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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of antineoplastic prostaglandins (PG) on human ovarian cancer cell growth were examined by using HR cells derived from ascites of a patient with serous cystadenocarcinoma of the ovary. With regard to inhibition of cancer cell proliferation in vitro, the effects of delta 7-PGA1 was most marked, followed by that of delta 12-PGJ2, PGJ2 and PGD2. When antineoplastic prostaglandins were administered to nude mice bearing HR cells, tumor growth in groups treated with PGJ2 and delta 12-PGJ2 alone was significantly inhibited 63 days after tumor inoculation, compared to that in an untreated group. Consequently, a significant prolongation of median survival was obtained with delta 12-PGJ2, compared to that in untreated groups and in groups with cisplatin alone. In addition, when prostaglandins were administered together with cisplatin, adjuvant inhibitory effects on the tumor growth were obtained 35, 56 and 63 days after tumor inoculation. Subsequently a significant prolongation of median survival was observed when cisplatin was combined with PGD2 or delta 7-PGA1, compared to the results in groups treated with PGD2 alone, delta 7-PGA1 alone or cisplatin alone. Combination of PGJ2 or delta 12-PGJ2 and cisplatin resulted in a significant decrease of hematocrit and body weight 63 days after tumor inoculation, suggesting a deterioration of the median survival. These results suggest that combination of PGD2 or delta 7-PGA1 with cisplatin may be of clinical use for ovarian cancer resistant to cisplatin.
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PMID:Adjuvant effects of antineoplastic prostaglandins to cisplatin in nude mice bearing human ovarian cancer cells. 161 93

We have elucidated the importance of a transforming growth factor (TGF) alpha and epidermal growth factor receptor autocrine mechanism on the growth of a human ovarian serous cystadenocarcinoma-derived cell line (SHIN-3) in vitro. In this study, we studied the biological significance of this autocrine mechanism in vivo using female athymic nude (nu/nu) mice. We measured the mouse plasma epidermal growth factor and TGF alpha levels by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. Plasma epidermal growth factor concentrations were remarkably decreased by sialoadenectomy (Sx): 410 +/- 65 (SE) pg/ml (n = 10) in intact animals; and undetectable in Sx mice (n = 5). Plasma TGF alpha levels were 90 and 40 pg/ml in intact and in Sx animals, respectively. Ten million SHIN-3 cells inoculated into nu/nu mice formed tumors in 100% of mice, and tumors grew progressively. Implantabilities and tumor growth rates of inoculated cells were not affected by Sx and even by Sx and anti-mouse epidermal growth factor antibody treatment. However, anti-TGF alpha monoclonal antibody (mAb) administered to SHIN-3 cell-inoculated Sx animals drastically reduced the tumor growth. Although 10(7) SHIN-3 cells formed tumors in this group, tumor growth was significantly inhibited by 10 micrograms of anti-TGF alpha mAb given 3 times a week, and growth inhibitions were more by 20 micrograms of anti-TGF alpha mAb. Moreover, as aggressive tumor growth as that in Sx animals was resumed by the cessation of anti-TGF alpha mAb treatments. All these data suggested the biological importance of a TGF alpha/epidermal growth factor receptor autocrine mechanism on the growth of this cell line in vivo.
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PMID:Importance of transforming growth factor alpha/epidermal growth factor receptor autocrine growth mechanism in an ovarian cancer cell line in vivo. 193 59

In vitro and in vivo effects of ginsenoside Rh2 on human ovarian tumor growth were examined by using a cell line (HRA) derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HRA cell proliferation in vitro was inhibited in a dose-dependent manner with dosages of 10-100 microM of ginsenoside RH2. DNA, RNA and protein synthesis by the HRA cells was inhibited in a dose-dependent manner at more than 15 microM of ginsenoside RH2. However, the growth of HRA cells transplanted in nude mice was not significantly inhibited by ginsenoside RH2. On the contrary, when cisplatin was administered together with 10 microM (but not 1 microM or 100 microM) ginsenoside RH2, the tumor growth was significantly inhibited 31 days after inoculation and the survival was also significantly prolonged, compared with not only the untreated group but also the groups given cisplatin alone or ginsenoside RH2 alone. This indicates synergistic effects between cisplatin and ginsenoside RH2. From monitoring of body weight and hematocrit, concentrations of ginsenoside RH2 used in this study did not seem to cause any adverse effect.
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PMID:Inhibition of human ovarian cancer cell proliferation in vitro by ginsenoside Rh2 and adjuvant effects to cisplatin in vivo. 195 54

In vitro and in vivo effects of prostaglandin D2 on human ovarian cancer growth were examined by using a cell line, designated HR, derived from ascites of patient with serous cystadenocarcinoma of the ovary. The HR cell proliferation in vitro was dose-dependently inhibited at prostaglandin D2 concentrations between 0.1 and 4.0 micrograms per ml. The results of a 51Cr-release assay seemed to indicate that the inhibition resulted from a direct cytotoxic effect exerted by prostaglandin D2. All DNA, RNA, and protein synthesis by the HR cells was also inhibited in a dose-dependent manner with 48 hr exposure to prostaglandin D2. When nude mice were inoculated with 5 X 10(5) HR cells, the 50% survival time in the untreated group was 52 days. The 50% survival time of nude mice treated with 12 mg (but not 4 mg) of prostaglandin D2 per kg was significantly prolonged to 67 days, in addition to a significant inhibition of the tumor growth. Adjuvant effects of prostaglandin D2 on cisplatin in relation to tumor growth were also studied. Combinations of 0.2 or 0.4 microgram cisplatin per ml and 0.05 or 0.1 microgram prostaglandin D2 per ml, which did not affect the HR cell proliferation alone, resulted in a significant inhibition of cell proliferation. In addition, the tumor take of HR cells by nude mice in groups treated with a combination of cisplatin and prostaglandin D2 was inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapeutic values of prostaglandin D2 in nude mice bearing human ovarian carcinoma]. 231 42

The cell line HTOA was established from a well-differentiated human ovarian serous cystadenocarcinoma. This line grew well and without interruption for 51 months and was subcultivated over 130 times. The cells were epithelial in shape, and neoplastic and pleomorphic features, a jigsaw puzzle-like arrangement, desmosomal junctional complexes, and multilayering without contact inhibition. The chromosome number was stable at a hypertetraploid range. The culture cells transplanted into BALB/c nude mice and or hamster cheek pouch produced serous cystadenocarcinomas. The cells were found to produce an antigen (CA125) of ovarian cancer, both in vitro and in vivo. The CA125 levels correlated with cellular proliferation in vitro and also with tumor growth, in the nude mouse. These results indicate that the amount of CA125 in the serum is a good marker for detecting early stages of ovarian cancer and in particular for the evaluation of anticancer drugs.
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PMID:Characterization of newly established human ovarian carcinoma cell line--special reference of the effects of cis-platinum on cellular proliferation and release of CA125. 243 20

Direct inhibitory effects of neuroendocrine hormones on human ovarian cancer cell proliferation in vitro were examined. Except for melatonin, all neuroendocrine hormones used in this study inhibited proliferation of KF cells derived from human serous cystadenocarcinoma of the ovary in a dose-dependent manner. The degree of inhibition of prostaglandin D2 was most marked being comparable to that of 5-fluorouracil and followed by beta-endorphin, alpha-endorphin, and Met-enkephalin. More than 200 microM melatonin stimulated the cell proliferation. The inhibitory effects by endorphins were partially reversible by 20 microM naloxone. From analyses of uptakes of radiolabeled precursors by the KF cell, endorphins were considered to inhibit protein and RNA syntheses but not DNA synthesis. These results suggest that neuroendocrine hormones may play an important role in regulation of tumor growth.
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PMID:Inhibition of human ovarian cancer cell proliferation in vitro by neuroendocrine hormones. 252 Dec 12

The effects of prostaglandin D2 (PGD2) on human ovarian tumor growth were examined in vitro and in vivo by using a cell line, designated HR, derived from patients with serous cystadenocarcinoma of the ovary. The cell proliferation was dose-dependently inhibited by PGD2 between concentrations of 0.1 and 4.0 micrograms/ml after 24 hrs, 48 hrs and 72 hrs of contact time. Concentrations of PGD2 required for 50% inhibition of the cell proliferation were 2.0, 1.1 and 0.55 micrograms/ml with 24, 48 and 72 hrs of contact time, respectively. From the results of 51Cr-release assay, the inhibition of cell proliferation by PGD2 was considered to result from the direct cytotoxic effects. The incorporations of 3H-thymidine, 3H-uridine and 3H-valine were inhibited in a dose-dependent fashion with more than 1.0 micrograms/ml of PGD2. Tumor growth in nude mice treated with 0.3 mg/mouse PGD2 was significantly inhibited, compared to that of untreated nude mice. In untreated nude mice the tumor growth curve was parallel to the changes in the plasma alpha-hydroxybutyrate dehydrogenase (HBD). In both PGD2-treated groups with 0.1 mg/mouse and 0.3 mg/mouse, the HBD activity markedly decreased on the 14th and the 21st day after inoculation. The 50% survival time in untreated mouse, 0.1 mg/mouse and 0.3 mg/mouse PGD2-treated groups was 52 days, 55 days and 67 days, each respectively.
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PMID:[Inhibition of human ovarian cancer cell growth by prostaglandin D2]. 302 47

The patient was a 57-year-old woman with ovarian serous cystadenocarcinoma in FIGO clinical stage IV. Cancer antigen 125 (CA125), tissue polypeptide antigen (TPA) and carcinoembryonic antigen (CEA) were immunohistochemically demonstrated in tumor cells, and the variations of serum CA125 and TPA levels reflected the clinical course. The tumor tissue obtained at exploratory laparotomy was minced with scissors, and transplanted subcutaneously into female nude mice for in vivo maintenance. The tumor cells from 5th generation nude mice were dispersed in Eagle's minimal essential medium supplemented with 10% fetal calf serum, and incubated in Falcon tissue culture dishes at 37 degrees C in 5% CO2 in air for in vitro maintenance. The results were as follows: Histopathologically the tumor transplanted into nude mice showed a cystadenocarcinoma, which closely resembled the original human tumor. Immunohistochemically CA125, TPA and CEA were demonstrated in the tumor transplanted into nude mice as well as in the original human tumor. From the growth curve in nude mice, the doubling time was estimated to be about 3.5 days. Serum TPA levels in nude mice were increased in proportion to the tumor growth after transplantation, but serum levels CA125 and CEA were normal. The concentrations of CA125 and TPA were increased in the conditioned media compared with the control media, although the elevated values were decreased with subsequent passages. CEA concentrations in the conditioned media were unchanged.
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PMID:Experiments with tissue cultures from a human ovarian serous cystadenocarcinoma producing cancer antigen 125 (CA125), tissue polypeptide antigen (TPA) and carcinoembryonic antigen (CEA). 316 55

In vitro and in vivo effects of prostaglandin D2 on human ovarian tumor growth were examined by using a cell line, designated HR, derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HR cell proliferation in vitro was dose dependently inhibited between concentrations of 0.1 and 4.0 micrograms of prostaglandin D2 per ml. From results of 51Cr release assays and trypan blue dye exclusion tests the inhibitory effect seemed to result from a direct cytotoxic effect by prostaglandin D2. All DNA, RNA, and protein syntheses by the HR cells were also inhibited in a dose-dependent manner with exposure time of 48 h to prostaglandin D2. When 5 X 10(5) HR cells were inoculated to nude mice, the 50% survival time of them in untreated groups was 52 days after inoculation. Although 4 mg of prostaglandin D2 per kg caused inhibition of the tumor growth, a significant prolongation of the survival time was not observed. On the other hand, the 50% survival time of nude mice treated with 12 mg of prostaglandin D2 per kg was significantly (P less than 0.05) prolonged to 67 days, in addition to a significant inhibition of the tumor growth.
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PMID:Inhibition of human ovarian cancer cell growth in vitro and in nude mice by prostaglandin D2. 345 25

Copy number alteration (CNA) represents an important class of genetic variations that may contribute to tumorigenesis, tumor growth and metastatic spread. CNA can directly affect the expression of genes within the CNA regions; however, genes within the CNA regions exhibit heterogeneity in gene dosage sensitivity. In this study, a computational framework was built to identify 1170 dosage-sensitive genes (DSGs) and 1215 dosage-resistant genes (DRGs) that were related to ovarian serous cystadenocarcinoma (OV) through the association between CNA and gene expression. To analyze the different functions of the genes within the two groups, the functional annotation results indicated that DRGs were involved in cancer-related processes like immune response, cell death and apoptosis, while DSGs were enriched in essential processes like the cell cycle and the DNA metabolic process. Meanwhile, two three-dimensional regulatory networks for differentially expressed miRNAs, differentially expressed transcription factors (TFs) and DSGs or DRGs were constructed based on feed-forward loops. We identified key regulators (such as miR-16-5p, miR-98-5p, MYB and HOXA5) and cancer prognosis-related network motifs (such as miR-98-5p-HOXA5-TP53 and miR-16-5p-MYB-IGF1R) after the analysis of network topological features. Our results lead us to speculate that these genes and associated regulators may be potential mechanistic biomarkers for tumorigenesis and progression of cancer. Research on the network characteristics and the role of feed-forward loops in OV tumorigenesis and development could lead to feasible suggestions for the prevention and early diagnosis of OV, which will shed light on understanding the functional mechanism of CNA in cancer.
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PMID:The functional consequences and prognostic value of dosage sensitivity in ovarian cancer. 2806 83


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