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We present BKG´s current activities in the area of combined data processing of different space-geodetic techniques. The primary goal of the combined analyses is the improvement of the consistency between the techniques through common parameters, mainly Earth Orientation Parameters (EOP), and thereby to improve also the resulting EOP. In previous studies, we have investigated different combination approaches using VLBI and GNSS data. We generate EOP series with latencies of about 1 to 14 days, depending on the input data we used. In this way, a significant improvement in accuracy compared to the individual technique-specific solutions was achieved, especially for the highly variable dUT1. The processing is based on homogenized datum-free normal equations, which allow a rigorous combination on the normal equation level.Our main objective is to generate a continuous, daily and regular EOP product with the shortest possible latency, especially for the parameter dUT1. The requirement for achieving these goals is the daily and rapid availability of the input data. Especially the VLBI Intensive sessions play an important role for the precise and rapid estimation of dUT1. In the last two years, an increasing number of VGOS Intensive campaigns has been conducted in addition to the legacy Intensives. In our recent studies, we integrate the new data into our combination process to improve the continuity and regularity of our EOP series.Based on the improved combination method, we intent to establish an operational EOP product at BKG. We present our future plans regarding the generation and availability of the new product., The 28th IUGG General Assembly (IUGG2023) (Berlin 2023)

Summary Chronic myeloid leukemia (CML) is induced by BCR-ABL1 and can be effectively treated for many years with Imatinib until leukemia cells acquire drug resistance through BCR-ABL1 mutations and progress into fatal B lymphoid blast crisis (LBC). Despite its clinical significance, the mechanism of progression into LBC is unknown. Here, we show that LBC but not CML cells express the B cell-specific mutator enzyme AID. We demonstrate that AID expression in CML cells promotes overall genetic instability by hypermutation of tumor suppressor and DNA repair genes. Importantly, our data uncover a causative role of AID activity in the acquisition of BCR-ABL1 mutations leading to Imatinib resistance, thus providing a rationale for the rapid development of drug resistance and blast crisis progression.