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1 lar endothelial cell growth factor (VEGF) in malignant ascites.
2 loid dendritic cells (MDCs) were absent from malignant ascites.
3                   Such mice began to develop malignant ascites about 6 months after injection, which
4  in tumor cells harvested from patients with malignant ascites and in tumor samples taken at a second
5     CS-682 also decreased the development of malignant ascites and the formation of metastases, which
6 is in the tumor microenvironment, we studied malignant ascites and tumors of patients with untreated
7 arization of lesions, decreased formation of malignant ascites, and prolonged survival of mice.
8 omal-derived factor (CXCL-12/SDF)-1 in their malignant ascites, attracting PDCs into the tumor enviro
9 n cancer, were examined from patient derived malignant ascites cells.
10                       Treatment of mice with malignant ascites due to mesothelioma with rapamycin led
11                             We observed that malignant ascites fluid induced potent in vivo neovascul
12  may have clinical application in inhibiting malignant ascites formation in ovarian cancer.
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
16 extensively, and produced a larger amount of malignant ascites in IFN-gamma(-/-) mice.
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
19                                              Malignant ascites is a common complication in the late s
20                                              Malignant ascites is a known consequence of vascular dys
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
23 toward a safe and effective means to control malignant ascites of EOC.
24 amniotic fluid, liver cirrhosis ascites, and malignant ascites of ovarian cancer patients.
25 er cells secrete PN, which can accumulate in malignant ascites of ovarian cancer patients.
26                Using cells isolated from the malignant ascites of patients with advanced ovarian canc
27 is in the tumor microenvironment, we studied malignant ascites of patients with untreated ovarian car
28 detected against cells freshly isolated from malignant ascites of previously treated patients.
29 itoneal fluid samples from 258 patients with malignant ascites randomized to catumaxomab or control g
30                                              Malignant ascites resolved in three patients, one each w
31                             Fractionation of malignant ascites revealed that extracellular matrix-deg
32                                Patients with malignant ascites secondary to primary carcinomas benefi
33 in vivo efficacy within the immunosuppressed malignant ascites tissue microenvironment.
34                   Natural fluidic streams of malignant ascites triggered by physiological factors, in
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
37                       Membrane vesicles from malignant ascites were also found to contain activated M
38                            Tumor biopsies or malignant ascites were collected from patients before tr
39 erous liver metastases and a large amount of malignant ascites, whereas IFN-beta-secreting cells did

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