Abstract: Provided are methods and compositions for treating myeloproliferative neoplasms in patients carrying an IDH2 mutation and a JAK2 mutation.

Abstract: The present invention provides a variety of methods for the identification and/or treatment of subjects that are at risk for developing life-threatening complications of SARS-CoV-2 infection and other infections. Such methods involve determining if a subject has clonal hematopoiesis.

Abstract: In the present invention, inventors have used high throughput sequencing to identify novel mutations in ABCA1 in CM ML patient samples. Further studies in a mouse model of myelomonocytic leukemia driven by hematopoietic Tet2 deficiency have shown that these somatic mutations abrogate the tumor suppressor function of WT ABCA1, resulting in the failure to suppress canonical IL3-receptor beta signaling-driven myelopoiesis. The loss of the myelo-suppressive function of ABCA1 mutants can be overcome by raising HDL levels through overexpression of the human apolipoprotein A-1 (apoA-1) transgene. Inventors have also shown that both IL-3Rbeta blocking antibody and cyclodextrin prevented the proliferation of ABCA1 mutant-transduced Tet2 deficient BM cells similar to the effect of ABCA1-WT overexpression.

Abstract: Provided are methods and compositions for treating myeloproliferative neoplasms in patients carrying an IDH2 mutation and a JAK2 mutation.

Abstract: Provided are methods and compositions for treating myeloproliferative neoplasms patients carrying an IDH2 mutation and a JAK2 mutation.

Abstract: Provided are methods and compositions for treating myeloproliferative neoplasms patients carrying an IDH2 mutation and a JAK2 mutation.

Abstract: Gene mutations are associated with the progression of acute myeloid leukemia (AML). The invention relates to methods and systems for evaluating the progression of AML based on these gene mutations. The present invention also relates to methods and compositions for treating AML patients by modulating the expression or activity of certain genes involved in AML progression and/or their encoded proteins. The invention further relates to methods and compositions for determining the responsiveness of an AML patient to induction chemotherapy therapy.