Christoph Schürch

TL;DR: It is shown in patient cells and in mice that oncogenic K-Ras activatesNLRP3 inflammasome to drive myeloproliferation, which can be reversed by genetic or pharmacologic NLRP3 blockade, which paves the way for a therapeutic approach based on immune modulation via NL RP3 blockade in KRAS-mutant myeloid malignancies.

TL;DR: The last 20 years of research in zebrafish models for hematopoietic disorders are summarized, highlighting how these models were created and are being applied for translational research.

TL;DR: It is shown that the activity of the transcription factor NFAT is chronically elevated in both DLBCL subtypes and constitutive NFAT signaling is identified as a crucial functional driver of ABCDLBCL and calcineurin inhibition is highlighted as a novel strategy for the treatment of ABC DLBCl.

TL;DR: Necrotic tumor zone volumes are proposed as a surrogate marker for the assessment of glioma invasive potential, corresponding to higher invasive capacities of tumors, while autologous necrotic cells are capable of inducing higher invasion in SOX2 overexpressing or OPA1 knocked‐down relative to parental LN319.

TL;DR: Interestingly, injection of human SRP54 mRNAs carrying mutations observed in patients aggravated neutropenia and induced pancreatic defects in srp54+/- fish, mimicking the corresponding human clinical phenotypes, suggesting that the variable phenotypes observed in customers may be due to mutation-specific dominant negative effects on the functionality of the residual wildtype SRP 54 protein.