SVEP1 (Sushi, Von Willebrand Factor Type A, EGF And Pentraxin Domain Containing 1)

We identified several novel plasma proteins for VTE that reflect biological processes outside established VTE pathophysiology, including extracellular matrix regulation, immunity, immune-vascular endothelium interactions, and vascular senescence. Results may provide new modifiable targets to improve VTE risk stratification, prevention, or treatment.

These effects were mediated by EMT phenotype switching through the activation of the Jag2/Notch1/Hes5 pathway. Our findings enhance the understanding of the novel mechanisms driving ICC progression and metastasis, suggesting that SVEP1 is a potential biomarker for ICC diagnosis.

Overall, this study confirmed that LYMS is an independent prognostic risk factor in GC patients. The LYMS demonstrates significant predictive ability for responses to immunotherapy, suggesting its potential to guide future immunotherapy interventions for GC patients.

Functional enrichment analysis revealed that several pathways were altered in tumour and immune cells. In conclusion, distinctive changes in gene expression patterns were observed as AK progressed to SCC.

SVEP1 emerges as a potential mechanism of mTOR activation in iMCD-TAFRO, while multiple pathways influence coagulopathy. Immunothrombosis emerges as a potential therapeutic target for iMCD.

Doxorubicin-exacerbated evasion and migration through VWF upregulation. Berberine as an inhibitor of VWF was able to reversed the doxorubicin-exacerbated VWF upregulation and evasion and migration in breast cancer cells.

PCNSL occurs somatic missense mutations frequently, mainly point mutations, and the mutation type is mainly C>T. The driver genes are mainly involved in RTK-RAS, Wnt, NOTCH and Hippo pathways, indicating that the above pathways may be related to the pathogenesis of PCNSL. PCNSL has a significantly high tumor mutation burden, which may explain the efficacy of PD-1 inhibitors in PCNSL.

These results suggest that BVES-AS1 plays a crucial role in the progression of CRC through the miR-1269a/b-SVEP1-PI3K/AKT axis, providing new insights into the therapeutic strategies for CRC.

Numerous serum proteins linked to metabolic, coagulation, and extracellular matrix regulatory pathways were associated with worse HFpEF prognosis. SVEP1, a cell adhesion protein recently identified as a HFrEF prognosis biomarker, also strongly predicted risk in HFpEF. Our results demonstrate substantial similarities in serum proteomic risk markers across the EF spectrum.

We constructed a six-gene BM-related prognostic model for predicting GC prognosis, immune cell infiltration, TMB status, and chemotherapy response. This research provides new ideas for developing more effective individualized treatment of GC patients.