ANG elevation

Our studies show that the NRASQ61R mutation in endothelial cells induces Ang-2 expression in vitro and in vivo. In cultured human endothelial cells, NRASQ61R drives elevated Ang-2 through MAP kinase and mTOR-dependent signaling pathways.

Latent phase analysis demonstrated that patients with low biomarker levels aside from TNF-α and TNFR-1 (Class 2) fared worse than other patients. Future research may benefit from considering other tools to predict and prevent development of ARDS in this population.

A 28.6% reduction in maximum target lesion diameter was achieved when PRL3-zumab was administered concurrently with hypofractionated radiation. These findings support wider exploration of PRL3 expression in embryonal and mesenchymal tumors and further clinical application of PRL3-zumab in pediatric patients.

Regarding our findings and observations, we can affirm that: An inverse and statistically significant association were observed between Ang1 and Ang2. The behavior of these angiogenic biomarkers described an increase in Ang2 in those cases where the disease progressed, compared to Ang1 that decreased. After the results described above, we can suggest that obtaining a low Ang1/Ang2 ratio (<6) was correlated with a greater probability of having an unfavorable response to treatment and a torpid evolution of MM.