methotrexate

The ABLE risk-stratification model can effectively differentiate prognostic subgroups in patients with PCNSL.

MTX when used in combination with AICAR, rescued human Tfh cell differentiation in vitro from MTX-mediated suppression. In the 4T1 mouse model, the synergistic administration of MTX and AICAR significantly enhanced the proliferation of Tfh cells, along with increases in germinal centre B cells, memory B cells, and plasma cells in both circulation and tumor-draining lymph nodes.

P3, N=1186, Recruiting, Children's Oncology Group | Trial completion date: Sep 2027 --> Jun 2029 | Trial primary completion date: Sep 2027 --> Jun 2029

P2, N=80, Recruiting, Children's Oncology Group | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

A standard drug group receiving methotrexate (MTX) was included to benchmark the efficacy of aloesin. MTX, as a standard comparator, allowed for direct benchmarking of aloesin anti-psoriatic effects. Psoriasis treatment could benefit from this approach in the future.

However, the patient relapsed within a few months and needed to be treated with methotrexate. This example highlights the importance of careful clinical, histological, and immunohistochemical testing for timely HMF detection as well as the need for vigilant monitoring to effectively manage recurrences.

This pathway-informed approach identifies genetic contributors to methotrexate-induced mucositis and supports polygenic risk prediction. Our findings provide a foundation for individualized toxicity risk profiling and suggest potential therapeutic targets to mitigate treatment-limiting mucositis in pediatric oncology.

It was also shown to have a protective effect on the lungs against acute Methotrexate toxicity, preventing alveolar epithelial damage, congestion, inflammatory cell infiltration and alveolar degeneration despite the presence of mild fibrosis and interstitial edema. Alpha Pinene can be considered to be a highly valuable protective agent against Methotrexate-induced lung injury.

The condition remained poorly controlled despite administration of Prednisone combined with Hydroxychloroquine, and showed no significant improvement after adding methotrexate. reported here findings suggest that T-DXd may trigger multi-system involvement through immune-mediated mechanisms, resulting in drug-induced dermatomyositis and interstitial pneumonia. Our findings highlight the need for heightened vigilance regarding such immune-related adverse events during T-DXd therapy, where early recognition and intervention are critically important to avoid irreversible and possibly fatal complications.

The simultaneous inversion of the IL-10/IL-6 ratio with edema onset suggests a cytokine shift unmasking an inflammatory response previously suppressed by malignant lymphoproliferation. This pattern supports an immune reconstitution inflammatory syndrome-like mechanism as the most likely cause.

In summary, decreased ZFP36L1 expression serves as an inherent mechanism enabling osteosarcoma to develop resistance to MTX therapy. These results highlight ZFP36L1 as a promising therapeutic target for overcoming MTX chemoresistance in osteosarcoma.

These LMNSC-EVs (collected from undifferentiated LMNSCs) demonstrated neuroprotective effects in a brain organoid model of methotrexate-induced toxicity when added to corresponding LMNSC01- or LMNSC02-derived brain organoids. LMNSC01- and LMNSC02-derived EVs restored neuronal and astrocytic populations but failed to rescue OPCs. These findings demonstrate the therapeutic potential of LMNSC-derived EVs to counter chemotherapy-induced neurotoxicity by preserving neurones and astrocytes, while highlighting the need for repeated or complementary interventions to restore oligodendrocyte populations.