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.

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 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.

It was revealed that the lymphoma cells of both lymphoplasmacytic lymphoma/Waldenström macroglobulinemia and primary central nervous system lymphoma derived from a common cell possessing MYD88. The utility of adding chemotherapy for low-grade lymphoma in addition to therapy for primary central nervous system lymphoma is not clear. While lymphoplasmacytic lymphoma is a low-grade lymphoma that does not always require chemotherapy, combining treatment for lymphoplasmacytic lymphoma and primary central nervous system lymphoma may contribute to the effectiveness of both treatments.

For over 70 years, methotrexate (MTX) has remained a first-line chemotherapeutic agent for acute lymphoblastic leukemia (ALL), playing a pivotal role in maintenance therapy...Mechanistically, dual-luciferase reporter and electrophoretic mobility shift assays revealed that rs1544105 A > G enhanced the binding affinity of the SNP-containing sequence for the transcription factor CREB1, thereby increasing FPGS transcriptional activity and ultimately augmenting MTX efficacy. Our multidimensional study, integrating data analysis with cellular, molecular, and animal experiments, highlights the remarkable regulatory role of a single SNP, rs1544105, in modulating MTX therapeutic response and provides a basis for individualized MTX-based maintenance therapy in ALL patients.

These improvements were greater in the group that received the higher dosage of LIR than in the group that received the lower dosage of LIR. In conclusion, LIR improved MTX-induced cardiotoxicity more significantly at a dosage of 0.4 mg/kg/day, probably through the interruption of oxidative stress and autophagy pathways and the activation alleviation of inflammatory cytokines.