Improved tumor control with antiangiogenic therapy after treatment with gemcitabine and nab‐paclitaxel in pancreatic cancer.

The baseline is referring to the patient before therapy administration gl Interesting, VEGF promotes gemcitabine resistance in pancreatic cancer cells (Figures 2A and 2B). Finally, we silenced c-Myc in VEGF-stimulated MIA PaCa-2 and SW1990 cells, and found that c-Myc suppression or knockdown could reverse the effects of VEGF on the IC50 values of gemcitabine of pancreatic cancer cells (Figures S2E and S2F). The baseline is referring to the patient before therapy administration. gl GLO:F2H7/01aug21:ctm2398-sup-0002-FigureS2.jpg PHOTO (COLOR): Figure S2 Silencing c-Myc reverses the effect of VEGF on RRM1. Dear Editor, The regimen of nab-paclitaxel and gemcitabine (AG) has been widely used as the first-line chemotherapy for advanced pancreatic cancer; the prolonged survival time is still less than 2 months.1 Kim et al demonstrated that paclitaxel can induce vascular endothelial growth factor-A (VEGF) expression which could facilitate the survival of neoplastic and tumor cells, thus protecting both endothelial and stroma cells from cytotoxic death while promoting angiogenesis.2-4 To explore the neovascularization in patients with pancreatic ductal adenocarcinoma (PDAC) treated with AG or gemcitabine alone, we first examined the I K SP trans sp i value in the tumor by Dynamic contrast enhancement magnetic resonance imaging (DCE-MRI). [Extracted from the article]