CEACAM1 (CEA Cell Adhesion Molecule 1)

Mechanistically, SETD2 methylates SRSF2P95H at lysine-17 and lysine-65 to inhibit aberrant splicing of CEACAM1-4 (isoforms of carcinoembryonic antigen cell adhesion molecule), which enhances interleukin-1β (IL-1β) signaling through Slc7a11 (solute carrier family 7 member 11)-mediated cystine uptake, thereby promoting HSPC differentiation into MDSCs, establishing an IL-1β-driven immunosuppressive microenvironment. These findings identify the SRSF2P95HK17me1K65me2-CEACAM1-4 signaling axis as a promising therapeutic target in SRSF2P95-Mut MDS.

In vivo, pharmacologic inhibition of SAA enhanced sensitivity to ICI plus TKI combination therapy, while blockade of the CEACAM1-TIM-3 axis in humanized PD-1 mouse models significantly potentiated anti-PD-1 efficacy. Our study establishes a single-cell atlas of the aRCC tumor microenvironment under treatment pressure and identifies a previously unrecognized SAA-CEACAM1-TIM-3 axis driving drug resistance, highlighting potential targets to improve therapy efficacy.

ProB leukemias with low CD66c expression were more likely to exhibit detectable MRD, increased mortality, and reduced survival. Low CD66c expression induces molecular stealth that could favor immune evasion and niche persistence, thereby increasing the risk of relapse and therapeutic failure.

Pharmacological inhibition of USP7 with FT671 and XL177A reduces KDM6A stability and viral receptor expression, and confers resistance to MERS-CoV, SARS-CoV, and all major SARS-CoV-2 variants of concern, including those resistant to remdesivir in primary human airway and intestinal epithelial cells. In mice, FT671 treatment was well tolerated, reduced Ceacam1 expression, and protected against MHV-A59 infection. Collectively, our findings unveil an antagonistic ubiquitin-mediated regulatory circuit that controls KDM6A stability, viral receptor levels, and coronavirus infection.

In summary, CEACAM6 was found to promote GC aggressiveness and alter macrophage polarisation. This information could be harnessed to develop future therapeutics for targeting GC.

Yeast-displayed C1ND specifically bound HopQ-GFP and GFP-expressing H. pylori. Yeast surface display of CEACAM1's N-domain is an effective model for studying HopQ-CEACAM1 binding and offers potential for identifying inhibitors to block H. pylori adhesion and associated disorders.

Plausible dissemination along an oral-gut-systemic axis, hematogenous, lymphatic, microaspiration, and direct mucosal transfer enables distal effects. While causality is not yet definitive, cumulative data support oral dysbiosis as a clinically relevant cofactor, motivating biomarker-based risk stratification, saliva/stool assays for early detection, and microbiome-targeted interventions (periodontal care, antimicrobials, probiotics, and microbiota modulation) alongside conventional cancer control.

This study provides a spatially resolved molecular map of IPMN progression, delineating key transcriptomic and immune signatures. These findings advance the understanding of IPMN biology and highlight potential biomarkers for risk stratification and therapeutic strategies.

The NK cell/PDO co-culture platform allows the identification of both common and patient-specific impacts of the tumor microenvironment on NK cell function and can aid the development of patient-tailored immunotherapies. The majority of CRC (CMS2/CMS3) PDOs from our cohort were susceptible to NK cell-mediated killing and induced NK cell activation, highlighting the potential of NK cells for CRC immunotherapies.

These markers, when integrated with cytology, could enhance the diagnostic precision and reduce dependence on invasive cystoscopy. The proposed cutoffs (10%-20% positive cells or Allred score ≤2) offer clinically actionable threshold for histopathological practice.

CEACAM1 regulates the PPAR signaling pathway key molecules, affecting OSCC cell autophagy, mitochondrial balance, and apoptosis.

This investigation elucidates the potential role of immune dysregulation underlying GWI, emphasising the importance of immune exhaustion pathways in disease progression. Further investigations in a larger cohort may further elucidate or confirm these identified markers for potential screening or therapeutic applications in GWI.