Resource allocation and feedback in wireless multiuser networks

This thesis focuses on the design of algorithms for resource allocation and feedback in wireless multiuser and heterogeneous networks. In particular, three key design challenges expected to have a major impact on future wireless networks are considered: cross-layer scheduling; structured quantization codebook design for MU-MIMO networks with limited feedback; and resource allocation to provide physical layer security. The first design challenge is cross-layer scheduling, where policies are proposed for two network architectures: user scheduling in single-cell multiuser networks aided by a relay; and base station (BS) scheduling in CoMP. These scheduling policies are then analyzed to guarantee satisfaction of three performance metrics: SEP; packet delay; and packet loss probability (PLP) due to buffer overflow. The concept of the τ-achievable PLP region is also introduced to explicitly describe the tradeoff in PLP between different users. The second design challenge is structured quantization codebook design in wireless networks with limited feedback, for both MU-MIMO and CoMP. In the MU-MIMO network, two codebook constructions are proposed, which are based on structured transformations of a base codebook. In the CoMP network, a low-complexity construction is proposed to solve the problem of variable codebook dimensions due to changes in the number of coordinated BSs. The proposed construction is shown to have comparable performance with the standard approach based on a random search, while only requiring linear instead of exponential complexity. The final design challenge is resource allocation for physical layer security in MU-MIMO. To guarantee physical layer security, the achievable secrecy sum-rate is explicitly derived for the regularized channel inversion (RCI) precoder. To improve performance, power allocation and precoder design are jointly optimized using a new algorithm based on convex optimization techniques

Imatinib treatment of poor prognosis mesenchymal-type primary colon cancer: A proof-of-concept study in the preoperative window period (ImPACCT)

Background: The identification of four Consensus Molecular Subtypes (CMS1-4) of colorectal cancer forms a new paradigm for the design and evaluation of subtype-directed therapeutic strategies. The most aggressive subtype - CMS4 - has the highest chance of disease recurrence. Novel adjuvant therapies for patients with CMS4 tumours are therefore urgently needed. CMS4 tumours are characterized by expression of mesenchymal and stem-like genes. Previous pre-clinical work has shown that targeting Platelet-Derived Growth Factor Receptors (PDGFRs) and the related KIT receptor with imatinib is potentially effective against mesenchymal-type colon cance

Ccaat/enhancer-binding protein delta (C/ebpδ): A previously unrecognized tumor suppressor that limits the oncogenic potential of pancreatic ductal adenocarcinoma cells

CCAAT/enhancer-binding protein δ (C/EBPδ) is a transcription factor involved in growth arrest and differentiation, which has consequently been suggested to harbor tumor suppressive activities. However, C/EBPδ over-expression correlates with poor prognosis in glioblastoma and promotes genomic instability in cervical cancer, hinting at an oncogenic role of C/EBPδ in these contexts. Here, we explore the role of C/EBPδ in pancreatic cancer. We determined C/EBPδ expression in biopsies from pancreatic cancer patients using public gene-expression datasets and in-house tissue microarrays. We found that C/EBPδ is highly expressed in healthy pancreatic ductal cells but lost in pancreatic ductal adenocarcinoma. Furthermore, loss of C/EBPδ correlated with increased lymph node involvement and shorter overall survival in pancreatic ductal adenocarcinoma patients. In accordance with this, in vitro experiments showed reduced clonogenic capacity and proliferation of pancreatic ductal adenocarcinoma cells following C/EBPδ re-expression, concurrent with decreased sphere formation capacity in soft agar assays. We thus report a previously unrecognized but important tumor suppressor role of C/EBPδ in pancreatic ductal adenocarcinoma. This is of particular interest since only few tumor suppressors have been identified in the context of pancreatic cancer. Moreover, our findings suggest that restoration of C/EBPδ activity could hold therapeutic value in pancreatic ductal adenocarcinoma, although the latter claim needs to be substantiated in future studies