TET2 mutation

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These findings demonstrate that Tet2 is essential for balancing proliferation and terminal differentiation of IgG1+ GC B-cells during the humoral response. The impaired regulation of this balance due to Tet2 loss provides mechanistic insight into a contributory pathway that may facilitate DLBCL transformation in TET2-mutated cases.

To our knowledge, this is the first reported case demonstrating the use of tagraxofusp in a patient with BPDCN and advanced chronic kidney disease, showing that even a minimum of tolerated treatment dose can induce a sustained response. Despite the risk of adverse events, tagraxofusp should be considered a viable treatment option for elderly patients with poor performance status and significant comorbidities who are ineligible for intensive chemotherapy or stem cell transplantation, as even limited exposure may achieve meaningful clinical responses.

Emerging therapeutic strategies, including inflammasome inhibition, STING modulation, and epigenetic restoration, highlight its potential as a modifiable risk factor. This narrative review synthesizes current epidemiological, mechanistic, and translational insights, framing CHIP as an emerging causal factor in cardiometabolic disease and as a promising target for precision medicine in aging populations.

The overall survival of MDS patients with ASXL1mut is poor. The patients with p.Gly646fs sequence mutation have a higher proportion of bone marrow blasts and a worse prognosis. There are no statistical differences in efficacy of different treatment strategies in ASXL1mut group. ASXL1 mutation shows no significant effect on the response of MDS to hypomethylating agent therapy.

Allogeneic hematopoietic stem cell transplantation was associated with better survival, underscoring its significance. These findings reveal the genetic and clinical heterogeneity of NUP98-rearranged AML in adults and support its classification as a distinct entity, highlighting the need for fusion partner-specific therapeutic strategies.

Single-cell genotyping confirmed the presence of mutated progenitors in 3 follicular, 2 mantle cell and 2 marginal zone lymphoma patients, providing direct evidence of a pre-neoplastic state in disease pathogenesis. Our findings offer novel insight into the cellular origin of nodal B-NHLs and highlight a previously underappreciated role for early clonal events involving the stem/progenitor cell compartment.

Cytogenetic analysis revealed triple molecular aberrations including a t(1;6) (p31;q25) translocation, a TET2 frameshift deletion (44.1% VAF), and a KDM6A missense mutation (c.262G>A, 46.6% VAF). The patient died within 6 months post-diagnosis, suggesting that this aggressive clinical course may be associated with a novel clinicogenetic subtype of BPDCN.

These observations highlight the critical role of TET2 mutations in the development and progression of BPDCN and related hematologic neoplasms. However, the hierarchical structure of clonal evolution remains unclear, so this report also discusses the potential clonal relationships between different tumors.

This study showed that CHIP was associated with diseases and mortalities of multiple systems, suggesting CHIP was a candidate risk factor for human health.

HSC expansion assays using ECM-functionalized hydrogels confirm a selective effect on the expansion of Tet2-mutant HSCs. Taken together, our study represents a comprehensive molecular characterization of Tet2-mutant HSCs and identifies a previously unanticipated role of ECM molecules in regulating self-renewal of disease-driving HSCs.