In this week's episode, we'll hear about new insights into PU.1-mutated agammaglobulinemia. Researchers show that haploinsufficiency of the master transcriptional regulator PU.1 causes agammaglobulinemia and dendritic cell deficiencies. These patients experience an array of infectious and non-infectious complications, but not leukemia. After that: venetoclax-based induction therapy in younger patients with AML. Venetoclax plus decitabine was associated with superior safety and non-inferior response rates compared to intensive chemotherapy. Is it time to consider lower-intensity therapy beyond older and unfit patients? Finally, a focus on venous thromboembolism. Researchers link BGAT, an enzyme pivotal to determining blood type, to risk of future VTE. They say high plasma levels of BGAT contribute to risk above and beyond what can be explained by von Willebrand factor and Factor VIII.Featured Articles:One hundred thirty-four germ line PU.1 variants and the agammaglobulinemic patients carrying themVenetoclax and decitabine vs intensive chemotherapy as induction for young patients with newly diagnosed AMLHisto–blood group ABO system transferase plasma levels and risk of future venous thromboembolism: the HUNT study

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“What did the council decide on item 42?” — answered with the speaker and the moment.

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