IGFBP7 (Insulin Like Growth Factor Binding Protein 7)

The validated six-protein risk-score improves prognostic stratification beyond standard clinical factors in stage-III CC, providing a robust framework for risk-adapted clinical investigation. Prospective, treatment-stratified clinical trials are warranted to determine whether this prognostic information can inform adjuvant therapy decision-making.

We showed that the editing activity of ADAR2 on IGFBP7 abolishes its proliferative effect on osteosarcoma cells and triggers terminal differentiation. Overall, our results indicate that ADAR2 acts as a tumor suppressor in osteosarcoma and may represent a novel therapeutic target for this aggressive pediatric tumor.

This association was also confirmed in patients receiving tafamidis. In patients with ATTR-CM, MR-proADM levels are associated with disease severity and worse prognosis. MR-proADM improves prediction of all-cause mortality and captures heart failure events.

In TH-MYCN mice, which have a high frequency of NB development, Tagln overexpression by induction of the murine Tagln gene significantly reduced tumor formation and prolonged survival. In conclusion, these in vitro and in vivo analyses suggest that TAGLN is a candidate tumor suppressor gene in NB.

CSF IGFBP7 was found to be closely associated with CSF TNF-α, showing potential diagnostic utility in MS. A dual-marker model combining CSF IGFBP7 and TNF-α improved diagnostic performance, suggesting that IGFBP7 reflects inflammatory processes relevant to MS.

A panel of protein biomarkers, some new (IGFBP7, HGF) and some previously known in PLWH (CLEC6A), could help identify PLWH at higher risk of developing CVD. If confirmed, these scores could be used with CVD and HIV-related factors to identify PLWH at risk for CVD who would benefit from proactive risk reduction strategies.

Moreover, we identified the GALNT10 inhibitor Luteolin, which effectively suppresses ovarian cancer metastasis, modulates the immunosuppressive tumor microenvironment through tumor vascular-immune crosstalk, and exhibits synergistic effects with anti-PD1 therapy. Collectively, our findings indicate that GALNT10 facilitates ovarian cancer metastasis through the induction of tumor cell EMT and tumor vascular dysfunction, suggesting that GALNT10 inhibitors represent a promising avenue for the development of novel therapeutic strategies in ovarian cancer.

This study establishes iCAFs and γδT cell loss as central drivers of cSCC aggressiveness and nominates CXCL8/TGFβ/IGFBP7 dysregulation as a biomarker framework for risk stratification. Collectively, these findings unveil actionable therapeutic targets and provide a molecular basis for personalizing management strategies, particularly for identifying and treating very highrisk cSCC patients who may benefit from intensified surgical approaches, adjuvant therapies, or novel targeted interventions.

More importantly, CBP-D8 peptide combined with radiotherapy significantly abrogated tumor growth and elicited systemic antitumor immune response. Our study identified a novel peptide blocking CD93/IGFBP7 interaction to normalize tumor vascular function, as well as revealed an approach to promote a favorable tumor microenvironment for the therapeutic intervention.

At markedly reduced intravenous doses, IGFBP7-sEVs efficiently concentrated temozolomide (TMZ) within glioma and elicited pronounced tumor growth inhibition...Our data suggest that IGFBP7-modified sEVs represent a novel platform that enables highly efficient, glioma VECs-targeted delivery of therapeutics into glioma, and are adaptable to a broad spectrum of agents, especially immunomodulators. It is a novel and effective strategy for treating gliomas.

This study underscores the biological relevance of RNA editing in CRC, highlighting its impact on chemoresistance, the tumor microenvironment, and subtype-specific gene regulation. Our findings suggest that RNA editing represents a critical post-transcriptional regulatory layer in CRC and holds potential as a biomarker and therapeutic target.