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How will the study be rolled-out? The study has been launched in September 2004 in 70 centers and 14 countries, including the United States, Canada and the following European countries: Austria, Belgium, France, Finland, Germany, Greece, Italy, Spain, Sweden, Turkey, Switzerland, United Kingdom. Approximately 740 patients diagnosed with idiopathic Parkinson's disease PD ; and requiring the initiation of levodopa therapy will be randomized into the study. Patient recruitment has started in September 2004. Patients will be randomized to be either treated with the new and optimized levodopa medication or with a traditional formulation of levodopa carbidopa. Treatment will continue until all patients in the study have been treated for 2 years. The study will employ a blinded rater system to evaluate the onset of dyskinesias. Raters will be trained using a video specifically produced for this purpose to ensure consistent evaluations across the study. First study results are expected in 2007.
Our study provides the first description of the influence of population factors on TMZ pharmacokinetics in the plasma and the CSF. We demonstrate that TMZ oral clearance is only slightly influenced by BSA and gender and is associated with a remarkably small inter-patient variability 4.7% ; . The volume of distribution is influenced by BSA only. These results are in good agreement with Jen et al. 43 ; reporting an oral clearance of 11.2 liter h with a 15% inter-patient variability and a similar influence of BSA and gender. In our study, neither individual determinants such as genetic background or organ failure nor comedications commonly used in gliomas patients anticonvulsants, antiemetics, corticosteroids, antacids, and cytoprotective agent ; altered TMZ oral clearance. The AUC values estimated in our analysis revealed that CSF values corresponding to 20% 5% of those observed in plasma. These results are comparable to the limited information reported in preclinical studies with TMZ and the camptothecins, irinotecan and topotecan. The AUCCSF AUCplasma ratio observed in nonhuman primate models were 33% 6% for TMZ, 14% 3% for irinotecan, and 32% 3% for topotecan 17, 44, 45 ; . Irinotecan and other camptothecins are currently in clinical trials as new treatments for malignant gliomas 46 ; . This AUCCSF AUCplasma ratio of 20% 5% is somewhat lower than the average CSF plasma concentration ratio mean, 29.4% 15%; increasing up to 40% until 4 h after TMZ intake ; reported previously on the same study population 29 ; . This difference is constructed as AUCCSF AUCplasma ratio integrates the entire dosing interval. The ratio of the AUCs estimates more accurately the penetration into the central nervous system than only a CSF plasma ratio obtained with plasma and CSF concentrations 30 ; . A penetration of at least 20% of the AUCplasma into the CSF may be used as a benchmark for comparison with other agents with a presumed activity in the CSF. The lack of a significant relationship between AUCplasma or AUCCSF beyond the cumulative dose and efficacy outcomes is likely to be explained by the very low inter-patient variability in TMZ pharmacokinetics, thus minimizing the predictive value added by AUC over the cumulative dose alone. Similarly, AUCplasma was not a predictor of decrease of platelets or neutrophils. Detection of decrease in blood counts is obscured by the large normal fluctuation of leukocyte and platelet counts. Furthermore, severe hematological toxicity with the treatment of TMZ is rare and observed in 10% of patients only. Decrease in blood counts is also dependent on O6-methylguanine-DNA methyltransferase MGMT ; expression in hematopoietic stem cells 47 ; . This ubiquitous DNA repair enzyme, which removes methylating and chloroethylating lesions at the O6 position of guanine, is to a large extent variably expressed in peripheral blood mononuclear cells 48 ; and thus seems to be a stronger predictor for toxicity than systemic drug exposure. It must be recognized that TMZ by itself is not the biologically active agent, but merely a prodrug which undergoes a spontaneous hydrolysis to generate the methylating agent MTIC. The determination of this compound in plasma and CSF could have a better chance to predict efficacy or safety outcomes and will be assessed in an additional investigation. Moreover, the biotransformation of TMZ may have a significant variability between organ, tissue, or cell compartments. This possibly lim.

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Bertrand, F. 1987. The main steps in manufacture. In: Eck, A. ed. ; . Cheesemaking: Science and Technology. Paris: Lavoisier Publishing. Pp. 413 421. Bjarnason, J. B. & sgeirsson, B. 1993. Psychrophilic proteolytic enzymes from Atlantic Cod: their characteristics and applications. Gen. Eng. Biotechnol., Vol. 13, pp. 3139. Bjarnason, J. B., Kristjnsson, M. M., lafsdttir, S., Benediktsson, B., Gudmundsdttir, E. & Gudmundsdttir, A. 1997. Characteristics and application of cryotin, a mixture of psychrotrophic marine proteinases. In: Hopsu-Havu, V. K. ed. ; . Proteolysis in cell function. IOS Press. Pp. 104111. Blakistone, B., Chuyate, R., Kautter, D., Charbonneau, J. & Suit, K. 1999. Efficacy of Oxonia active against selected spore-formers. J. Food Prot., Vol. 63, pp. 262267. Block, S. 1991. Disinfection, sterilization and preservation, 4 ed. Philadelphia: Lea & Febiger. Bloomfield, S. F. 1988. Cosmetics and pharmaceuticals: Biodeterioration and disinfectants. In: Houghton, D. R., Smith, R. N. & Eggins, H. O. W. eds. ; . Biodeterioration 7. Essex: Elsevier Publishers Ltd. Pp. 135145. Bloomfield, S. F. 1992. Resistance of bacterial spores to chemical agents. In: Russel, A. D., Hugo, W. B. & Ayliffe, G. A. J. eds. ; . Principles and practices of disinfection, preservation and sterilization. Oxford: Blackwell Scientific Publications. Pp. 230245. Bloomfield, S. F. & Arthur, M. 1994. Mechanisms in inactivation and resisitance of spores to chemical biocides. J. Appl. Bacteriol. Symp. Suppl., Vol. 76, pp. 91S104S. Bolton, K. J., Dodd, C. E. R., Mead, G. C. & Waites, W. M. 1988. Chlorine resistance of strains of Staphylococcus aureus isolated from poultry processing plants. Lett. Appl. Microbiol. Vol. 6, pp. 3134.

Recurrent or persistent squamous cell carcinoma of the cervix. Proc Soc Gynecol Oncol 32: 21, 2001 abstr 5 ; 26. Petersen IA, Long HJ, Abu-Ghazaleh S, et al: North Central Cancer Treatment Group NCCTG ; study of neoadjuvant methotrexate, vincristine, adriamycin, cisplatin MVCA ; in locally advanced cervical carcinoma. Proc Soc Clin Oncol 14: 274, 1995 abstr 765 ; 27. Papadimitriou CA, Dimopoulos MA, Giannakoulis N, et al: A Phase II trial of methotrexate, vinblastine, doxorubicin, and cisplatin in the treatment of metastatic carcinoma of the uterine cervix. Cancer 79: 2391-2395, 1997 Wilson TO: Neoadjuvant MVAC methotrexate, vinblastine, doxorubicin, cisplatin ; chemotherapy for locally advanced or metastatic cervical and vaginal cancer, in Salmon SE ed ; : Adjuvant Therapy of Cancer VII. Philadelphia, PA, J B Lipincott Co, 1997, pp 366-371 29. Murad AM, Triginelli SA, Ribalta JC: Phase II open label multicentric trial of MVAC: Methotrexate M ; , vinblastine V ; , doxorubicin D ; and cisplatin C ; plus granulocyte colony simulating factor Filgrastim ; in advanced recurrent cervical carcinoma final report. Proc Soc Clin Oncol 14: 276, 1995 abstr 774 ; 30. Long HJ, Langdon RM, Cha SS, et al: Phase II trial of methotrexate, vinblastine, doxorubicin, and cisplatin in advanced recurrent carcinoma of the uterine cervix and vagina. Gynecol Oncol 57: 239-245, 1995 Muderspach LI, Blessing JA, Levenback C, et al: A phase II trial of topotecan in patients with advanced squamous cell carcinoma of the cervix. Gynecol Oncol 81: 213-215, 2001.

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Secretarial assistance of Deb Strauss; and advice of Udo Kellner during the course of these studies are gratefully acknowledged. This study was made possible by the skillful care provided by Ken Hall, Louann Morrell, and the attendings, fellows, housestaff, and nurses of the Adult Leukemia Service. REFERENCES 1. Dive C, Evans CA, Whetton AD: Induction of apoptosis--New targets for cancer chemotherapy. Semin Cancer Biol 3: 417, 1992 Sachs L, Lotem J: Control of programmed cell death in normal and leukemic cells: New implications for therapy. Blood 82: 15, 1993 Kerr JF, Winterford CM, Harmon BV: Apoptosis. Its significance in cancer and cancer therapy. Cancer 73: 2013, 1994 Hannun YA: Apoptosis and the dilemma of cancer chemotherapy. Blood 89: 1845, 1997 Mesner P, Budihardjo I, Kaufmann SH: Chemotherapy-induced apoptosis. Adv Pharmacol 41: 461, 1997 Li X, Gong J, Feldman E, Seiter K, Traganos F, Darzynkiewicz Z: Apoptotic cell death during treatment of leukemias. Leuk Lymph 13: 65, 1994 Seiter K, Feldman EJ, Halicka HD, Traganos F, Darzynkiewicz Z, Lake D, Ahmed T: Phase I clinical and laboratory evaluation of topotecan and cytarabine in patients with acute leukemia. J Clin Oncol 15: 44, 1997 Miyashita T, Reed JC: Bcl-2 oncoprotein blocks chemotherapyinduced apoptosis in a human leukemia cell line. Blood 81: 151, 1993 Lowe SW, Bodis S, McClatchey A, Remington L, Ruley HE, Fisher DE, Housman DE, Jacks T: p53 status and the efficacy of cancer therapy in vivo. Science 266: 807, 1994 Green DR, Bissonnette RP, Cotter TG: Apoptosis and cancer. Import Adv Oncol 37, 1994 11. Bedi A, Barber JP, Bedi GC, el-Deiry WS, Sidransky D, Vala MS, Akhtar AJ, Hilton J, Jones RJ: BCR-ABL-mediated inhibition of apoptosis with delay of G2 M transition after DNA damage: A mechanism of resistance to multiple anticancer agents. Blood 86: 1148, 1995 Hickman JA: Apoptosis and chemotherapy resistance. Eur J Cancer 32A: 921, 1996 Wu GS, El-Deiry WS: Apoptotic death of tumor cells correlates with chemosensitivity, independent of p53 or Bcl-2. Clin Cancer Res 2: 623, 1996 Craig RW: The Bcl-2 gene family. Semin Cancer Biol 6: 35, 1995 Hacker G, Vaux DL: A sticky business. Curr Biol 5: 622, 1995 Yang E, Korsmeyer SJ: Molecular thanatopsis: A discourse on the Bc1-2 family and cell death. Blood 88: 386, 1996 Lotem J, Sachs L: Control of apoptosis in hematopoiesis and leukemia by cytokines, tumor suppressor and oncogenes. Leukemia 10: 925, 1996 Reed JC: Double identity for proteins of the Bcl-2 family. Nature 387: 773, 1997 Tsujimoto Y, Cossman J, Jaffe E, Croce C: Involvement of the bcl-2 gene in human follicular lymphoma. Science 228: 1440, 1985 Hockenbery DM, Nunez G, Milliman C, Schreiber RD, Kors~ meyer SJ: Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death. Nature 348: 334, 1990 Krajewski K, Tanaka S, Takayama S, Schibler MJ, Fenton W, Reed JC: Investigation of the subcellular distribution of the Bcl-2 oncoprotein: Residence in the nuclear envelope, endoplasmic reticulum, and outer mitochondrial membranes. Cancer Res 53: 4701, 1993 Reed JC: Regulation of apoptosis by Bcl-2 family proteins and its role in cancer and chemoresistance. Curr Opin Oncol 7: 541, 1995 Kitada S, Takayama S, De Riel K, Tanaka S, Reed JC: Reversal of chemoresistance of lymphoma cells by antisense-mediated reduction of Bcl-2 gene expression. Antisense Res Dev 4: 71, 1994 Keith FJ, Bradbury DA, Zhu YM, Russell NH: Inhibition of.

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It was agreed that semi-sodium valproate Depakote ; should be added to the Additional List for Specialist Use only in acute cases, where patients cannot tolerate or do not respond to first choice drugs. FC September 2005 It was agreed that topotecan Hycamtin ; should be added to the Additional List. FC September 2005 and toradol. In all models, encapsulated topotecan, or topotecan tcs, was compared with free form topotecan. By bleomycin in mice. J Respir Crit Care Med 162: 225-231. MEDLINE Hiraoka W, Vazquez N, Nieves-Neira W, Chanock SJ, Pommier Y 1998 ; Role of oxygen radicals generated by NADPH oxidase in apoptosis induced in human leukemia cells. J Clin Invest 102: 1961-1968. MEDLINE Hug H, Strand S, Grambihler A, Galle J, Hack V, Stremmel W, Krammer PH, Galle PR 1997 ; Reactive oxygen intermediates are involved in the induction of CD95 ligand mRNA expression by cytostatic drugs in hepatoma cells. J Biol Chem 272: 28191-28193. MEDLINE Hulka BS, Stark AT 1995 ; Breast cancer: cause and prevention. Lancet 346: 883-887. MEDLINE Kahlos K, Soini Y, Sormunen R, Kaarteenaho-Wiik R, Paakko P, Linnainmaa K, Kinnula VL 2001 ; Expression and prognostic significance of catalase in malignant mesothelioma. Cancer 91: 1349-1357. MEDLINE Kaufmann SH, Peereboom D, Buckwalter CA, Svingen PA, Grochow LB, Donehower RC, Rowinsky EK 1996 ; Cytotoxic effects of Topotecan combined with various anticancer agents in human cancer cell lines. J Natl Cancer Inst 88: 734-741. MEDLINE Kinnula K, Linnainmaa K, Raivio KO, Kinnula VL 1998 ; Endogenous antioxidant enzymes and glutathione S-transferase in protection of mesothelioma cells against hydrogen peroxide and epirubicin toxicity. Br J Cancer 77: 1097-1102. MEDLINE Koster JF, Biemond P, Swaak AJ 1986 ; Intracellular and extracellular sulphydryl levels in rheumatoid arthritis. Ann Rheum Dis 45: 44-46. MEDLINE Levine RL, Garland D, Oliver CN, Amici A, Climent I, Lenz AG, Ahn BW, Shaltiel S, Stadtman ER 1990 ; Determination of carbonyl content in oxidatively modified proteins. Methods Enzymol 186: 464-478. MEDLINE Lowry OH, Rosebrough NJ, Farr AL, Randall RJ 1951 ; Protein measurement with the Folin phenol reagent. J Biol Chem 193: 265-275. MEDLINE Mans DR, Lafleur MV, Westmijze EJ, Horn IR, Bets D, Schuurhuis GJ, Lankelma J, Retel J 1992 ; Reactions of glutathione with the catechol, the ortho-quinone and the semi-quinone free radical of etoposide. Consequences for DNA inactivation. Biochem Pharmacol 43: 1761-1768. MEDLINE Mansat-de Mas V, Bezombes C, Quillet-Mary A, Bettaieb A, D'Orgeix AD, Laurent G, Jaffrezou JP 1999 ; Implication of radical oxygen species in ceramide generation, c-Jun N-terminal kinase activation and apoptosis induced by daunorubicin. Mol Pharmacol 56: 867-874. MEDLINE Minotti G, Ronchi R, Salvatorelli E, Menna P, Cairo G 2001 ; Doxorubicin irreversibly inactivates iron regulatory proteins 1 and 2 in cardiomyocytes: evidence for distinct metabolic pathways and implications for iron-mediated cardiotoxicity of antitumor therapy. Cancer Res 61: 8422-8428. MEDLINE Misra HP, Fridovich I 1972 ; The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem 247: 3170-3175. MEDLINE Mosmann T 1983 ; Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. J Immunol Methods 65: 55-63. MEDLINE Muluk NB, Kisa U, Kacmaz M, Apan A, Koc C 2005 ; Efficacy of Topotecan treatment on antioxidant enzymes and TBARS levels in submandibular glands of rabbits: an experimental study. Otolaryngol Head Neck Surg 132: 136-140 and toremifene.

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Yusuf TRKZ, nder CEL K, eyma HASALIK, Yilmaz REM , Mehmet HASALIK, Blent MIZRAK, and Saim YOLO LU Inonu University, School of Medicine and Art and Science, Departments of Biochemistry, Obstetrics and Gynecology, Anaesthesiology, Pathology, Biostatistics, and Biology, 44069, Malatya TURKEY yturkoz inonu .tr Objective: This experimental study was designed to determine the changes in ovarian malondialdehyde.
Recognized for having the largest and most diverse assembly of extinct Ice Age plants and animals in the world. Visitors can learn about Los Angeles as it was between 10, 000 and 40, 000 years ago, during the last Ice Age, when animals such as saber-toothed cats and mammoths roamed the L.A. basin. The museum features a glass enclosed live-action room where people can watch scientists clean and repair real bones. Outside the museum, life-size replicas of several extinct mammals are featured. For more information, visit tarpits . 323 ; 934-PAGE 7243 ; MUSEUM OF RADIO AND TELEVISION 465 North Beverly Dr., Beverly Hills, 90210 This unique museum collects radio shows, television programs, and commercial advertisements in both media and makes the programming available to the general public. In the museum you can view programming of your choice alone in a console or with a group in a family console. For a true L.A. experience, attend a screening in one of the museum's theaters where you can see any number of thematic series such as a tribute to Johnny Cash or the short films of "Saturday Night Live." Currently the museum is featuring Celebrating Fifty Years of Jim Henson and the Muppets. For more information, visit mtr . 310 ; 786-1025 and torsemide Topotecan hycamtin ; recommendation from the new drugs committee scottish medicines consortium topotecan 1mg, 4mg powder for concentrate for solution for infusion hycamtin ; no 366 07 ; glaxosmithkline 6 april 2007 the scottish medicines consortium smc ; has completed its assessment of the above product and advises nhs boards and area drug and therapeutic committees adtcs ; on its use in nhs scotland.
The gift of the graduating class ; at St. Michael's College was highly successful this past year. The campaign's student committee, led by Misha Beline, Olivia de Souza, Katie DiTomaso and Mark Sokolski received the award for "best large campaign" from the University of Toronto and the Department of Alumni and Development. Over , 000.00 was raised for the Class Project - beautification of Elmsley Place, better known to some as "Flower Pot Lane and tracleer.

Cat al og # 04434 04444 04534 Cont ai ns hSCF, hIL-3, hGM-CSF, hEpo hSCF, hIL-3, hGM-CSF hSCF, hIL-3, hGM-CSF, hIL-6, hG-CSF, hEpo hSCF, hIL-3, hGM-CSF, hIL-6, hG-CSF hEpo Ap p l Routine colony assays of CFU-E, BFU-E, CFU-GM and CFU-GEMM in bone marrow BM ; , cord blood CB ; , mobilized peripheral blood MPB ; and peripheral blood PB ; . Routine colony assays of CFU-GM in BM, CB, MPB and PB.

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The rdl of cohort 1 was paclitaxel 175 mg m2 3 h, cisplatin 50 mg m2 and topotecan 5 mg m2 daily x 5 with filgrastim and trandolapril. The number of tumoral organs P 0.0058 ; and the number of mitoses P 0.049 ; showed a significant effect on survival on multivariate analysis. Based on the number of tumoral organs one or two and more than two ; and the number of mitoses less than 20 and more than 20 ; , a model is proposed to predict survival Fig. 1 ; : a 2.8-, 1.2-, and 0.8-yr median survival was observed in ACC patients with none, one, and two deleterious prognostic factors, the 5-yr survival being 25, 0, and 0%, respectively P 0.0008 ; . Objective responses to o, p DDD- or cisplatinum-based chemotherapy in ACC patients with none, one, and two deleterious prognostic factors were observed in three of 21 14% ; , three of 14 21% ; , and none of nine patients, respectively trend test: non significant.
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Traditionally state governmental function of operating a prison through contractual relationships with the City of Burlington and State of Colorado. In its treatment of the decedent, Jeffrey A. Buller, at the Kit Carson Correctional Center, Defendant CCA employed all Defendants who are herein sued in their individual and official capacities. Defendant CCA knew of, supported, adopted, approved and ratified the policy, custom, or practice of ignoring and violating the constitutional rights of the decedent. CCA, a private operator of Kit Carson Correctional Center, is not a healthcare professional or healthcare institution. 7. At all pertinent times mentioned herein, all of the Defendants sued in both their and tranylcypromine. Untreated cells, whereas cellular accumulation of topotecan scarcely increased in MCF-7 cells treated with 3 nmol L E2 when compared with cells treated with 0.03 nmol L E2 Fig. 3B ; . The results coincided with BCRP down-regulation in E2-treated MCF-7 cells Fig. 1A ; . As for MCF-7 BCRP cells, intracellular topotecan accumulation only marginally increased in the presence of 0.03 nmol L E2 as compared with untreated cells Fig. 3B ; . Also, cellular accumulation of topotecan only marginally increased in MCF-7 BCRP cells treated with 3 nmol L E2 when compared with those treated with 0.03 nmol L E2 Fig. 3B ; . The results suggest that down-regulation of exogenous BCRP in MCF-7 BCRP cells would not be enough for abrogation of topotecan efflux out of the cells, even after treatment xwith 3 nmol L E2. Effects of Tamoxifen and ERa Knockdown by siRNA on E2a mediated BCRP Down-regulation in MCF-7 and MCF-7 BCRP Cells. MCF-7 cells expressed similar amounts of endogenous BCRP in the presence of increasing concentrations of tamoxifen Fig. 4A, left ; . In MCF-7 BCRP cells, marginally higher levels of exogenous BCRP were produced by increasing dosages of tamoxifen Fig. 4B, left ; , possibly by competition with residual estrogens in the culture medium. Tamoxifen was also found to partially reverse the E2-mediated down-regulation of either endogenous or exogenous BCRP in a dose-dependent manner Fig. 4A and B, right ; . In these tamoxifen reversal experiments using MCF-7 BCRP cells, a concentration of 0.3 nmol L E2 was used to down-regulate BCRP, because tamoxifen even at levels of 0.5 Amol L failed to reverse 3 nmol L E2-mediated BCRP downregulation data not shown ; . These results suggest that E2mediated BCRP down-regulation in MCF-7 and MCF-7 BCRP cells may be associated with the interaction of E2 and ERa. We therefore did an experiment in which ERa expression was repressed using siRNA, and investigated the effects of this gene silencing on E2-mediated modification of BCRP expression. Transfection of 100 nmol L ERa siRNA resulted in a nearly complete loss of ERa expression in MCF-7 BCRP cells after 48 hours Fig. 4C-1 ; . In addition, this down-regulation of ERa expression persisted for at least 6 days after the siRNA transfections data not shown ; . Gene silencing of ERa in MCF7 BCRP cells by RNA interference was also found to attenuate E2-mediated BCRP down-regulation Fig. 4C-2 ; , indicating that ERa is necessary for the repression of BCRP. Semi-quantitative RT-PCR and Northern Blot Analysis of BCRP Expression in MCF-7 and MCF-7 BCRP Cells. RT-PCR and Northern blot analyses revealed that the treatment of MCF-7 cells with E2 for 4 days did not affect the expression of endogenous BCRP mRNA Fig. 5A and B, left ; . Similarly, the same treatment of MCF-7 BCRP cells with E2 for 4 days did not affect exogenous HaBCRP mRNA levels Fig. 5B, right ; . Considering that these treatments dramatically reduce BCRP protein expression levels up to 10-20% of control levels following exposure to 3 nmol L E2 ; , we speculated that the mechanism of E2-mediated inhibition would be a posttranscriptional process. Metabolic Labeling of BCRP in MCF-7 BCRP Cells. The biosynthesis and degradation of BCRP was further investigated by pulse-chase experiments. An outline of the experimental procedure is presented in Fig. 6A. MCF-7 BCRP cells produce a large amount of exogenous BCRP, driven by a constitutive long terminal repeat promoter, which could be successfully immunoprecipitated with the anti-BCRP antibody BXP-21, whereas the quantity of endogenous protein in parental MCF-7 cells is below the minimum detectable level Fig. 6B and C ; . BCRP is initially detectable as a and topotecan.

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Phase II Study of Paclitaxel Therapy for Unresectable Biliary Tree Carcinomas Dennie V. Jones, Jr, Richard Lozano, Ashraful Hoque, Avi Markowitz, and Yehuda Z. Patt 2306 Phase II Trial of Intravenous Fluorouracil and Subcutaneous Interferon Alfa-2b for Biliary Tract Cancer . Yehuda Z. Patt, Dennie V. Jones, Jr, Ashraful Hoque, Richard Lozano, Avi Markowitz, Isaac Raijman, Patrick Lynch, and Chusilp Charnsangavej 2311 Head and Neck Cancer Phase II Study of Paclitaxel in Patients With Recurrent Malignant Glioma . Michael D. Prados, S. Clifford Schold, Alexander M. Spence, Mitchel S. Berger, Leslie D. McAllister, Minesh P. Mehta, Mark R. Gilbert, Dorcas Fulton, John Kuhn, Kathleen Lamborn, Dorothy J. Rector, and Susan M. Chang 2316 Chemotherapy Followed by Accelerated Fractionated Radiation for Larynx Preservation in Patients With Advanced Laryngeal Cancer . Avraham Eisbruch, Allan F. Thornton, Susan Urba, Ramon M. Esclamado, William R. Carroll, Carolyn R. Bradford, Mark B. Hazuka, Fred J. Littles, Myla Strawderman, and Gregory T. Wolf 2322 Cisplatin-Fluorouracil Exclusive Chemotherapy for T1-T3NO Glottic Squamous Cell Carcinoma Complete Clinical Responders: Five-Year Results . Ollivier Laccourreye, Daniel Brasnu, Vincent Bassot, Madeleine Menard, David Khayat, and Henri Laccourreye 2331 Lung Cancer Randomized Trial Comparing Induction Chemotherapy Versus Induction Chemotherapy Followed by Maintenance Chemotherapy in Small-Cell Lung Cancer . J.P. Sculier, M. Paesmans, G. Bureau, V. Giner, J. Lecomte, J. Michel, M.C. Berchier, O. Van Cutsem, U. Kiistner, F. Kroll, R. Sergysels, P. Mommen, and J. Klasterskyfor the European Lung Cancer Working Party 2337 Phase II Study of Topotecan in Patients With Extensive-Stage Small-Cell Carcinoma of the Lung: An Eastern Cooperative Oncology Group Trial . Joan H. Schiller, KyungMann Kim, Paul Hutson, Russell DeVore, John Glick, James Stewart, and David Johnson 2345 Sarcoma Randomized Phase III Trial of Liposomal Daunorubicin Versus Doxorubicin, Bleomycin, and Vincristine in AIDS-Related Kaposi's Sarcoma . Parkash S. Gill, James Wernz, David T. Scadden, Philip Cohen, Geoffrey M. Mukwaya, Jamie Hayden von Roenn, Mark Jacobs, Sanford Kempin, Ivan Silverberg, Guillermo Gonzales, Mark U. Rarick, Adam M. Myers, Frances Shepherd, Carol Sawka, Malcolm C. Pike, and Michael E. Ross 2353 Radiation in Management of Patients With Dermatofibrosarcoma Protuberans . Herman Suit, Ira Spiro, Henry J. Mankin, Jimmy Efird, and A.E. Rosenberg 2365 PediatricOncology Comparative Cytotoxicity of Dexamethasone and Prednisolone in Childhood Acute Lymphoblastic Leukemia . Chikako Ito, William E. Evans, Lisa McNinch, Elaine Coustan-Smith, Hazem Mahmoud, Ching-Hon Pui, and Dario Campana 2370 REVIEW ARTICLE Bronchioloalveolar Carcinoma . John E. Barkley and Mark R. Green 2377 and treprostinil.
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