Oncogenic mutations in the small GTPase Ras contributes to ~30% of human cancers. However, tissue growth induced by oncogenic Ras is restrained by induction of cellular senescence and additional mutations are required to induce tumor progression. Therefore, it is paramount to identify cooperating cancer genes. Recently, the tensin family of focal adhesion proteins, TNS1-4, have emerged as regulators of carcinogenesis, yet their role in cancer appears somewhat controversial. Around 90% of human cancers are of epithelial origin. We have used the Drosophila wing imaginal disc epithelium as model system to gain insight into the roles of two orthologs of human TNS2 and 4, blistery (by) and PVRAP, in epithelial cancer progression. We have generated null mutations in PVRAP and found that, as it is the case for by and mammalian tensins, PVRAP mutants are viable. We have also found that elimination of either PVRAP or by potentiates RasV12-mediated wing disc hyperplasia. Furthermore, our results have unravelled a mechanism by which tensins may limit Ras oncogenic capacity, the regulation of cell shape and growth. These results demonstrate that Drosophila tensins behave as suppressors of Ras-driven tissue hyperplasia, suggesting that the roles of tensins as modulators of cancer progression might be evolutionary conserved.

D-type cyclins encode G1/S cell cycle checkpoint proteins, that play a crucial role in defining cell cycle exit and progression. Precise control of cell cycle exit is vital during embryonic development, with defects in the pathways regulating intracellular D-type cyclins resulting in abnormal initiation of stem cell differentiation in a variety of different organ systems. Furthermore, stabilisation of D-type cyclins is observed in a wide range of disorders characterised by cellular over-proliferation, including cancers and overgrowth disorders. In this review, we will summarise and compare the roles played by each D-type cyclin during development and provide examples of how their intracellular dysregulation can be an underlying cause of disease.

Almost all modern inorganic light-emitting diode (LED) designs are based on double heterojunctions (DHJs) whose structure and current injection principle have remained essentially unchanged for decades. Although highly efficient devices based on the DHJ design have been developed and commercialized for energy-efficient general lighting, the conventional DHJ design requires burying the active region (AR) inside a pn-junction. This has hindered the development of emitters utilizing nanostructured ARs located close to device surfaces such as nanowires or surface quantum wells. Modern DHJ III-N LEDs also exhibit resistive losses which arise from the DHJ device geometry. The recently introduced diffusion-driven charge transport (DDCT) emitter design offers a novel way to transport charge carriers to unconventionally placed ARs. In a DDCT device, the AR is located apart from the pn-junction and the charge carriers are injected into the AR by bipolar diffusion. This device design allows the integration of surface ARs to semiconductor LEDs and offers a promising method to reduce resistive losses in high power devices. In this work, we present a review of the recent progress in gallium nitride (GaN) based DDCT devices, and an outlook of potential DDCT has for opto- and microelectronics.