Background: Tumor resistance to chemotherapy may be present at the beginning of treatment, develop during treatment, or become apparent on re-treatment of the patient. The mechanisms involved are usually inferred from experiments with cell lines, as studies in tumor-derived cells are difficult. Studies of human tumors show that cells adapt to chemotherapy, but it has been largely assumed that clonal selection leads to the resistance of recurrent tumors.

A terminal deletion of chromosome 3 at p25.3 was observed during prenatal diagnosis. A similar deletion is also present in the phenotypically normal mother. The deletion was confirmed by FISH. The breakpoint is distal to the region responsible for the 3p-syndrome. A normal baby girl was born with no apparant phenotypic abnormalities.

Background: We wished to evaluate the clinical response following ATP-Tumor Chemosensitivity Assay (ATP-TCA) directed salvage chemotherapy in a series of UK patients with advanced ovarian cancer. The results are compared with that of a similar assay used in a different country in terms of evaluability and clinical endpoints.

Time-critical applications, such as early warning systems or live event broadcasting, present particular challenges. They have hard limits on Quality of Service constraints that must be maintained, despite network fluctuations and varying peaks of load. Consequently, such applications must adapt elastically on-demand, and so must be capable of reconfiguring themselves, along with the underlying cloud infrastructure, to satisfy their constraints. Software engineering tools and methodologies currently do not support such a paradigm. In this paper, we describe a framework that has been designed to meet these objectives, as part of the EU SWITCH project. SWITCH offers a flexible co-programming architecture that provides an abstraction layer and an underlying infrastructure environment, which can help to both specify and support the life cycle of time-critical cloud native applications. We describe the architecture, design and implementation of the SWITCH components and describe how such tools are applied to three time-critical real-world use cases.

Background: Activation of the epidermal growth factor receptor (EGFR) triggers downstream signaling pathways that regulate many cellular processes involved in tumour survival and growth. Gefitinib ('Iressa') is an orally active tyrosine kinase inhibitor (TKI) targeted to the ATP-binding domain of EGFR (HER1; erbB1).