The cell lines did not harbor the most commonly reported KRAS or

The cell lines did not harbor the most commonly reported KRAS or BRAF mutations nor the most common BRCA1 and BRCA2 mutations identified in the French Canadian breast and ovarian cancer families. Imatinib Mesylate Cell growth rate and oncogenic assays The growth rates of the cell lines was determined and compared with TOV112D and TOV1946, cell lines previously developed by our labora tory derived from endometrioid and serous EOC re spectively. The proliferation of the cell lines is depicted in Figure 5. There was no difference in the doubling time for the three cell lines derived from 2295. Inhibitors,Modulators,Libraries OV1369 Inhibitors,Modulators,Libraries had a greater proliferation rate than TOV1369. OV3133 had a slower growth rate than the other 3133 cell lines. Similarly, the growth rates, as measured by doubling time, of all nine cell lines was slower than the pre chemotherapy highly aggressive cell line TOV112D.

Doubling times ran ged from 2. 5 to 3. 2 days, compared to 1. 5 for TOV112D. There was no consistent difference in doubling between cell lines Inhibitors,Modulators,Libraries derived pre versus post chemotherapy among the three patients. Saturation densities were typically lower than what we could observed for TOV112D, being between 25% to 50% of the value obtained for TOV112D, and more in line with the previously densities described for other serous ovarian cancer cell lines, such as TOV1946 and TOV2223. The cell lines ability to form spheroids was measured using the hanging droplet method as previously described. Although there was some variation among the repli cates, none of cell lines consistently formed compact spheroids, as was clearly observed with TOV112D.

Four Xenograft tumor formation cell lines, OV2295, OV2295 TOV3133G, TOV3133D, could form semi compact spheroids, while OV1369, TOV2295, OV3133, and TOV1946 formed numer ous individual small aggregates and TOV1369 and OV3133 would not form spheroids. The migration potential of the cell lines was measured using an established scratch migration assay. There were no notable differences Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries in migration rates between the cell lines. All cell lines migrated slowly and did not fill the gap within 48 hours, which is slower than what was observed with TOV1946. Using the soft agarose assay, the anchorage depend ency of the cells lines was investigated. After three weeks second there were visible colonies formed with the OV1369, OV2295, TOV2295, TOV3133D and OV3133 cell lines. The in vivo growth potential of the cell lines was deter mined by subcutaneous injection of cells into SCID mice. TOV1946 and TOV112D. Only OV3133 formed tumors in SCID mice, whereas all other cell lines failed to induce any tumor formation. The tumorigenic cell lines, TOV112D and TOV1946, both formed tumors in all mice.

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