Skull base chordomas presenting with abducens nerve deficits: clinical characteristics and predictive factors for deficit improvement or resolution.

Objective: Skull base chordomas (SBCs) often present with cranial nerve (CN) VI deficits. Studies have not assessed the prognosis and predictive factors for CN VI recovery among patients presenting with CN VI deficits.

Methods: The medical records of patients who underwent resection for primary chordoma from 2001 to 2020 were reviewed.

Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial.

Background: Olutasidenib is a potent, selective, oral, small molecule inhibitor of mutant IDH1 (mIDH1) which induced durable remissions in high-risk, relapsed/refractory (R/R) mIDH1 AML patients in a phase 1/2 trial. We present a pooled analysis from multiple cohorts of the phase 1/2 trial of patients with R/R AML who received combination olutasidenib and azacitidine therapy.

Methods: Adult patients with mIDH1 AML received 150 mg olutasidenib twice daily plus standard-of-care azacitidine (OLU + AZA) and were evaluated for response and safety.

Hemophagocytic Lymphohistiocytosis (HLH) Following Immune Checkpoint Therapy (ICT).

In the past decade, the use of immune checkpoint therapy (ICT) has increased across many malignancies, including metastatic renal cell carcinoma as an option for frontline and subsequent lines of therapy. Despite the many therapeutic benefits of ICT, its use is complicated by the potential risk of immune-related adverse events (irAEs). One rare but potentially life-threatening irAE is hemophagocytic lymphohistiocytosis (HLH).

Macrophage-based pathogenesis and theranostics of vulnerable plaques.

Vulnerable plaques, which are high-risk features of atherosclerosis, constitute critical elements in the disease's progression due to their formation and rupture. Macrophages and macrophage-derived foam cells are pivotal in inducing vulnerability within atherosclerotic plaques. Thus, understanding macrophage contributions to vulnerable plaques is essential for advancing the comprehension of atherosclerosis and devising novel therapeutic and diagnostic strategies.