SFRT was associated with longer survival in non-elderly patients, possibly reflecting selection of poorer-risk patients for HFRT. In elderly patients, HFRT was noninferior regardless of MGMTp status, supporting its use as a less intensive approach with comparable survival and reduced treatment burden.
Combined radiomics-clinical models achieved numerically higher performance, but current evidence remains limited by retrospective designs, internal validation, and methodological heterogeneity. These models should be considered adjunctive rather than replacement tools, and prospective multicenter external validation with standardized workflows is required before clinical implementation.
Maximal safe resection remains the cornerstone of management, with radiotherapy or chemotherapy reserved for selected cases. Despite potential morbidity, long-term survival and functional outcomes are favorable for many patients.
Although paraspinal peripheral nerve sheath tumors (including neurofibromas and schwannomas) occur frequently in the NF conditions, there is also a risk of intramedullary spinal cord tumors in people with NF1 and NF2-SWN. Here, we discuss the presentation and diagnosis of the various forms of NF, the intramedullary spinal cord tumors that occur in NF1 and NF2-SWN, and their diagnostic and treatment considerations.
P1, N=12, Not yet recruiting, Washington University School of Medicine | Trial completion date: Nov 2027 --> Mar 2028 | Initiation date: Apr 2026 --> Aug 2026 | Trial primary completion date: Oct 2027 --> Feb 2028
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Trial completion date • Trial initiation date • Trial primary completion date
Early detection of pathogenic mutations, appropriate surgical intervention, and long-term follow-up are essential to reduce complications. Multidisciplinary care and emerging targeted therapies, such as MEK inhibitors, may further improve management and prognosis for patients with complex NF1 manifestations.
This case highlights diagnostic pitfalls in cytokeratin-positive pleomorphic chest-wall tumors and the limitations of core biopsy. En bloc resection with rigid reconstruction is feasible, while positive margin status warrants multidisciplinary consideration of adjuvant local therapy and structured surveillance.
Importantly, CD206 expression was not increased in M1 macrophages after contact with spheroids, and was lower in M2 macrophages loaded with B4C nanoparticles compared to control M2 macrophages. BMDMs are promising carriers of B4C nanoparticles for BNCT due to their ability to cross the in vitro BBB model toward the glioblastoma microenvironment.
Despite palliative chemotherapy (cyclophosphamide and vincristine), the patient experienced rapid tumor recurrence and progressive clinical deterioration, culminating in death three weeks post-intervention. In resource-limited settings, where advanced molecular diagnostics are scarce, maintaining a high index of clinical suspicion and ensuring multidisciplinary management are paramount. Early histopathological confirmation is critical to addressing the rapid progression and therapeutic resistance characteristic of this malignancy.
FAM135B acts as a critical negative regulator of GBM angiogenesis, whose low expression contributes to high tumor angiogenic potential and poor patient prognosis. Mechanistically, HNF4A transcriptionally upregulates FAM135B, which then binds to and stabilizes the IKK complex, inactivating the NF-κB signaling pathway and downregulating IL-6 expression, ultimately inhibiting the JAK/STAT-mediated angiogenic process. FAM135B also remodels the GBM tumor microenvironment by reducing M2 macrophage infiltration. Targeting the HNF4A/FAM135B/NF-κB/IL-6 signaling axis provides a novel and promising therapeutic strategy for GBM anti-angiogenic therapy.
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IL6 (Interleukin 6) • CD31 (Platelet and endothelial cell adhesion molecule 1) • PECAM1 (Platelet And Endothelial Cell Adhesion Molecule 1) • HNF1A (HNF1 Homeobox A)
Mechanistic analysis revealed that the active peptide uniquely competes with Wnt5a, the endogenous ligand of ROR1, for receptor binding. To our knowledge, this report provides the first evidence implicating ROR1/2 as a viable therapeutic target in DIPG and establishes macrocyclic peptides as a promising modality for its pharmacological inhibition.
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ROR1 (Receptor Tyrosine Kinase Like Orphan Receptor 1)