CDCP1 (CUB Domain Containing Protein 1)

Notably, we develop a pH-sensitive nanoparticle delivering siCDCP1, which effectively restores chemosensitivity and impairs tumor growth in cisplatin-resistant patient-derived xenograft (PDX) models with favorable safety profile. These findings establish PDOs as robust preclinical models for mechanistic explorations and therapeutics development and highlight CDCP1-targeting strategies as promising approaches to overcome cisplatin resistance in OSCC.

Mechanistically, CD318 inhibited T cell receptor signaling independently of SHP2, while its induction required interleukin-2-dependent mTOR activation. These findings identify CD318 as a marker of human CD8+ T cells with implications for immune regulation and autoimmunity.

Furthermore, risk models incorporating specific protein signatures effectively stratified patients by platinum sensitivity/resistance (9-protein panel: ILK, CDCP1, CD86, CLDN4, CLEC1B, CDHR5, CLDN11, JAM2, FOLH1), lymph node metastasis status (7-protein panel: APOE, CD28, CLDN4, FOLH1, ITGAL, JAML, ULBP3), and post-surgical residual disease burden (4-protein panel: CD44, CLMP, ITGA4, AMIGO1), with Cluster 13 (ITGB1-high) also significantly associated with residual disease. This work demonstrates the power of single-EV proteomics combined with machine learning for non-invasive diagnosis and clinical outcome assessment in advanced ovarian cancer, though the absence of early-stage patients limits its applicability for early detection.

Quantitative ex vivo fluorescence analysis of excised xenografts demonstrated that combining ch10D7ICG and amatuximabICG enhances tumor-associated fluorescence by 2.8- to 12.5-fold compared with either agent alone. The results support the potential of dual-targeted, antibody-based fluorescence imaging for enhanced intraoperative visualization and excision of PDAC, including for tumors with heterogeneous expression of either or both of the targeted receptors CDCP1 and MSLN.

CDCP1 defines a transcriptionally distinct PDAC subtype characterized by immune evasion, stromal depletion, and genomic instability. These findings highlight CDCP1 as a potential therapeutic target and biomarker reflecting interplay between oncogenic signaling and the TME.

Detailed smoking history provides crucial insights for optimizing IO selection in advanced NSCLC through mechanistic alterations in both the tumor microenvironment and systemic plasma protein profiles.

Together, our findings revealed shared molecular features across MPN and AML, identified a prognostic gene signature for risk stratification, and provided rationale for PI3K/mTOR inhibition as a promising therapeutic strategy in myeloid malignancies.

Mechanistic interrogation combined NSUN2 knockout, CRISPR knock-in mutants at K692 (K692R/E), co-immunoprecipitation, RIP-seq, MeRIP-qPCR, and actinomycin-D chase to test mRNA binding, m5C modification, and stability of CDCP1/STC1... This study identifies lactate-driven NSUN2 K692 lactylation as a key driver of perineural invasion in PDAC. We define a lactate-NSUN2-m5C-CDCP1/STC1 axis that links metabolic stress-induced lysine lactylation to mRNA methylation-dependent stabilization of pro-invasive transcripts, highlighting actionable therapeutic targets to restrain neural invasion and improve patient outcomes.

This study provides insight into unique biomarker profile in patients on ocrelizumab. Increased BAFF was associated with lower IgG and IgA levels, biomarkers of neuroaxonal damage and inflammation in MS patients without recent acute inflammatory activity on ocrelizumab.

The SMYD3-CDCP1 axis drives CRC progression by epigenetically promoting CDCP1 transcription and remodeling the tumor microenvironment. Targeting this pathway may provide a promising therapeutic strategy to restrain metastasis and enhance chemotherapy efficacy in CRC.

Furthermore, the combination of TAVO423 in combination with other solid tumor cell targeting modalities such as 5-fluorouracil (5-FU), anti-PD-L1 monoclonal antibody, a PD-L1 × CD3 bispecific T-cell engager (TCE), and a CD318-targeting antibody-drug conjugate (ADC) all demonstrated enhanced tumor growth inhibition (TGI) values of 49-67% as compared to the respective monotherapy TGI values of 1-28%...Conclusions. These findings demonstrated the broad potential of the modular AbEn platform for targeted HA degradation to overcome barrier entry in stromal HA-rich solid tumors.

A prognostic signature composed of CDCP1, CLIC6, FURIN, KRT6A, MFI2, and P2RY13, based on PANR-DEGs, provides a theoretical framework and reference for further LUAD research.