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.

HA-mEXO carrying ZNF516 suppress ABCC5 expression, thereby enhancing the sensitivity of A549 and PC-9 LAUD drug-resistant cells to PMX.

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.

While interleukin (IL)-1β is known to promote lung cancer growth in humans and mice, we show here that IL-1β administration or overexpression overcomes resistance to classical chemo-immunotherapy (cisplatin/pemetrexed/anti-PD-1) in mouse lung cancer models. Additionally, drug screening identifies MEK and MDM2 inhibitors as inducers of TXNIP expression capable of reversing resistance to chemo-immunotherapy. This study highlights a positive role of IL-1β in lung cancer treatment and suggests that enhancing IL-1β production at the tumor site can overcome resistance to chemo-immunotherapy.