CEACAM6 (CEA Cell Adhesion Molecule 6)

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.

ALK mutations drive tumor stemness and drug resistance by blocking epithelial cell differentiation, activating CEACAM6-mediated signaling, enhancing chromatin accessibility, and remodeling the EGR1/PRC regulatory network. Targeting CEACAM6 and its downstream effector EGR1 may represent an effective strategy to overcome ALK-TKI resistance.

We developed a prognostic signature based on triaptosis-related genes (TRGs) that robustly stratifies HER2-low BC patients. Our findings support the clinical relevance of TRGs as biomarkers rather than direct evidence of triaptotic cell death, and identify PYDC1 as a functionally relevant suppressor of PI3K/AKT signaling in HER2-low BC.

Collectively, these findings highlight CEACAM6-containing EVs as mediators of tumorigenesis. This study also showcases the technical, translational and clinical advantages of considering CEACAM6 as a diagnostic biomarker for the detection of GC in a minimally-invasive manner.

CEACAM6 exhibits high diagnostic accuracy and tumor-specific overexpression in pan-gastrointestinal cancers. CEACAM6 could promote angiogenesis/metastasis and suppress anti-tumor immunity. Spatially localized in tumors with immune cell exclusion, CEACAM6 correlates with poor survival and immune-excluded subtypes, positioning it as a therapeutic target in precision immunotherapy for pan-gastrointestinal cancers.

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.

CD97, CD73, CD86, and CD58 are the best amongst newer markers in B-ALL MRD assessment. Our findings support integrating these into MRD panels to enhance post-therapy MRD detection, thus improving prognostication and guiding treatment decisions.

Using a novel data-driven approach, six potential imaging targets were successfully identified and validated. CEACAM5 and CEACAM6 emerged as strong targets that, regardless of neoadjuvant therapy, covered nearly the entire CRLM population-supporting their further probe development and clinical translation.

The high expression of LAD1 in cancer cells, its associations with LUAD-related genes, and its links to biological processes and pathways suggest its potential biological relevance and that it merits further investigation. Overall, this study provides insights into LUAD and supports LAD1 as a gene worthy of further investigation.

Our study demonstrated that CEACAM6 regulates glycolysis via the ENO1-AKT/mTOR axis. These results offer new evidence about previously unexplored molecular mechanisms driving BCa progression.

GSK-3b blockade synergizes with FFX by modulating PDAC plasticity while promoting the development of a tumor suppressive immune microenvironment.

Tier 3 proteins, supported by logistic regression and MR only, included CD5L, GNPDA, ACAN, C7, DMP1, HEPH, CEACAM6, COX6B1, CPXM2 and IL12RB2. Druggability evaluation suggests that existing drugs targeting ITGB2, GP1BA, ACADSB and COX6B1 could potentially be repurposed for the treatment of specific lung cancer subtypes.