Human ovarian carcinoma cell lines

The toxicity of the four purified cytochalasins (61—64) was measured against human tumor cell lines 2780S (ovarian carcinoma), SW-620... 

Loh S Y, Mistry P, Kelland LR, Abel G, Harrap KR. Reduced drug accumulation as a major mechanism of acquired resistance to cisplatin in a human ovarian carcinoma cell line circumvention studies using novel platinum (II) and (IV) ammine/amine complexes. BrJ Cancer 1992 66 1109-1115. 

Kelland LR, Mistry P, Abel G, et al. Mechanism-related circumvention of acquired cis-diammine-dichloroplatinum(II) resistance using two pairs of human ovarian carcinoma cell lines by ammine/ amine platinum(IV) dicarboxylates. Cancer Res 1992 52 3857-3864. 

The implementation of animal test protocols in the 1980s has been accompanied by the development of a host of alternative methods to study adverse effects of chemicals on reproductive and developmental parameters. For example, rat whole embryo culture stems from the seventies (16), as does the rat limb bud organ culture (17) and rat limb bud and brain micromass was developed in the eighties (18). An elegant nonvertebrate alternative model used regeneration of polyps of Hydra atUnuata from dissociated cells (19). Animal-free in vitro alternatives include those employing the proliferation of a human embryonic palatal mesenchymal cell line (20), the attachment of a mouse ovarian tumor cell line (21), and the differentiation of a neuroblastoma cell line (22) and a embryonal carcinoma cell line (23). Various overviews of methods have been published over the years (24). The predictability of... 

Cytotoxicity. JM216 was evaluated in vitro using the sulforhodamine B (SRB) assay against a panel of human ovarian carcinoma cell lines, established to be representative of the range of clinical responsiveness to platinum-based chemotherapy observed in patients presenting with advanced ovarian cancer (see below) [30]. JM216 showed a similar in vitro potency to that of cisplatin itself mean /C50 values across the ovarian cell line pan-... 

Fig. 3. Cross-resistance profiles for the 41M/41McisR, CH 1/CH1 c sR and A2 780/A2780cisR pairs of human ovarian-carcinoma cell lines for cisplatin itself carboplatin, tetraplatin (1,2-diaminocyclohexane)tetrachloroplatinum(IV)), JM216, JM118 (the major metabolite of JM216) andAMD473. Resistance Factor = IC50 resistant/parent cell line. Drug exposure was for 96 h, sulforhodamine B growth-inhibition assay, bars = SEM, n = 3-4.

V anhoefer U, Harstrick A, Wilke H, Schleucher N, WaUes H, Schroder J, Seeber S. Schedule-dependent antagonism of paclitaxel and cisplatin in human gastric and ovarian carcinoma cell lines in vitro. Eur J Cancer 1995 31 A(l) 92-7. 

Ormerod, M. G., O Neill, C. F Robertson, D and Harrap, K. (1994) Cisplatin induced apoptosis in a human ovarian carcinoma cell line without concomitant intemucleosomal degradation of DNA. Exp. Cell Res. 211, 231-237. 

The human ovarian carcinoma cell line NIH OVCAR-3 originates from ATCC (Manassas, USA). OVCAR-3 cells are passaged when confluency is reached to provide new maintenance cultures in 75 cm culture flasks. For maintenance, in general, 1 10 part of the last passage is transferred into a new flask. This procedure is done twice a week. 

Kellard LR, Abel G. Comparative in vitro cytotoxicity of Taxol and Tax-otere against cisplatin-sensitive and resistant human ovarian carcinoma cell lines. Cancer Chemother Pharmacol 1992 30 444-450. 

Indirect evidence for DNA repair as a determinant in acquired resistance was obtained with the discovery that a mouse leukemia cell line 50-fold resistant to cis-DDP had a fourfold increase in the level of DNA polymerase p, an enzyme involved in DNA repair (73). This hypothesis was supported by a study in which a human ovarian carcinoma cell line 20-fold resistant to cis-DDP showed two to three times more repair synthesis than the parental cell line after a 1-h exposure to the drug (74). Also, studies in L1210 cells found that, although d(GpG), d(ApG), and d(ApNpG) crosslinks formed by [ H][Pt(en)Cl2] were all repaired, resistant cells repaired fourfold more adducts during an initial 6-h phase of repair (39). 

Comparisons of reactions of cis- versus fran -DDP with sulfur donors and other cellular components may afford some insight into their relative biological effects, however. /rans-DDP is much more reactive than the cis isomer with GSH (6, 27). Depletion of GSH with use of the inhibitor BSO had no effect on the cisplatin sensitivity of two human ovarian carcinoma cell lines, but made them 2.7 times more sensitive to trans-DY) (4). In a related finding, it was necessary to add 14 times more trans- than ds-DDP to cells in culture to achieve the same percent inhibition of in vivo SV40 DNA replication (23). These results suggest that part of the differential activity of these isomers in biological systems may arise from the differential reactivity of fran -DDP toward cellular components other than DNA. Thus trani-DDP could be more effectively inactivated prior to encountering DNA, or be better blocked as monofunctional platinum-DNA cross-links. 

Minko, T., Kopeckova, P., Pozharov, V. and Kopecek, J. (1998) HPMA copolymer bound adriamycin overcomes MDRl gene encoded resistance in human ovarian carcinoma cell line. J. Controlled Rel. 54 223-233. 

PTX-2 was toxic to KB (human epidermoid carcinoma) cells in vitro at a concentration of 58 nM [14]. In contrast, no evidence of a toxic effect in these cells was seen with PTX-2 seco acid or l-epi-VTX-2 seco acid at a concentration of 2 pM [14]. PTX-2 has been screened for selective cytotoxic activity against 60 human tumour cell lines by the US National Cancer Institute. It was selectively toxic to several cell lines of ovarian, renal, pulmonary, colonic, cerebral, and mammary tumors at nanomolar concentrations, but was ineffective against leukemia or prostate cancer cell lines [37]. PTX-2 was toxic to Vero (monkey renal epithelial) cells at a concentration of 0.58 pM... 

Minko T, Kopeckova P, Kopecek J. Chronic exposure to HPMA copolymer-bound adriamycin does not induce multidrug resistance in a human ovarian carcinoma cell line. J Cont Rel 1999 59 133-148. 

Kunath K, Kopeckova P, Minko T, Kopecek J. HPMA copolymer-anticancer drug-OV-TL16 antibody conjugates. 3. The effect of free and polymer-bound adriamycin on the expression of some genes in the OVCAR-3 human ovarian carcinoma cell line. Eur J Pharm Biopharm 2000 49 11-15. 

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