Abstract. Neutrinos, and in particular their tiny but non-vanishing masses, can be considered one of the doors towards physics beyond the Standard Model. Precision measurements of the kinematics of weak interactions, in particular of the 3 H β-decay and the 163 Ho electron capture (EC), represent the only model independent approach to determine the absolute scale of neutrino masses. The electron capture in 163 Ho experiment, ECHo, is designed to reach sub-eV sensitivity on the electron neutrino mass by means of the analysis of the calorimetrically measured electron capture spectrum of the nuclide 163 Ho. The maximum energy available for this decay, about 2.8 keV, constrains the type of detectors that can be used. Arrays of low temperature metallic magnetic calorimeters (MMCs) are being developed to measure the 163 Ho EC spectrum with energy resolution below 3 eV FWHM and with a time resolution below 1 μs. To achieve the sub-eV sensitivity on the electron neutrino mass, together with the detector optimization, the availability of large ultra-pure 163 Ho samples, the identification and suppression of background sources as well as the precise parametrization of the 163 Ho EC spectrum are of utmost importance. The high-energy resolution 163 Ho spectra measured with the first MMC prototypes with ion-implanted 163 Ho set the basis for the ECHo experiment. We describe the conceptual design of ECHo and motivate the strategies we have adopted to carry on the present medium scale experiment, ECHo-1K. In this experiment, the use of 1 kBq 163 Ho will allow to reach a neutrino mass sensitivity below 10 eV/c 2 . We then discuss how the results being achieved in ECHo-1k will guide the design of the next stage of the ECHo experiment, ECHo-1M, where a source of the order of 1 MBq 163 Ho embedded in large MMCs arrays will allow to reach sub-eV sensitivity on the electron neutrino mass.

Gastrointestinal stromal tumors (GISTs) are composed of various molecular subtypes, with differing prognostic and predictive relevance. Previously, tumors lacking mutations in the KIT and PDGFRA genes have been designated as 'wild-type' GISTs; however, they represent a heterogeneous group currently undergoing further subclassification. Primary and secondary resistance to imatinib poses a significant clinical challenge, therefore ongoing research is trying to evaluate mechanisms to overcome resistance. Thorough understanding of the prognostic and predictive relevance of different genetic subtypes of GIST can guide clinical decision-making both in the adjuvant and the metastatic setting. Further work is required to identify tailored therapies for specific subgroups of GISTs wild-type for KIT and PDGFRA mutations and to identify predictive factors of resistance to currently approved systemic therapies.

This series confirms the activity of TEMIRI in both adults and pediatric patients. This schedule offers a 71% DCR, independently of the line of chemotherapy. Predictive factors of response are ECOG and LDH.