5 research outputs found

    Software Requirements and Prototype Development of a Web Application for Quality Assurance (QA) in Radiation Therapy - a QAlender

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    The implementation of a web based portal QA solution will lead to a high acceptance of the staff as the usage of commonly known standard software (e.g. web browser) allows intuitive handling. In the daily use a significant simplification of the workflow and Performance enhancement can be achieved by easy access to the check documents. As the data is now saved in a database it can easily be processed and long-term trends can be displayed. Therefore possible errors can be detected much easier and earlier. By the usage of time stamps and user authentication procedures and user responsibilities are comprehensibly documented. As the software is browser based, integration into an existing software Environment is not critical. As only technical QA data is processed, no further data security measures are necessary. A certification as a medical product is not required

    Increased malignant behavior in neuroblastoma cells with acquired multi-drug resistance does not depend on P-gp expression.

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    Acquisition of P-gp-mediated multidrug-resistance does not always correlate with observed malignant behavior of NB. To characterize alterations accompanying development of multidrug-resistance in NB we established two neuroblastoma cell sublines resistant to vincristine (UKF-NB-3rVCR10) and doxorubicin (UKF-NB-3rDOX20). UKF-NB-3rVCR10 and UKF-NB-3rDOX20 overexpressed functional P-gp and developed an increased malignant phenotype: presented constitutive phosphorylation of AKT, resistance to gamma-irradiation, and had increased survival in serum-free medium. Inhibition of P-gp restored chemosensitivity but did not affect increased survival in serum-free medium and sensitivity to gamma-irradiation. Inhibition of AKT had no influence on chemoresistance but restored sensitivity to serum starvation. Both resistant cell lines acquired additional chromosomal changes. UKF-NB-3rVCR10 cells acquired a missense P53 mutation in exon 5, an increased MYCN amplification, an enhanced adhesion to endothelium, a decreased NCAM expression, a distinctly higher clonogenicity, and an increased in vivo tumorigenicity. We conclude that acquisition of increased malignant behavior in neuroblastoma occurs concomitantly with multidrug-resistance and is P-gp-independent
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