LYPD3 (LY6/PLAUR Domain Containing 3)

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.

erlotinib-, gefitinib-, and osimertinib-resistant HCC827 cell lines were established by exposing them to increasing EGFR-TKIs concentrations. A nomogram (C-index = 0.7) integrated RiskScore with clinical factors for personalized prognosis. This model bridges in vitro resistance mechanisms with clinical immune landscapes, offering a tool to stratify patients for EGFR-TKIs, immunotherapies, or combinatorial strategies.

Notably, 3C-toxin showed superior target promiscuity compared to traditional DT3C methods, expanding applicability to a broader range of antigens. This platform provides a scalable solution for antibody internalization analysis, positioned to accelerate ADC discovery by providing reliable early-stage screening metrics.

Drug sensitivity analysis revealed differential therapeutic vulnerabilities, with high-risk patients showing increased sensitivity to EGFR-TKIs, including Gefitinib (p < 0.001). The model demonstrated significant prognostic value in kidney chromophobe (p = 0.040), kidney clear cell carcinoma (p < 0.001), and cervical squamous cell carcinoma (p = 0.004). Our study establishes a robust epigenetic-based prognostic model for NSCLC and identifies LYPD3 as a novel oncogenic driver, providing insights into tumor biology and treatment response, offering potential clinical utility for personalized therapeutic strategies.

Further experiments indicated that LYPD3 promoted the malignant progression in LUAD cell lines. Our study constructed the PMRS model, highlighting its potential value in the treatment and prognosis of LUAD patients and providing new insights into the individualized precision treatment for LUAD patients.

Finally, we experimentally validated one of the biomarkers, HMGA1, confirming its role in promoting malignant phenotypes of NSCLC. This study provides valuable insights into the role of lactate metabolism-related biomarkers and their impact on patient outcomes, it was expected to provide important reference value for prognosis assessment and personalized treatment decision of NSCLC patients.

Our study provides novel, high-affinity, fully human, anti-AGR2 MAbs that neutralize the pro-tumor effects of extracellular AGR2 in PDAC.

In vitro experimental findings demonstrated a marked decrease in the proliferative and migratory capacities of LUAD cells upon knockdown of MKI67. Conclusively, we successfully constructed the PCDS, providing important assistance for prognosis prediction and treatment optimisation of LUAD patients.

This process is orchestrated by methyltransferase-like 3 (METTL3) and mediated by a newly identified reader, heterogeneous nuclear ribonucleoprotein U (hnRNP U). These findings collectively underscore the significance of the METTL3/miR-151-5p/LYPD3 axis serves as a prominent driver in the malignant progression of HNSCC.

Additionally, the median half maximal inhibitory concentration (IC50) of bexarotene, cyclopamine, etoposide, and paclitaxel in LYPD3 high group was significantly lower than that in LYPD3 low group. LYPD3 is involved in many BPs of LC, such as regulating immune cell infiltration and affecting prognosis. Therefore, LYPD3 may have potential value as a biomarker for prognosis and immunotherapy in LC.

APOBEC family was associated with genomic instability, DNA damage-related pathways, and cell cycle in LUAD. The AMES-related gene signature had a great potential to indicate the prognosis and guide immunotherapy/chemotherapy for patients suffering from LUAD.