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1 lar endothelial cell growth factor (VEGF) in malignant ascites.
2 loid dendritic cells (MDCs) were absent from malignant ascites.
4 in tumor cells harvested from patients with malignant ascites and in tumor samples taken at a second
6 is in the tumor microenvironment, we studied malignant ascites and tumors of patients with untreated
8 omal-derived factor (CXCL-12/SDF)-1 in their malignant ascites, attracting PDCs into the tumor enviro
13 test this novel therapeutic peptide, serous malignant ascites from highly resistant recurrent ovaria
14 d in peritoneal exudate cells (PEC) from the malignant ascites from patients with ovarian cancer.
15 jection of VR cells into athymic mice formed malignant ascites in 100% of the animals when injected i
17 intraperitoneal therapy for the treatment of malignant ascites in patients with EpCAM-positive carcin
18 ffects of the CatmAb on the major subsets of malignant ascites-infiltrating leukocytes and the molecu
21 correlates with microvessel density, stage, malignant ascites, metastasis, and survival in ovarian c
22 rian carcinoma cell lines and the cells from malignant ascites of chemotherapy-treated patients with
27 is in the tumor microenvironment, we studied malignant ascites of patients with untreated ovarian car
29 itoneal fluid samples from 258 patients with malignant ascites randomized to catumaxomab or control g
35 nctions to reverse the vascular pathology of malignant ascites using fluid from human patients and an
36 ate macrophages' role in the pathogenesis of malignant ascites, we blocked macrophage function in ID8
39 erous liver metastases and a large amount of malignant ascites, whereas IFN-beta-secreting cells did
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