MUC5B (Mucin 5B, Oligomeric Mucus/Gel-Forming)

Drug sensitivity analysis based on oncoPredict revealed compounds with differential efficacy between risk groups, and the model also predicted response to PD-1 blockade in an external immunotherapy cohort. In summary, polyamine metabolism is closely linked to the immune microenvironment and prognosis of ESCA, providing a potential biomarker for patient stratification and treatment optimization.

P3, N=80, Recruiting, Boehringer Ingelheim | Not yet recruiting --> Recruiting

Lower serum total protein was independently associated with mucus plug formation. These findings refine the pathophysiological understanding of RMPP with mucus plugs and may inform targeted anti-inflammatory and mucus-modulating therapeutic strategies.

Newer tools, including quantitative imaging and artificial intelligence, may help detect subtle disease earlier and refine risk assessment. Despite advances, challenges remain in defining progression thresholds and treatment strategies, highlighting the need for further research.

MUC5B facilitates LUAD lymph node metastasis, potentially by regulating the GINS complex and promoting oncogenic signaling. These findings highlight MUC5B as a promising biomarker and therapeutic target for advanced LUAD.

However, there has been less research on other consequences of screening for RA-ILD, including cost, anxiety, radiation exposure, incidental findings, and downstream clinical follow-up. Trials are needed to identify an intervention that alters the natural history for those found to have subclinical RA-ILD on screening.

Non-sinonasal ITACs are rare, aggressive malignancies requiring accurate diagnosis and further molecular investigation to improve management and outcomes.

This study reveals novel genes and mechanisms in osimertinib resistance. The prognostic model stratifies LUAD patients effectively, and LHX2 represents a promising therapeutic target for reversing resistance.

Mutations in TP53 and MUC5B, as well as deletion of CASP8, may be early driver events in carcinogenesis and could precede the emergence of the APOBEC mutation signature. Moreover, ploidy alterations confer a selective advantage to genomically unstable cells, thereby promoting their progression toward malignant transformation. Collectively, our results demonstrate that genomic instability is prevalent in precancerous lesions and intensifies during the late stages of tumor progression. Cells with a certain level of genomic instability appear to possess a competitive advantage for malignant transformation.

SA1 was found to suppress MUC5B and elevate APOB expression in A549 cells, while inhibiting MFGM, ANGL4 and increasing GCN1 expression in exosomes. This study demonstrates that SA1 exhibits anti-NSCLC effects by regulating exosome function and related protein expression, providing novel insights for NSCLC treatment.

In addition, interrogation of the Drug-Gene Interaction Database highlighted putative therapeutic targets such as CDK13, MUC16, and MUC17. While preliminary, these findings establish the first comprehensive mutational blueprint of HNLEC, providing novel insights into its pathogenesis, potential prognostic determinants, and therapeutic vulnerabilities, and laying a foundation for future translational and clinical research.

ScRNA-seq delineated three PCa cell clusters, with high-risk subtypes being sensitive to bendamustine/dacomitinib and resistant to apalutamide/neratinib. This study establishes a TME-driven prognostic framework that connects immune heterogeneity, genomic instability, and therapeutic resistance in PCa. By pinpointing metabolic dependencies and subtype-specific vulnerabilities, our findings provide actionable strategies to circumvent treatment failure, such as targeting energy metabolism or tailoring therapies based on resistance signatures.