NT5E (5'-Nucleotidase Ecto)

These findings suggest that the expression of PD-L1 and PD-1 in CC tissues is strongly correlated with the expression of CD73 and TGF-β1. Therefore, the joint analysis of these biomarkers could be highly useful for evaluating disease prognosis and for developing strategies to improve the efficacy of immunotherapy protocols in CC patients treated with immune checkpoint inhibitors (ICIs).

P2, N=150, Active, not recruiting, TJ Biopharma Co., Ltd. | Recruiting --> Active, not recruiting

P2/3, N=450, Active, not recruiting, TJ Biopharma Co., Ltd. | Recruiting --> Active, not recruiting

PIK3R1 overexpression is linked to poor prognosis in GC and influences the extent of immune cell infiltration within the tumor microenvironment. A novel prognostic model integrating PIK3R1 and CD73 expression with clinical parameters was established to stratify GC patients into distinct risk groups, offering potential value for personalized therapeutic strategies.

In summary, we demonstrate that protein profiling of EVs in relation to osimertinib refractoriness has the potential to identify possible biomarkers that can indicate osimertinib treatment resistance, for example, CSPG4, HSPG2, TAGLN, TNC, THBS1, ANXA1 and CD73/NT5E. Studies in expanded cohorts should be conducted to further validate these putative osimertinib biomarkers.

TCGA analyses, GeoMx digital spatial profiling, and functional analyses showed that CD73 loss drives distinct Wnt-TCF/LEF-dependent gene expression programs linked to cancer cell stemness. These findings identify CD73 as a key regulator of mutant β-catenin, providing mechanistic insight into the variability of recurrence in CTNNB1-mutant EC.

CD73 expression was observed in 45.8% of patients whose disease was under control with sorafenib, while 80% of patients who did not respond to sorafenib showed CD73 expression (p = 0.02).ConclusionsPositive lymphocyte activation gene 3 expression was correlated with better survival in patients with advanced or metastatic hepatocellular carcinoma. In addition, CD73 expression in patients with advanced or metastatic hepatocellular carcinoma was a negative predictive factor in those receiving sorafenib.

Here, we identify that immunosuppressive eADO signaling in the TME is a major barrier to oHSV therapy and CD73 blockade prevents tumor immune escape. The combination of oHSV with CD73 blockade supports the development of an antitumor immune memory response in solid tumors. This study supports clinical development of this combination strategy.

This study identifies potential therapeutic targets for BTC. Drugs designed to target these genes have a higher likelihood of clinical success and are expected to facilitate BTC drug development while reducing associated costs.

The CD73+CD39+CD146+ cell subset showed self-renewal and multipotency abilities and was located in perivascular areas of BM. Such cell subset was also reported in single and dual-mobilized leukopaks.

These findings identify CD73 as a direct hypoxia-responsive effector of HIF-1α in EAC and demonstrate that dual inhibition of HIF-1α and CD73 synergistically disrupts tumor cell survival and pro-metastatic signaling. This combinatorial strategy represents a mechanistically integrated therapeutic approach to overcome hypoxia-driven resistance in esophageal adenocarcinoma.

To our knowledge, this is the first study to construct a comprehensive ceRNA network specifically for posttreatment recurrent NPC. These findings highlight the ceRNA network as a valuable framework for elucidating the mechanisms of NPC relapse and for identifying potential biomarkers for prognosis and therapeutic targets in recurrent nasopharyngeal carcinoma.