalizing abnormal tumor vasculature, eventually result in tumor resistance whereby a highly infiltrative and invasive phenotype may be adopted. Here we review recent anti-angiogenic therapy for malignant glioma and highlight implantable devices and nano/microparticles as next-generation methods for chemotherapeutic delivery. Intrinsic and adaptive modes of glioma resistance to anti-angiogenic therapy will be discussed with particular focus on the glioma stem cell paradigm.