This case highlights the diagnostic challenge posed by TTF-1-positive gastric tumors, which may be mistaken for metastatic lesions from lung cancer. As TTF-1 expression is not entirely specific to tissues of lung or thyroid origin, diagnosis should be based on a comprehensive evaluation of morphological and immunohistochemical findings, together with clinical information, including treatment response and disease course.

We predicted potential therapeutic small molecular drugs by targeting subtype-specific oncogenic pathways and validated drug sensitivity (C1-GBM: Methotrexate and Cisplatin; C2-GBM: Cytarabine) by assessing IC50 values against GBM cell lines (divided into C1/C2 subtypes based on the nine hub genes) from the Genomics of Drug Sensitivity in Cancer database. This study introduces a pathway-based prognostic molecular classification of GBM with "hot" (C1-GBM) and "inherent driving" (C2-GBM) tumor subtypes, providing a prediction model based on hub biomarkers and potential therapeutic targets for treatments.

This study presents a method to improve the therapeutic effect of methotrexate against rheumatoid arthritis using the Exo/MTX/HA.

In this prospective, randomized, open-label, single-center study, 76 children with non-systemic JIA in stable remission for ≥24 months on etanercept or adalimumab were enrolled. Early significant clinical response, absence of subclinical disease activity, and concomitant low-dose methotrexate therapy were key predictors of sustained drug-free remission. These findings may inform personalized strategies for biologic tapering in pediatric JIA.

The ORR was higher in the PD-L1 1 %-49 % group; however, the PFS and OS were similar in both groups.

P2, N=90, Recruiting, University of Pennsylvania | Trial completion date: Dec 2025 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2028

In the pre-biologic era, immunomodulators such as azathioprine, 6-mercaptopurine, and methotrexate (MTX) were widely used as first-line maintenance therapies in Crohn's disease. In light of evolving treatment goals that prioritize safety, cost-effectiveness, and individualized care, this editorial argues that MTX should no longer be viewed as a fallback but as a strategic first-line option in well-defined high-risk populations. The survey underscores a persistent gap between guidelines and real-world practice, reinforcing the urgent need for clearer algorithms and education to support the repositioning of MTX in modern Crohn's disease management.

The patient was refractory to corticosteroids, dapsone, and roflumilast, and developed recurrent Gram-negative infections. Brodalumab may offer a safe and effective treatment option in refractory pyoderma gangrenosum, particularly in patients with contraindications to conventional therapies. This case supports further evaluation of IL-17 pathway inhibition in neutrophilic dermatoses.

Rats were randomly divided into five groups: healthy control (Control), untreated RA model (Model), SIL (25 mg/kg/day), SIL (50 mg/kg/day), and methotrexate (7.6 mg/kg/day) groups, with 10 mice in each group...SIL effectively mitigates myocardial fibrosis and oxidative stress in adjuvant-induced RA rats, primarily through inhibition of IRAK4-mediated inflammatory signaling. These findings highlight SIL as a promising therapeutic candidate for RA-related cardiac injury.

Collectively, our findings uncover that METTL3-mediated m6A modification of CACNA1E contributes to OS progression and chemoresistance through enhancing WNT7B-mediated non-canonical Wnt/Ca2+ signaling. Targeted inhibition of CACNA1E in combination with MTX may be a promising alternative therapeutic strategy for patients with MTX-resistant OS.

The combination of IT via Ommaya reservoir and WBRT may result in better survival in EGFR-mutant NSCLC patients with LM and represents a promising treatment strategy for this patient population.

CAEO considerably alleviated the oxidative and nitrosative stress, mitochondrial dysfunction, inflammatory and apoptosis responses caused by MTX. This shielding effect may be due to the decline in JAK2/STAT3/NF-κB and the triggering in Nrf2/HO-1/NQO1 pathways.