SOCS1 (Suppressor Of Cytokine Signaling 1)

P2, N=12, Active, not recruiting, Pharming Technologies B.V. | Recruiting --> Active, not recruiting | Trial completion date: Oct 2025 --> Nov 2026 | Trial primary completion date: Oct 2025 --> Nov 2026

Combining CTX with the next generation MERTK-selective inhibitor UNC2371 (MRX-2843) drives complete remissions in both models, but durable long-term responses occurred selectively in the basal-like subtype model. Suppressive myeloid programing limits effective adaptive immune engagement in TNBC usually resulting in ICB treatment resistance and tumor recurrence. This study identifies a therapeutically actionable myeloid interferon checkpoint in which MERTK inhibition stabilizes CXCL9⁺ monocyte-macrophage programming to promote CD4⁺ T cell dependent immune memory and durable tumor control in basal-like TNBC.

Mechanistically, HD15 effectively degraded SKP2 (DC50 = 0.29 μM), stabilizing SOCS1 expression and modulating immunoproteasome expression via the JAK/STAT pathway, thereby suppressing tumor cell proliferation. The discovery of HD15 demonstrates the promise of PROTAC technology in enhancing the efficacy of natural products and identifying therapeutic targets, offering a novel strategy for developing therapeutics from natural products.

This study demonstrates that tumor-specific DNA methylation changes, particularly when evaluated using multi-gene panels can enhance prognostic stratification in GC. These findings support the potential use of methylation-based biomarkers for personalized management of GC.

IFNG, PTPN6, SLC38A1, and SOCS1 may serve as potential biomarkers of poor prognosis in SKCM patients. These genes demonstrate predictive value for immunotherapy response and drug sensitivity, particularly indicating susceptibility to selumetinib treatment, and therefore show substantial potential for clinical translation.

In clinical samples from patients with BC, serum levels of miR‑155 align with both tumor miR‑155 levels and the immune status of the tumor. The present review emphasizes the importance of understanding the dynamics between TILs and miRNAs to identify new prognostic and predictive biomarkers, proposing a more integrated and personalized approach in the management of BC..

It promotes cutaneous MM tumorigenicity by regulating the SOCS1/STAT3 signaling. Hence, the targeted regulation of SIRPB1 and USF2 could be a promising therapeutic strategy for MM.

In the two external GEO (GSE71014 and GSE6891) datasets, area under the curve values of 1, 3, 5 years were 0.847, 0.857, 0.822, and 0.830, 0.863, 0.891 respectively. Our seven signature genes containing risk-scoring model performed excellently in evaluating the OS of AML patients.

Selinexor and azacitidine offer a promising strategy to overcome therapeutic resistance and improve outcomes in TET2/RHOA-mutated PTCL, supporting further clinical evaluation.

Given the modest, single-center sample size and lack of external validation, these findings should be considered exploratory. Larger, multi-center validation studies are essential before clinical translation.

These findings suggest that the DNA methylation biomarkers panel could revolutionize HCC diagnostics by enabling earlier, more accurate, and cost-effective detection, particularly in high-risk populations.

These integrated molecular effects were superior to those of free apigenin or blank EVs. Collectively, our findings highlight Apig-exo as a potent, multi-modal therapeutic platform capable of overcoming TNBC resistance via coordinated modulation of microRNA networks, apoptotic pathways, and epigenetic landscapes.