Higher risk profile among patients with TET2-mutated giant cell arteritis: a cluster analysis.

Objective: We aimed to assess the prevalence of clonal haematopoiesis (CH) in patients with giant cell arteritis (GCA) compared with controls and individuals with other autoimmune diseases (AIDs) and to identify high-risk clinical/genetic profiles that could influence disease outcomes.

Methods: In a prospective observational study at three hospitals, we included 49 patients diagnosed with GCA, 48 patients with other AIDs and 27 control participants. We used next-generation sequencing to detect clonal haematopoiesis (CH) among them.

Inflammatory Waldenström Macroglobulinemia is associated with clonal hematopoiesis: a multicentric cohort.

Inflammation in Waldenström Macroglobulinemia (iWM) predicts outcomes after immuno-chemotherapy and BTK inhibitors, but its origin is unknown. Here, we unravel increased clonal hematopoiesis in iWM patients (61% versus 23% in non-inflammatory WM), suggesting a contribution of environmental cells to iWM.

Conditional survival of younger patients with mantle cell lymphoma: Results from a randomized phase III trial of the European MCL Network.

During a fatal disease, patients often request updated information on their prognosis. After patients have already survived a certain time, conditional survival captures their future survival probability. We investigated conditional overall and failure-free survival in 473 younger mantle cell lymphoma (MCL) patients from a randomized phase III trial comparing immunochemotherapies R-CHOP and alternating R-CHOP/R-DHAP before autologous transplantation.

Modeling NK-cell lymphoma in mice reveals its cell-of-origin and microenvironmental changes and identifies therapeutic targets.

Extranodal NK/T-cell lymphoma (ENKTCL) is an Epstein-Barr virus (EBV)-related neoplasm preferentially involving the upper aerodigestive tract. Here we show that NK-cell-specific Trp53 disruption in mice leads to the development of NK-cell lymphomas after long latency, which involve not only the hematopoietic system but also the salivary glands. Before tumor onset, Trp53 knockout causes extensive gene expression changes, resulting in immature NK-cell expansion, exclusively in the salivary glands.