Topotecan

William F. "Bill" Boland, Jr. began his career with Amtrak Nov. 18, 1989, in Engineering's Communications and Signal department. Over the years, Bill has held several positions in C&S, and is currently Advanced Civil Speed Enforcement System ACSES ; manager, which allows Amtrak to run 150 mph trains. Bill was instrumental in the conversion of leased data circuits to Amtrakowned circuits. The Amtrak-owned circuits provide users with higher speed, better quality and improve reliability. Bill also installed a new fiber optic transport system, which gives Amtrak the ability to ship video anywhere within the New England Division. Bill's unique understanding of Amtrak's right of way and telecommunication assets enable him to work with a variety of telecommunications companies in the New England region. Bill continues to search for ways to protect and improve Amtrak's infrastructure, always with an eye on cost savings and increased productivity. In this ever-changing world of technology, he maintains a high level of technical expertise and continues to stay updated with the latest innovations that will benefit the company. William F. "Bill" Boland is highly regarded by his peers and subordinates. The personification of a team player, he will roll up his sleeves and work with his employees. With his can-do attitude and positive demeanor, he accomplishes his tasks in a proficient manner and represents Amtrak with the utmost professionalism. Bill has earned the respect and trust of those he works with at Amtrak, as well as outside contractors.

Put a check ; against the answer which does not agree with the others. 14. Stocktaking should be done in the pharmacy: a ; Once every four years. b ; Each time there is a burglary. c ; At least once every year. d ; Anytime it becomes necessary. 15. The doors of the pharmacy must: a ; Be transparent so that patients can see through. b ; Have a metal bar across with padlocks. c ; Have locks that are functioning well. d ; Have metallic door shutters. 16. The pharmacy must be handed over to another staff when going on: a ; Maternity leave. b ; Sick leave. c ; Annual leave. d ; Lunch break.
There is evidence that the cytotoxic potential of both topotecan and gemcitabine is also related to the dosing schedule [21, 24, 28]. This might explain the somewhat different findings made by Greggi et al. [25] compared with the present data. Thrombocytopenia of CTC grade 4 occurred in five patients. In concordance to the preceding dose finding study, severe toxicities were observed exclusively after the first course of chemotherapy. With the exception of anaemia, cumulative toxicities were absent in this study. In terms of serum creatinine and creatinine clearance, combination chemotherapy did not impair renal function. There was no correlation between renal function and haematological toxicity. Dose escalation up to 0.75 mg m2 was realised in nine participants, with two more subjects receiving 1.0 mg m2. Even this increase in dose was not accompanied by severe haematological toxicity. In conclusion, the present data support the available evidence of various favourable characteristics of the topotecan gemcitabine combination. The distinct features of the application schedule chosen for the purpose of this study including dose escalation ; might facilitate long-term treatment with the goal of tumour control. Meanwhile, the planned three-arm, multiinstitutional randomised trial was initiated and certified by.

Topotecan

Of 1.75 mg m2 used in another clinical trial.18 The dose escalation of topotecan was allowed with an increment of 0.5 mg m2 to a maximum dose of 6 mg m2. Both drugs were administered as 30minute infusions, with topotecan given one hour before docetaxel. This protocol was revised with reduced docetaxel doses 40-50 mg m2 ; when the maximum tolerable dose was reached among the first 6 patients. Both the original and the revised dose levels are given in Table 1. The administration of the agents was on a bi-weekly basis with one cycle of 3 infusions followed by a one-week rest. Patient Inclusion Criteria Patients were eligible for enrollment if they had metastatic or locally advanced malignancy by histologic or cytologic diagnoses. All the patients had malignancies that were either refractory to standard therapy or for which no standard therapies existed. Patients were males or females of at least 18 years of age. Prior radiation therapy was allowed if it was completed at least 4 weeks before the study entry. Prior chemotherapy was also allowed if it was completed at least 4 weeks prior to study entry, and if the patient had recovered from the 55.

C8 column Pro RPC HR 5 10, Pharmacia LKB Biotechnology Inc. ; using gradient elution from 0 to 60% CH&N in 0.1% CF3COOH Hz0a t a flow rate of 500 pl min Fig. 3 ; . The inhibitory activity was eluted in asingle peak which was collected and rechromatographed using a large-pore C8-derivatized silica HPLC column Yamamura Co., Japan, 4.6 mm inner diameter X 250 mm ; under two elution schedules. The active fraction was first eluted using a gradient of CH&N from 36 to 42% in 0.156 CF3COOH H20at a flow rate of 1 ml min Fig. 4a ; and thsen reapplied to thecolumn and eluted with a gradient of 3 7 CH&N in 0.1% CF3COOH H20 at a flow rate of 1 ml min Fig. 4b ; . Data on the purification procedure are presented. in TableI and demonstrate 77.6-fold purification with a 17% yield. SDS-polyacrylamide gel electrophoresis of the purified trehalase inhibitor yielded a single band which showed a positive glucoprotein pattern with periodic acid-Schiff reagent Fig. 5 ; . Comparison of the electrophoretic mobility of the protein with that of standard proteins indicates a molecular weight of about 86, 000 Fig. 5 ; . The amino acid composition of the purified inhibitor is. Results of phase ii studies suggest considerable antitumor activity of single agent topotecan in small cell lung cancer and ovarian cancer patients and toradol Fig. 3. Cell growth inhibition induced by DDP A ; , UV B ; , MNNG C ; , and topotecan D ; in empty vector-transfected and p73-overexpressing clones. Values reported are the mean SD from at least three independent experiments, each consisting of four replicates. f, A2780 pCDNA3; , A2780 p73.4; E, A2780 p73.5. Cells were treated for 2 h with DDP and for 1 h with MNNG and topotecan.
29. Tong WM, Ellinger A, Sheinin Y, Cross HS. Epidermal growth factor receptor expression in primary cultured human colorectal carcinoma cells. Br J Cancer 1998; 77: 17921798. Baselga J. Targeting the epidermal growth factor receptor with tyrosine kinase inhibitors: small molecules, big hopes. J Clin Oncol 2002; 20: 22172219. Waksal HW. Role of an anti-epidermal growth factor receptor in treating cancer. Cancer Metastasis Rev 1999; 18: 427436. Formento JL, Francoual M, Formento P et al. Epidermal growth factor receptor assay: validation of a single point method and application to breast cancer. Breast Cancer Res Treat 1991; 17: 211216. Allred DC, Swanson PE. Testing for erbB-2 by immunohistochemistry in breast cancer. J Clin Pathol 2000; 113: 171 Koenders PG, Peters WH, Wobbes T et al. Epidermal growth factor receptor levels are lower in carcinomatous than in normal colorectal tissue. Br J Cancer 1992; 65: 189 Koretz K, Schlag P, Moller P. Expression of epidermal growth factor receptor in normal colorectal mucosa, adenoma, and carcinoma. Virchow Arch A Pathol Anat Histopathol 1990; 416: 343349. Spano JP, Lagorce C, Atlan D et al. Impact of EGFR expression on colorectal cancer patient prognosis and survival. Ann Oncol 2005; 16: 102 Karameris A, Kanavaros P, Aninos D et al. Expression of epidermal growth factor EGF ; and epidermal growth factor receptor EGFR ; in gastric and colorectal carcinomas. An immunohistological study of 63 cases. Pathol Res Pract 1993; 189: 133137. Steele RJ, Kelly P, Ellul B et al. Epidermal growth factor receptor expression in colorectal cancer. Br J Surg 1990; 77: 13521354. Steele RJ, Kelly P, Ellul B et al. Immunohistochemical detection of epidermal growth factor receptors on human colonic carcinomas. Br J Cancer 1990; 61: 325326. Moorghen M, Ince P, Finney KJ et al. Epidermal growth factor receptors in colorectal carcinoma. Anticancer Res 1990; 10: 605 Prewett MC, Hooper AT, Bassi R et al. Enhanced antitumor activity of anti-epidermal growth factor receptor monoclonal antibody IMC-C225 in combination with irinotecan [CPT-11] against human colorectal tumor xenografts. Clin Cancer Res 2002; 8: 9941003. Radinsky R. Modulation of tumor cell gene expression and phenotype by the organ-specific metastatic environment. Cancer Metastasis Rev 1995; 14: 323 McKay JA, Douglas JJ, Ross VG et al. Expression of cell cycle control proteins in primary colorectal tumors does not always predict protein expression in lymph node metastases. Clin Cancer Res 2000; 6: 113 McLeod HL, McKay JA, Collie-Duguid ESR, Cassidy J. Therapeutic opportunities from tumor biology in metastatic colon cancer. Eur J Cancer 2000; 36: 17061712. Paredes-Zaglul A, Kang JJ, Essig YP et al. Analysis of colorectal cancer by comparative genomic hybridization: evidence for induction of the metastatic phenotype by loss of tumor suppressor genes. Clin Cancer Res 1998; 4: 879886. Al Mulla F, Keith WN, Pickford IR et al. Comparative genomic hybrodization analysis of primary colorectal carcinomas and their synchronous metastases. Genes Chromosomes Cancer 1999; 24: 306 Saeki T, Salomon DS, Johnson GR et al. Association of epidermal growth factor-related peptides and type I receptor tyrosine kinase with prognosis of human colorectal carcinomas. Jpn J Clin Oncol 1995; 25: 240 Yasui W, Sumiyoshi H, Hata J et al. Expression of epidermal growth factor receptor in human gastric and colonic carcinomas. Cancer Res 1988; 48: 137 Neal DE, Marsh C, Bennett MK et al. Epidermal growth factor receptors in human bladder cancer: comparisons of invasive and superficial tumors. Lancet 1985; i: 366 368. 50. Mendelsohn J. Epidermal growth factor receptor as a target for therapy with antireceptor monoclonal antibodies. J Natl Cancer Inst Monogr 1992; 13: 125131. Mendelsohn J, Baselga J. Status of epidermal growth factor receptor antagonists in the biology and treatment of cancer. J Clin Oncol 2003; 21: 27872799. Niwa H, Wentzel AL, Li M et al. Antitumor effects of epidermal growth factor receptor antisense oligonucleotides in combination with docetaxel in squamous cell carcinoma of the head and neck. Clin Cancer Res 2003; 9: 50285035. Huang SM, Bock JM, Harari PM. Epidermal growth factor receptor blockade with C225 modulates proliferation, apoptosis, and radiosensitivity in squamous cell carcinomas of the head and neck. Cancer Res 1999; 59: 1935 Ye D, Mendelsohn J, Faz Z. Augmentation of a humanized abtiHER2 m Ab 4D5 induced growth inhibition by a human-mouse chimeric anti-EGF receptor mAb C225. Oncogene 1999; 18: 731738. Mandal M, Adam L, Mendelsohn J, Kumar R. Nuclear targeting of Bax during apoptosis in human colorectal cancer cells. Oncogene 1998; 17: 9991007. Liu B, Fang M, Schmidt M et al. Induction of apoptosis and activation of the caspase cascade by anti-EGF receptor monoclonal antibodies in DiFi human colon cancer cells do not involve the c-jun Nterminal kinase activity. Br J Cancer 2000; 82: 19911999. Wood RD, Mitchell M, Sgouros J, Lindahl T. Human DNA repair genes. Science 2001; 291: 1284 Bandyopadhay D, Mandal M, Adamn L et al. Physical interaction between epidermal growth factor receptor and DNA-dependent protein kinase in mammalian cells. J Biol Chem 1998; 273: 15681573. Luwor RB, Johns TG, Murone C et al. Monoclonal antibody 806 inhibits the growth of tumor xenografts expressing either the de2-7 or amplified epidermal growth factor EGFR ; but not wild-type EGFR. Cancer Res 2001; 61: 53555361. Mendelsohn J. Blockade of receptors for growth factors: an anticancer therapy. Clin Cancer Res 2000; 6: 747753. Huang SM, Harari PM. Modulation of radiation response after epidermal growth factor receptor blockade in squamous cell carcinomas: inhibition of damage repair, cell cycle kinetics and tumor angiogenesis. Clin Cancer Res 2000; 6: 21662174. Ciardello F, Caputo R, Bianco R et al. Antitumor effect and potentiation of cytotoxic drugs activity in human cancer cells by ZD-1839 Iressa ; , an epidermal growth factor receptor-selective tyrosine kinase inhibitor. Clin Cancer Res 2000; 6: 20532063. Hidalgo M, Siu LL, Nemunaitis J et al. Phase I and pharmacologic study of OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in patients with advanced solid malignancies. J Clin Oncol 2001; 19: 32673279. Mendelsohn J, Baselga J. The EGFR receptor family as targets for cancer therapy. Oncogene 2000; 19: 65506565. Erlichman C, Boerner SA, Hallgren CG et al. The HER tyrosine kinase inhibitor CI1033 enhances cytotoxicity of 7-ethyl-10-hydroxycamptothecin and topotecan by breast cancer resistance proteinmediated drug efflux. Cancer Res 2001; 61: 739 Milano G, Magne N. Pharmacological consequences of EGFR targeting. Bull Cancer 2003; 90: S197S201. 67. Azzariti A, Xu JM, Porcelli L, Paradiso A. The schedule-dependent enhanced cytotoxic activity of 7-ethyl-10-hydroxy-camptothecin and toremifene.

Topotecan blood brain barrier

Patients on dose levels 3 and 4 repeated topotecan for up to 5 days starting on day 15 after the initial topotecan and etoposide sequence. Avoid contact with the eyes or mucous membranes. Discontinue use if a sensitivity reaction occurs or if excessive irritation develops on uninvolved skin areas. Drug product is flammable. Keep away from open flame and torsemide.
Monolayer-cultured primary lung epithelial cells P-Z ; by lipofection. Twenty-four hours after transfection, cells were fixed and indirectly immunostained with anti-CBE1 antibodies or pre-immune serum A ; . Nuclei were stained with 7-AAD. C and Q are interference contrast images of B and P, respectively. F, I, L, O, T, W, and Z represent merged images of D and E, G and H, J and K, M and N, R and S, U and V, and X and Y, respectively. No fluorescent FITC signals were detected without either primary or secondary antibodies data not shown ; . In COS-7 and 16HBE 14o - ; cells, most FITC signals overlap with nuclear staining, but some are outside the nucleus arrowhead ; . In contrast, most signals are perinuclear when expressed in primary epithelial cells although intranuclear staining is also observed in some of the cells U-W ; . Nuclear localization in primary cells was also observed for ORF2 data not shown ; . Representative results from at least three independent transfection experiments are shown. Scale bars 40 m. Firmed in the CP70-ch3 and CP70-ch2 cells data not shown ; . Cells were exposed to 500 M temozolomide in the presence or absence of 400 nM AG14361 for 4 h. A representative elution profile is shown in Fig. 3A, and pooled relative elution data from three independent experiments are given in Fig. 3B. After exposure to temozolomide alone, there was a greater accumulation of DNA strand breaks in the CP70-ch2 cells compared with the CP70-ch3 cells. However, coincubation with AG14361 increased the relative elution 3-fold in CP70-ch3 cells but only 2-fold in CP70-ch2 cells, such that there was no significant difference between the relative elution of CP70-ch3 and CP70ch2 cells exposed to the combination of temozolomide and AG14361. Thus, the greater enhancement of temozolomideinduced growth inhibition by AG14361 in the CP70-ch2 cells could not be attributed to an increased number of DNA strand breaks. Investigation of the Potentiation of Topotecan by AG14361 in MMR-Proficient and -Deficient Cells. It has been shown previously that PARP-1 inhibitors are effective enhancers of topotecan-induced growth inhibition and cytotox and tracleer.
Chao-Sheng Liao, Hsin-Chih Lai, Chun-Pin Chiang, Hui-Ling Peng, Chuen-Den Tseng, Ming-Shyen Yen, Wei-Chih Hsu, Chih-Hung Chen An innovative community-based multiple disease screening model was created. The success of this model includes the enhancement of the attendance rate, the detection of a large proportion of asymptomatic neoplastic diseases and nonneoplastic chronic diseases, and the elucidation of the relations between certain neoplasms and nonneoplastic chronic disease. Discipline Epidemiology Cigarette advertising and female smoking prevalence in Spain, 19821997: Case studies in International Tobacco Surveillance Omar Shafey, Esteve Fernndez, Michael Thun, Anna Schiaffino, Suzanne Dolwick, Vilma Cokkinides The authors examined the correlation between the explosive increase in female smoking prevalence and tobacco industry cigarette marketing practices in Spain during a period of rapid social liberalization. Their findings indicate that strong cultural and traditional prohibitions against female smoking are not sufficient to withstand aggressive tobacco marketing in the context of social liberalization. Pediatric Oncology Oral topotecan in children with recurrent or progressive high-grade glioma: A Phase I II study by the German Society for Pediatric Oncology and Hematology Sabine Wagner, Bernhard Erdlenbruch, Alfred Lngler, Astrid Gnekow, Joachim Khl, Michael Albani, Sigrid Vlpel, Peter Bucsky, Angela Emser, Ove Peters, Johannes E. A. Wolff In children with recurrent high-grade glioma, oral topotecan median dose, 0.9 mg m2 per day ; administered once daily was well tolerated, with a response rate complete clinical remission, partial response, or stable disease ; of 71.3%. The primary dose-limiting toxicity was hematotoxicity. Soft tissue sarcoma as a second malignant neoplasm in the pediatric age group p 1758-1765 ; Gianni Bisogno, Guido Sotti, Yohann Nowicki, Andrea Ferrari, Alberto Garaventa, Ilaria Zanetti, Claudio Favre, Amalia Schiavetti, Paolo Tamaro, Modesto Carli The experience of the Italian Cooperative Group showed that children who developed soft tissue sarcomas as a second malignancy had a less dismal prognosis than reported previously and could be treated with the same strategies used in the treatment of children with de novo pediatric sarcomas. Correspondence Eighteen-year results in the treatment of early breast carcinoma with mastectomy versus breast conservation therapy Brian K. P. Goh, Wei-Sean Yong.

Topotecan drug

Please call 1-800-sentara 736-8272 ; to sign up for the "healthy living with diabetes" classes and trandolapril. Clinical trials safeguards participating in clinical trials the cost of clinical trials finding specific clinical trials the future of clinical trials clinical trials database overview caregivers healing environments support groups journaling birth control and sexuality home health financial & insurance issues advanced directives inspiration movement & exercise life after treatment online resources combination of cisplatin and topotecan improves survival in advanced cervical cancer a phase iii clinical trial published in the journal of clinical oncology reported that women with advanced cervical cancer treated with a combination of cisplatin platinol ; plus topotecan hycamtin ; chemotherapy lived longer than women treated with cisplatin alone. Dosing by body weight is preferred. ; The standard dose is 1.0 mg kg body weight, up to 100 mg ; Age Group and tranylcypromine.

For the purposes of the current study, CA125 values obtained at baseline and with each of the first two cycles of both PLD and topotecan were reviewed relative to a patient's best response on therapy. Serial CA125 values were obtained from assays performed at local or central laboratories according to standard practice. The percent change from baseline by agent PLD and topotecan ; and and topotecan. 149. Velasquez WS, Cabanillas F, Salvador P et al. Effective salvage therapy for lymphoma with , cisplatin in combination with high-dose Ara-C and dexamethasone DHAP ; . Blood. 1988; 71: 117-22. Velasquez WS, McLaughlin P Tucker S, et al. ESHAP--an effective chemotherapy , regimen in refractory and relapsing lymphoma: a 4-year follow-up study. J Clin Oncol. 1994; 12: 1169-76. Verschraegen CF, Sittisomwong T, Kudelka AP et al. Docetaxel for patients with paclitaxel, resistant mullerian carcinoma. J Clin Oncol. 2000; 18: 2733-39. Vogler WR, Velez-Garcia E, Weiner RS, et al. A phase III trial comparing idarubicin and daunorubicin in combination with cytarabine in acute myelogenous leukemia: A Southeastern Cancer Study Group study. J Clin Oncol. 1992; 10: 1103-11. von der Maase H, Hansen SW, Roberts JT, et al. Gembitabine and cisplatin versus methotrexate, vinblastine, doxorubicin, and cisplatin in advanced or metastatic bladder cancer: Results of a large, randomized, multinational, multicenter, phase III study. J Clin Oncol. 2000; 17: 3068-77. Von Pawel J, Schiller JH, Shepherd FA, et al. Topotecan versus cyclophosphamide, doxorubicin, and vincristine for the treatment of recurrent small-cell lung cancer. J Clin Oncol. 1999; 17: 658-67. Vose JM, Link BK, Grossbard ML, et al. Phase II study of rituximab in combination with CHOP chemotherapy in patients with previously untreated, aggressive non-Hodgkins lymphoma. J Clin Oncol. 2001; 19: 389-97. Wilke H, Preusser P Fink U, et al. Etoposide E ; leucovorin L ; 5-fluorouracil F ; ELF ; in , advanced gastric carcinoma--A phase I II trial. Proceedings of the NCI-EORTC Symposium on New Drugs in Cancer Therapy, Amsterdam, The Netherlands; March 710, 1989. Abstract 323. 157. Wilke H, Preusser P Fink U, et al. New developments in the treatment of gastric , carcinoma. Cancer Treat Res. 1991; 55: 363-73. Williams SD, Birch R, Einhorn LH, Irwin L, Greco FA, Loehrer PJ. Treatment of disseminated germ-cell tumors with cisplatin, bleomycin, and either vinblastine or etoposide. N Engl J Med. 1987; 316: 1435-40. Wils JA, Klein HO, Wagener DJ, et al. Sequential high-dose methotrexate and fluorouracil combined with doxorubicin--a step ahead in the treatment of advanced gastric cancer: a trial of the European Organization for Research and Treatment of Cancer Gastrointestinal Tract Cooperative Group [see comments]. J Clin Oncol. 1991; 9: 827-31. Wolmark N, Wieand HS, Hyams DM, et al. Randomized trial of postoperative adjuvant chemotherapy with or without radiotherapy for carcinoma of the rectum: National Surgical Adjuvant Breast and Bowel Project protocol R-02. J Natl Cancer Inst. 2000; 92: 388-96. Yang TS, Lin YC, Chen JS, Wang HM, Wang CH. Phase II study of gemcitabine in patients with advanced hepatocellular carcinoma. Cancer. 2000; 89: 750-56. Yung WKA, Prados MD, Yaya-Tur R, et al. Multicenter phase II trial of temozolomide in patients with anaplastic astrocytoma or anaplastic oligoastrocytoma at first relapse. J Clin Oncol. 1999; 17: 2762-71. Ziegler-Heitbrock HWL, Schlag R, Flieger D, Thiel E. Favorable response of early stage B CLL patients to treatment with IFN-alpha2. Blood. 1989; 73: 1426-30. Zinzani PL, Magagnoli M, Moretti L, et al. Randomized trial of fludarabine versus fludarabine and idarubicin as frontline treatment in patients with indolent or mantle-cell lymphoma. J Clin Oncol. 2000; 18: 773-79 and treprostinil.

Topotecan chemotherapy

I thought for many years that it was the injection that was creating my illness. There was nothing bothering me yet I was ill. "Abominable" is the word I use to describe such a situation. Specifically, at least about 85% of the topotecan in the composition is liposome-entrapped topotecan, and wherein about 85% of the liposomes in said composition have sizes of about 05 to about 25 microns and triac. In yet another embodiment, this invention provides a process for preparing a lyophilized liposomal topotecan which, after long-term storage, and subsequent reconstitution provides a ready to use liposome composition which has preselected liposome sizes, relatively little unencapsulated topotecan, and which passes usp 788 particulate matter testing and toradol.

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