PMID stringlengths 10 13 | sentence stringlengths 1 1.35k | embedding sequencelengths 384 384 |
|---|---|---|
PMID:9041188 | Nine human ovarian cancer cell lines that express wild-type (wt) or mutated p53 were used to evaluate the cytotoxicity induced by paclitaxel. | [
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PMID:9041188 | The IC50 calculated in the five mutated p53-expressing cell lines was not different from the four wt p53-expressing cell lines. | [
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PMID:9041188 | The introduction of wt p53, by using a temperature-sensitive mutant murine p53 or the human p53 under the control of a tetracycline-dependent promoter, did not change the cytotoxicity of paclitaxel as compared to mock-transfected cells. | [
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PMID:9041188 | By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected. | [
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PMID:9041188 | This increase in p53 levels led to an increase in the mRNA and protein levels of p53 downstream genes (WAF1, GADD45, and bax). | [
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PMID:9041188 | In none of the cell lines examined was paclitaxel able to induce apoptosis, evaluated by terminal deoxynucleotidyl transferase-mediated nick end labeling staining and filter binding assay at concentrations closed to the IC50. | [
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PMID:9041188 | By increasing the concentration of paclitaxel in the filter binding assay, we could see fragmentation of DNA in the different cell lines. | [
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PMID:9041188 | We conclude that the presence of p53 is not a determinant for the cytotoxicity induced by paclitaxel in human ovarian cancer cell lines. | [
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PMID:9041188 | Differences in the activation of p53 downstream genes could be observed in wt versus mutated p53-expressing cells, but this does not account either for a differential induction of apoptosis or for a change in cytotoxicity induced by paclitaxel. | [
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PMID:14991574 | Sulfamoylation of 2-methoxyestrone (2-MeOE1) was shown previously to enhance its potency as an anti-proliferative agent against breast cancer cells. | [
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PMID:14991574 | We have examined the ability of a series of 2-methoxyestradiol (2-MeOE2) and 2-ethylestradiol (2-EtE2) sulfamates to inhibit angiogenesis in vitro. | [
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PMID:14991574 | 2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate were potent inhibitors of human umbilical vein endothelial cell (HUVEC) proliferation with IC(50) values of 0.05 microM and 0.01 microM, respectively. | [
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PMID:14991574 | A novel co-culture system, in which endothelial cells were cultured in a matrix of human dermal fibroblasts, was also used to assess the anti-angiogenic potential of these drugs. | [
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PMID:14991574 | In this system endothelial cells proliferate and migrate through the culture matrix to form tubule structures. | [
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PMID:14991574 | Whereas 2-MeOE2 (1.0 microM) caused a small reduction in tubule formation, both 2-MeOE2 bis-sulfamate (0.1 microM) and 2-EtE2 sulfamate (0.1 microM) almost completely abolished tubule formation. | [
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PMID:14991574 | 2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate both induced BCL-2 phosphorylation, p53 protein expression and apoptosis in HUVECs. | [
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PMID:14991574 | Microarray analysis of a limited number of genes known to be involved in the angiogenic process did not show any gross changes in cells treated with the 2-substituted estrogens. | [
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PMID:14991574 | The sulfamoylated derivatives of 2-MeOE2 and 2-EtE2 are potent inhibitors of in vitro angiogenesis and both compounds should have therapeutic potential. | [
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PMID:15990222 | Treatment failures result from resistance to chemotherapy in ovarian cancer. | [
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PMID:15990222 | The effect of cisplatin and paclitaxel treatments on chemosensitivity was studied in ovarian cancer cells developed from a patient with stage IIIC disease. | [
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PMID:15990222 | Cells (UL-3A, UL-3B) that recovered from cisplatin (Cis) and paclitaxel (Tax) treatments showed higher levels of p53, mdr-1 and chemoresistance than untreated controls. | [
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PMID:15990222 | EC50 values of Cis and Tax for UL-3A clones were 7.2-34.6, average 20.9 microg/ml, while UL-3B clones ranged from 11.8-252.0 microg/ml, with a mean value of 73.2 microg/ml for Cis, and 260.0-4400.0 nM (mean 2555.0 nM) for Tax. | [
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PMID:15990222 | Selection pressures during treatment may contribute to drug resistance. | [
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PMID:9231689 | Tumors are thought to differ in their response to cytotoxic agents for a variety of reasons including cell cycle kinetics, degree of hypoxia, differential repair, and ability to survive when stressed. | [
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