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Cell line ovarian adenocarcinoma

Langdon, S. P, Hawkes,M. M., Hay,F. G.,Lawrie, S. S., Schol, D. J., Hilgers, J.,Leonard, R. C. F., Smyth, J. F. (1988). Effect of sodium-hutyrate and other differentiation inducers on poorly differentiated human ovarian adenocarcinoma cell-lines. Cancer Res. 48(21), 6161— 6165. [Pg.240]

In another study involving patients with metastatic breast, colorectal and ovarian cancer, increased anti-sTn titers were correlated with better survival. Even if before treatment, elevated titers of antibodies against the mucin MUC1, were correlated with a poor response to immunotherapy, CTL precursors to the MUC1 were detected in carcinoma patients [208], A vaccine using 10 pg/ml MUC1-KLH mixed with Detox was injected s.c. in breast cancer patients treated with cyclophosphamide. A weak antibody response, and an ex vivo CTL response against HLA-matched adenocarcinoma cell lines were seen. No correlation with the clinical outcome was available [209],... [Pg.544]

Some biflavonoids exhibited cytotoxic/anticancer activity.[34-38] For example, ginkgetin (7) was cytotoxic to hirnian ovarian adenocarcinoma (OVCAR)-3 cells, but not to other cells such as Hep G2 and HeLa.[39] Taiwanhomoflavone-A (8) showed cytotoxicity against several cancer cell lines. [40] Apoptotic cell death by caspase activation was involved in the cytotoxic effects of ginkgetin. [41] In other studies, several hinokiflavone (235)-type biflavonoids such as cryptomerin B (239) and isocryptomerin (237) exhibited potent cytotoxic effects, probably by apoptotic death at low pM concentrations. [3] In contrast, some biflavones such as ginkgetin (7) and sciadopitysin (15) enhanced proliferation of normal hmnan skin fibroblasts and increased collagen production. [42]... [Pg.173]

As described above, Mn-SOD is highly expressed in epithelial-type ovarian cancer (14) and is one of the best marker proteins for this cancer. For this reason, we investigated the effect of TNF on the induction of the Mn-SOD level prior to the effect of TNF on the induction of Mn-SOD in a cell line, Kuramochi, derived from adenocarcinoma of the ovary. In the case of Kuramochi cells, the Mn-SOD level prior to treatment with TNF was 110 ng/mg protein. Addition of TNF to achieve concentrations of 10-6, 10 5, and 10 4 mg/ml resulted in dose-dependent increases in Mn-SOD levels to 180,270, and 360 ng/mg protein, respectively (Fig. 26). On the other hand, even at 10-4 mg/ml, TNF did not induce Cu,Zn-SOD protein in the Kuramochi cells. [Pg.42]

The possible modes of action of 4HPR have been mostly investigated in already transformed tumor cells. 4HPR suppressed the proliferation of cell lines of different tumor types such as human breast carcinoma [24-27], prostate adenocarcinoma [28, 29], leukemias [30, 31], neuroblastoma [32, 33, 34], ovarian carcinoma [35, 36], cervical carcinoma [37, 38], head and neck squamous cell carcinoma [39], esophageal squamous carcinoma [40] and small-cell lung can-... [Pg.242]


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