To improve the therapy efficiency as a PTT agent, the MCP NPs are further modified with functional polyethylene glycol (PEG) and thiol terminal cyclic arginine-glycine-aspartic acid peptide, respectively: the first one is to increase the stability, biocompatibility, and blood circulation time of MCP NPs in vivo; the second one is to increase the tumor accumulation of MCP-PEG NPs and improve their therapeutic efficiency as photothermal agent.
Downregulated DEGs included TFs, such as the proto‑oncogene SPI1, pre‑B‑cell leukemia homeobox 3 (PBX3) and lymphoid enhancer‑binding factor 1 (LEF1), as well as tumor suppressors (TSs), such as capping actin protein, gelsolin like (CAPG) and tumor protein p53‑inducible nuclear protein 1 (TP53INP1).
The combination of CTNB1, XPO2, and CAPG achieved 95% sensitivity and 96% specificity for the discrimination of these subtypes.<b>Conclusions:</b> We developed two uterine aspirate-based signatures to diagnose EC and classify tumors in the most prevalent histologic subtypes.
The IHC results demonstrated that CapG was relatively highly expressed in CRC tissue compared with non-tumor tissue (P<0.001), and that the expression of CapG was significantly associated with the tumor site, differentiation, lymph node metastasis and clinical stage (P=0.021, P=0.036, P=0.012 and P=0.009, respectively).
We found that macrophage-capping protein (CapG) was up-regulated in the tumor tissues of patients with LNM, whereas it showed an equivalent expression level between nontumor and tumor tissues of patients without LNM.
One hundred six of 224 (47%) CNS tumors were positive for HHV-6 U57 Major Capsid Protein (MCP) gene by ISH compared to 0/25 non tumor control brain (P = 0.001).