CDH1 (Cadherin 1)

Our findings indicate that E-Cad-neg BLEC is a type of breast carcinoma characterized by extensive lymphocytic infiltration and high proliferative activity and is associated with a relatively favorable prognosis.

These findings suggest that cellular MT1B overexpression has the potential to promote lung cancer growth. [BMB Reports 2026; 59(2): 161-168].

BXD intervention demonstrated significant therapeutic effects in GPL mice. The underlying mechanisms are associated with the restoration of gastric microbiota dysbiosis, promotion of beneficial bacterial growth, suppression of potential pathogens, modulation of the inflammatory response, and alleviation of mucosal damage.

This study provides robust genetic evidence for the causal roles of SELE, CDH1, and ALPI in reducing BC risk. The integrative proteomic-genetic-transcriptomic approach identifies potential therapeutic targets and offers new insights into BC pathogenesis, presenting hypotheses for clinical validation.

Nevertheless, the prognostic value of selected genes should be established in wide genomic clinical trials, regarding drug response and overall survival rate (OSR). This article aims to elucidate the clinical utility of several genetic alterations towards a genetically informed prognostication and rationalized combination of novel targeted therapeutic tools.

The strong correlation between UNC93B1 overexpression and adverse clinical outcomes underscores its potential as a dual diagnostic biomarker and therapeutic target. This work not only provides a mechanistic foundation for novel precision immunotherapies in PDAC but also establishes a robust methodological paradigm for multi-omics-driven discovery in oncology.

Similarly, there was no effect of unglycosylated EpCAM on cell viability, migration, invasion, or homotypic adhesion, although we did observe slight increases in homotypic cell-cell adhesion in EpCAM overexpressing cells. These findings show that N-glycosylation has a significant impact on stability and subcellular localization of EpCAM, but not on several critical breast cancer cell properties important for cancer progression and metastasis in human triple-negative MDA-MB-468 breast cancer cells.

Importantly, siRNA-mediated silencing of FAM83A abolished its overexpression and inhibited EMT activation, confirming its essential role in M2-Exo-induced programming of EMT. Collectively, these findings highlight exosome-mediated immune-tumor interactions as critical drivers of EMT and the progression toward an invasive, mesenchymal-like phenotype.

E-cadherin dysregulation is strongly associated with histological tumor grade, adenocarcinoma type, tumor stage, nodal metastasis, and perineural invasion in GI adenocarcinomas. The significant loss of expression in poorly differentiated and infiltrating tumor types supports its role as an invasion suppressor. Loss of E-cadherin expression in advanced tumor stages, higher nodal metastasis, and perineural invasion elucidate the role of E-cadherin as a useful prognostic immunohistochemical marker in gastrointestinal adenocarcinomas.

Despite advancements in H. pylori research and technology over 20 years, no improvement was observed in H. pylori-positive tumor rates or early gastric cancer detection in Western Poland. Although molecular characteristics remained largely unchanged, the increased proliferation index in recently diagnosed cancers merits further study.

In vivo, the combination reduced tumor growth vs cisplatin alone without increasing toxicity. This is the first report that lycopene enhances cisplatin sensitivity in OSCC by coupling inhibition of MRP-1-mediated drug efflux with suppression of PI3K/Akt/mTOR and EMT/stemness-filling the gap of lycopene's synergistic mechanism with cisplatin, offering a strategy to improve therapeutic efficacy without exacerbating toxicity.

Inactivation of Cdh1 alone in Cd44-expressing cells is sufficient to induce DGC in mice. Tumour growth is significantly accelerated by concurrent Trp53 inactivation.