Metastatic disease is a major challenge for cancer cure, haematogenous spread and subsequent growth of tumour cells at distant sites being the cause of most cancer deaths. Molecular characterization and detection of the tumour cells responsible for haematogenous spread may increase understanding of the biology of metastasis, help improve patient management and allow evaluation of novel treatments to prevent and eradicate this disease. The bone marrow is a common site to which tumour cells metastasize, from which they may re-circulate to other organs with a favourable microenvironment for growth.
View Article and Find Full Text PDFThe European Network for Cancer Research in Children and Adolescents (ENCCA) provides an interaction platform for stakeholders in research and care of children with cancer. Among ENCCA objectives is the establishment of biology-based prioritization mechanisms for the selection of innovative targets, drugs, and prognostic markers for validation in clinical trials. Specifically for sarcomas, there is a burning need for novel treatment options, since current chemotherapeutic treatment protocols have met their limits.
View Article and Find Full Text PDFPURPOSE EWS-ETS fusion genes are the driving force in Ewing's sarcoma pathogenesis. Because of the variable breakpoint locations in the involved genes, there is heterogeneity in fusion RNA and protein architecture. Since previous retrospective studies suggested prognostic differences among patients expressing different EWS-FLI1 fusion types, the impact of fusion RNA architecture on disease progression and relapse was studied prospectively within the Euro-E.
View Article and Find Full Text PDFHerpesvirus saimiri (HVS) has the ability to infect a variety of human cell lines and establish a persistent infection by virtue of episomal maintenance. Moreover, the viral episome provides sustained expression of a heterologous transgene. HVS-based vectors can also persist for a long term in tumor xenografts generated from HVS-infected human carcinoma cell lines.
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