POU2AF1 (POU Class 2 Homeobox Associating Factor 1)

These findings suggest that active smoking creates an immunosuppressive TME, potentially facilitating rapid tumor growth and aggressive progression. Smoking cessation may reverse these changes, highlighting the clinical significance of smoking behavior in disease outcomes.

Our irAE-associated gene signature robustly stratifies NSCLC patients for immunotherapy response and survival. Integrating RS with clinical parameters provides a practical tool to balance efficacy and safety.

We develop first-in-class small molecule inhibitors of Oct1/OCA-B transcription complexes and show that administration into NOD mice also blocks diabetes emergence following α-PD-1 treatment. These results identify OCA-B as a promising therapeutic target for the prevention of autoimmunity and immune-related adverse events (irAEs).

None of the animals revealed the expected DGE pattern corresponding to a moderate to high H-ARS-severity degree. Hence, the Göttingen minipig did not qualify as another validation model for our specific gene set, which does not argue against their validity for other purposes.

Furthermore, increased activity of macrophages and reduced expression of B-cells support previous studies underlining their involvement in treatment resistance. Despite limitations in sample size, these findings shed light on the mechanisms behind resistance and early relapse in cHL, which could help guide the development of targeted therapies and potentially improve early risk assessment.

In the end, the core target and the active molecule were both given the green light for a molecular docking investigation. POU2AF1 is being considered as a possible therapeutic target for HCC, and the results of our work have presented novel concepts for the treatment of HCC.

An orally bioavailable mSWI/SNF ATPase degrader significantly inhibits tumor growth in preclinical models of SCLC-P and multiple myeloma without signs of toxicity. This study suggests that POU2F-POU2AF-driven malignancies have an intrinsic dependence on the mSWI/SNF complex, representing a therapeutic vulnerability.

However, the GE pattern of other genes differed between saliva and blood. In summary, the current human in vivo study, (I) reveals significant radiation-induced GE associations of five transcriptional biomarkers in salivary samples, (II) suggests genes predicting diverse clinical outcomes such as acute and late radiotoxicity as well as ARS severity, and (III) supports the view that blood-based GE response can be reflected in saliva samples, indicating that saliva is a "mirror of the body" for certain but not all genes and, thus, studies for each gene of interest in blood are required for saliva.

We show that early in viral infection, endogenously elevated OCA-B expression prospectively identifies memory precursor cells with increased survival capability and memory recall potential. Cumulatively, the results demonstrate that OCA-B is both necessary and sufficient to promote CD4 T cell memory in vivo and can be used to prospectively identify memory precursor cells.

Limitations related to leukemia type, associated reduced RNA amounts, suppressed GE changes, and methodological challenges must be considered as factors negatively affecting the total number of validated genes. Based on that, we propose additional controls including blood cell counts and preferably fluorescence-based RNA quantity measurements for selecting promising samples and using a more sensitive 96-well format for candidate genes with low baseline copy numbers.

Our results revealed that patients in the iTreg-related low-risk subgroup had a better prognosis and possibly greater sensitivity to traditional chemotherapy. Our study provides a novel iTreg-related signature to elucidate the mechanisms underlying LUAD prognosis and promote individualized chemotherapy treatment.

Our findings highlight the impact of sBCMA levels and its chronicity of exposure on anti-BCMA TCE and CAR T activities in MM. We further identified structural genomic events driving TNFRSF17 over-expression and their correlation to sBCMA levels facilitating tumoral immunotherapeutic escape.