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Overexpression of SPF45 confers a multidrug-resistant phenotype to A2780 ovarian carcinoma cells. We showed previously that transfection of SPF45 was sufficient to confer vincristine and doxorubicin resistance to HeLa cells 6 ; . To further explore the role of SPF45 as a drug resistance gene, we transfected a different cell line, A2780 ovarian carcinoma cells, with SPF45 expression constructs. Ninety-three clones were screened by Northern hybridizations to a SPF45 cDNA probe to identify transcripts derived from the transfected construct as well as the lower molecular weight transcripts of the endogenous gene. SPF45 transcripts derived from the expression construct were detected in approximately two-thirds of the clones but often at lower levels than endogenous SPF45 transcripts data not shown ; . Twenty-two independent clones with elevated SPF45 expression levels were screened for drug resistance to doxorubicin and etoposide in cytotoxicity assays done once, and 20 of these were resistant to both drugs data not shown ; . Four of these clones were analyzed in additional cytotoxicity assays and found to be 14- to 18-fold resistant to mitoxantrone, 3- to 5-fold resistant to doxorubicin, 3- to 12-fold resistant to etoposide, and 3- to 5-fold resistant to cisplatinum. Resistance values for individual clones are given in a footnote to Table 1. One of these, clone 51, with stable overexpression of SPF45 at high levels A2780-SPF45 ; was selected for further study. A2780-SPF45 cells and a stable transfectant of the empty vector A2780-Vector ; had similar doubling times of 21 and 23 hours, respectively. A2780-SPF45 cells had increased expression of SPF45 relative to A2780-Vector cells when analyzed by Western using a SPF45 polyclonal antibody and a h-actin antibody to control for protein loading Fig. 1A ; . In cytotoxicity assays, A2780-SPF45 cells were 2.8- to 20.9-fold resistant relative to A2780-Vector cells to several drugs with different mechanisms of action. A representative survival curve for vincristine is shown in Fig. 1B. EC50 and fold resistance values for seven anticancer drugs paclitaxel, carboplatin, vinorelbine, doxorubicin, etoposide, mitoxantrone, and vincristine ; are shown in Table 1. A2780-SPF45 cells were resistant to six drugs P 0.05 ; but were not resistant to paclitaxel Table 1 ; . Results from a single experiment also found that A2780-SPF45 cells were not resistant to 5-FU but were f5-fold resistant to cisplatinum. Sensitivity to gemcitabine and pemetrexed was also determined. As shown in Fig. 1C and D, the dose-response survival curves for gemcitabine and pemetrexed were only significantly different in the two transfectants at the highest drug concentrations where cell survival plateaued. Survival was significantly different at z0.02 Amol L for gemcitabine and z0.12 Amol L for pemetrexed P 0.05 ; . Taken together, these data indicate that overexpression of SPF45 in A2780 cells confers MDR. Ribozyme knockdown of SPF45 sensitizes A2780 cells to etoposide. To further explore the relationship between SPF45 levels in A2780 cells with sensitivity to anticancer drugs, we.

Forty-five patients with resectable, advanced squamous cell carcinoma of the head and neck, who were previously untreated, received paclitaxel 250 mg m 2 administered over three courses of 24-hour intravenous infusion every 21 days. Quicksilver Foamy Bells Zone 4-9. Mature Size: 18"h. Silver foliage with bronze veining turning to silver green in summer and red brown in the fall. Pink buds open to light pink and white flowers appear in June and papaverine.

1. Ginsberg RJ, Vokes EE, Rosenzweig K. Cancer of the lung. In: DeVita VT Jr, Hellman S, Rosenberg SA, editors. Cancer: Principles and Practice of Oncology, 6th ed. Philadelphia: Lippincott-Raven 2001; 9257. 2. Sch CI, Sch KE, Park SH, Chang HJ, Ko JW, Ahn DH. Annual report of the central cancer registry in Korea-1998 based on registered data from 124 hospitals ; . J Korean Cancer Assoc 2000; 32: 82734. Lilenbaum RC, Green MR. Novel chemotherapeutic agents in the treatment of non-small-cell lung cancer. J Clin Oncol 1993; 11: 1391402. Shepherd FA, Dancey J, Ramlau R, Mattson K, Gralla R, O'Rourke M, et al. Prospective randomized trial of docetaxel versus best supportive care in patients with non-small-cell lung cancer previously treated with platinumbased chemotherapy. J Clin Oncol 2000; 18: 2095103. Kosmas C, Tsavaris N, Vadiaka M, Stavroyianni N, Koutras A, Malamos, et al. Gemcitabine and docetaxel as second-line chemotherapy for patients with nonsmall cell lung carcinoma who fail prior paclitaxel plus platinumbased regimens. Cancer 2001; 92: 290210. Crino L, Mosconi MA, Scagliotti G, Selvaggi G, Novello S, Rinaldi M, et al. Gemcitabine as second-line treatment for advanced non-small-cell lung cancer: a phase II trial. J Clin Oncol 1999; 17: 20815. Rossi A, Perrone F, Barletta E, Tambaro R, Barzelloni ML, Scognamiglio F, et al. Activity of gemcitabine in cisplatin-pretreated patients with advanced non-small cell lung cancer: a phase II trial. Proc Soc Clin Oncol 1999; 18: 484a abstract 1868 ; . 8. Reddy GR, Gandara DR, Edelman MJ, Doroshow JH, Lau D, Lenz H, et al. Gemcitabine in platinum treated non-small cell lung cancer. Proc Soc Clin Oncol 1999; 18: 521a abstract 2007 ; . 9. Sculier JP, Lafitte JJ, Berghmans T, Thiriaux J, Lecomte J, Efremidis A, et al. A phase II trial testing gemcitabine as second-line chemotherapy for non small cell lung cancer. Lung Cancer 2000; 29: 6773. Fossella FV, DeVore R, Kerr RN, Crawford J, Natale RR, Dunphy F, et al. Randomized phase II trial of docetaxel versus vinorelbine or ifosfamide in patients with advanced non-small-cell lung cancer previously treated with platinum-containing chemotherapy regimens. J Clin Oncol 2000; 18: 235462. Pronzato P, Landucci M, Vaira R, Vigani A, Bertelli G. Failure of vinorelbine to produce responses in pretreated non-small cell lung cancer patients. Anticancer Res 1994; 14: 14136.

In other centers, paclitaxel and vinorelbine are being evaluated in sequential schedules of administration.
Confirm all of the inflammatory alterations that originate from stent implantation and their persistent disastrous consequences. Taking all these facts together, it has to be accepted that the clinical benefits from drug-eluting stents with regard to target vessel restenosis and target vessel revascularization have been overestimated and that they do not offer safety, efficacy and effectiveness. CONCLUSION In the present study, paclitaxel or rapamycin-eluting stent did not show any statistically significant difference with regard to avoiding the need for coronary-artery bypass grafting, or in relation to myocardial infarction or death from cardiac causes, in comparison with bare-metal stent and paromomycin.
Induced by carcinogens can give insight into their mechanism of action. In this study microarrays of 22K human genomewide cDNAs were used to identify gene expression alterations in MCF-7 and HepG2 cells following exposure to the carcinogen benzo a ; pyrene BaP ; and were related to DNA adducts measured by 32P-postlabelling. To further dissect the BaP expression response, cells were exposed to its ultimate carcinogenic metabolite, benzo a ; pyrene-diol-epoxide BPDE ; , to identify genes modulated in response to the DNA adducts and to 2, 3, 7, TCDD ; to identify genes modulated in response to activation of the aryl hydrocarbon receptor AhR ; . After exposure to BaP 05 mM ; for up to 48 h, 171 and 111 transcripts were modulated in the MCF-7 and HepG2 cells, respectively. Twenty-nine gene alterations were common to both cell lines. BPDE exposure resulted in 1081 and 95 modulated transcripts in the MCF-7 and HepG2 cells, respectively. Sixty-seven genes were found common between BaP and BPDE in the MCF-7 cells and 28 in the HepG2 cells. These included genes involved in cell cycle regulation, chromatin remodelling, apoptosis anti-apoptosis and DNA repair. Exposure to TCDD revealed 28 and 134 transcripts modulated in the MCF-7 and HepG2 cells, respectively. Both BaP and TCDD modulated 21 genes in the MCF-7 cells and 27 in the HepG2 cells. These genes included a number involved in xenobiotic metabolism. An overlap in the BPDE and TCDD gene expression patterns was also observed in the MCF-7 19 genes ; and HepG2 cells 14 genes ; highlighting the complex response of the cells to such compounds. These results demonstrate the capabilities of microarray technology to identify gene expression changes induced by carcinogens and to further elucidate the roles of gene-environment interactions that may be important in the process of carcinogenesis. 47. Aneuploid Events Detected by Non-Disjunction in Human Peripheral Blood Lymphocytes In Vitro Ann T.Doherty, Julie Hayes, Sean Evans and Mike O.Donovan AstraZeneca, Safety Assessment UK, Alderley Park, Macclesfield. SK11 7AH. UK Aneuploidy is the loss or gain of whole chromosomes from the normal diploid chromosome complement. Chemically induced aneuploidy may result from interaction with any part of the cell division apparatus, such as the mitotic spindle, the centrosomes, the centromere and it associated proteins, etc. Non-disjunction results from the failure of chromosomes on the mitotic spindle to segregate and results in daughter cells containing aneuploid chromosome complements. Compound X is a kinase in development at AstraZenca and was assessed for its ability to cause non-disjunction by examining chromosome malsegregation by labelling two pairs of human centromeres chromosomes 7 1 8 binucleate lymphocytes 1 ; . The presence of micronuclei in binucleate cells was also recorded. In addition mitotic index MI ; and polyploidy P ; were assessed in parallel cultures blocked with colcemid. In binucleate cells, increases in non-disjunction were observed at concentrations of Compound 3 from 0.0025 P 0.05 ; to 0.015 mmol L P 0.001 ; and increases in micronuclei in binucleate cells were seen at concentrations from 0.005 to 0.015 mmol L. Increases in aberrant cell divisions trinucleate and multinucleate ; were observed from 0.0025 to 290.

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