Carboplatin uses

Key Evidence Thirteen randomized trials compared various chemotherapy regimens for patients with recurrent ovarian cancer. In five of the thirteen trials where 100% of patients were considered sensitive to platinumcontaining chemotherapy: o Further platinum-based combination chemotherapy significantly improved response rates two trials ; , progression-free survival four trials ; , and overall survival three trials ; when compared with single-agent chemotherapy with carboplatin or paclitaxel. o Only two randomized trials compared the same chemotherapy regimen, carboplatin alone versus the combination of carboplatin and paclitaxel. Both trials were consistent in reporting improved survival outcomes with the combination of carboplatin and paclitaxel. o In one trial, the combination of carboplatin and gemcitabine resulted in significantly higher response rates and improved progression-free survival when compared with carboplatin alone. o Median survival with carboplatin alone ranged from 17 months to 24 months in four trials. In eight of the thirteen trials where 35% to 100% of patients had platinum refractory or resistant disease: o Three small trials compared the combination of paclitaxel with epirubicin or doxorubicin versus paclitaxel alone. No significant differences in response or survival outcomes were detected between treatment groups in the three trials. o Five trials compared non-platinum single-agents in this mixed platinum sensitivity setting.

Carboplatin maximum dose Four factors are critical determinants in the initial medical management of victims presenting at a hospital or clinic following an accidental or malevolent act involving radiological or nuclear materials: i ; The number of victims involved. The ability to assess, diagnose and provide initial therapy may be compromised when large numbers of patients arrive for treatment. Triage is essential when personnel and material resources are scarce. ii ; The presence absence of thermal or conventional injuries. In incidents involving thermal or conventional injuries, along with total body or large volume partial body irradiation i.e. combined injury ; , initial triage, assessment and treatment must first focus on the conventional injuries present. Diagnosis of the ARS and estimates of severity are made after the immediate lifesaving treatment of trauma, since the radiation injury does not present immediate life-threatening complications. iii ; The amount of time that has elapsed since the exposure s ; occurred is important since victims presenting soon after being irradiated i.e. minutes to 48 h ; will have signs and symptoms and laboratory results that are different from those found in patients presenting days or. 24. Neijt J. P., ten Bokkel Huinink W. W., van der Burg M. E., Van Oosteron A. T, Willemse P. H. B., Vermorken J. B., Van Lindert A. C. M., Heintz A. P. M., Aartsen E., Van Lent M., Trimbos J. B., De Meijer A. J.: Long term survival in ovarian cancer: mature data from the Netherlands Joint Study Group for ovarian cancer. Eur J Cancer 27, 1367-72 1991 ; 25. Omura G. A, Brady M. F, Homesley H. D. Yordan E., Major F. J., Buchsbaum H. J., Park R. C.: Long term follow-up and prognostic factor analysis in advanced ovarian carcinoma; the Gynecologic oncology group experience. J Clin Oncol 9, 1138-50 1991 ; 26. Ovarian Cancer Meta-analysis Project: Cyclophosphamide plus cisplatin versus Cyclophosphamide, doxorubicin and cisplatin chemotherapy of ovarian carcinoma: a meta-analysis. J Clin Oncol 9, 1668-1674 1991 ; 27. Rowinsky E. K., Gilbert M. R., Mc Guire W. P. Noe D. A., Grochow L. B., Forastiere A. A., Ettinger D. S., Lubejko B. G., Clerk B., Sartorius S. E.: Sequences of Taxol and Cisplatin: a phase I and pharmacologic study. J Clin Oncol 9, 1692-1703 1991 ; 28. Sarosy G., Kohn E., Stone A. D. et al.: Phase I study of Taxol and granulocyte colony-stimulating factor in patients with refractory ovarian cancer. J Clin Oncol 10, 1165-1170 1992 ; 29. Schiller J. H., Storer B., Tutsch K. Arzoomanian R., Alberti D., Feierabend C., Spriggs D.: Phase I trial of 3-hour infusion of Paclitaxel with or without granulocyte colony-stimulating factor in Patients with advanced cancer. J Clin Oncol 12, 241-248 1994 ; 30. Sutton G., Stehman F., Einhorn L., Roth L. M., Blessing J. A., Eherlich C. E.: Ten year follow up of patients receiving cisplatin, doxorubicin and cyclophosphamide chemotherapy for advanced epithelial ovarian carcinoma. J Clin Oncol 7, 223-229 1989 ; 31. ten Bokkel Huinink W. W., Dubbelmann R., Aartseen E., Franklin H., M. C. Vie J.: Experimental and clinical results with intraperitoneal cisplatin. Semin Oncol 3, 43- 46 ; 32. ten Bokkel Huinink, Van der Burg M, . Van Oosterom A., Neijy J. P., George M., Guastalla J. P., Veenhof C. H., Rotmensz N., Dalesio O. and Vermoken J. B.: Carboplatin in combination therapy for ovarian cancer. Cancer Treat Rev 15, 9-15 1988 ; 33. ten Bokkel Huinink W.W., Eisenhauer E. and Swenerton K.: Preliminary evaluation of a multicenter, randomized comparative study of Taxol. Carboplatin injection site HE EFFECTS OF thyroid hormone TH ; are dependent on the quantity of the hormone that reaches peripheral tissues and the availability of unaltered TH receptors in cell nuclei. Several classes of TH membrane transporters with different kinetics and substrate preferences have been identified that belong to different families of solute carriers, including organic anions organic anion transporting polypeptides, OATP ; , amino acids, and monocarboxylate transporters MCT ; 15 ; . Their characteristics in terms of tissue distribution and kinetics, as well as the binding of other possible ligands, provide them with potentially distinctive roles in the fine tuning of organ-specific TH availability. Until recently, the physiological role of TH membrane transporters has remained elusive. The identification of patients with mutations in the X-linked TH transporter, monocarboxylate transporter 8 MCT8 ; , has revealed the role played by this transmembrane carrier in the intracellular availability of TH. Hemizygous MCT8-deficient males present a syndrome with two components: a thyroid defect increased total and free serum T3 and decreased.

Taxol carboplatin cisplatin Band together, call City Hall. The transit contact is Alex Armstrong at 828-3702. The more people that make their needs known the more likely we will get some results. I spoke with Heather Archer at People in Motion. They have a 16-passenger bus for their members' use, but it is only used for group outings. So there are many people of all ages who are dependent on wheelchairs that cannot go out to dinner or to a late movie. I friends with a family here in town whose 29year-old son broke his neck last June and as a result is a paraplegic he has never looked back his return home is awe-inspiring. The B.C. Paraplegic Association wants him to try to organize some paraplegic games. He was very involved in Vancouver and loves the idea. This is, after all, the Tourna. Corepressors have also been directly implicated in negative transcriptional regulation by WT TR. Tagami et al. 35 ; have observed that with negatively regulated promoters, cotransfected corepressor SMRT or NCoR ; augments basal promoter activation by unliganded TR. When tested in transfection assays, we found that the unliganded R383H mutant activated a negatively regulated promoter and repressed a positively regulated reporter gene comparably to WT receptor, although, in both contexts, T3-induced changes--either reversal of unliganded activation or relief of silencing--were impaired. We hypothesized that both these effects might reflect altered R383Hcorepressor interaction, and indeed the mutant receptor dissociated less readily from SMRT than WT receptor Fig. 4a ; . Furthermore, when tested as a heterodimer bound to TREs, the corepressor release by the R383H mutant was impaired on both negative and positive response elements. Accordingly, our data suggest that another receptor region distinct from the C-terminal amphipathic -helix is involved in corepressor release, although the structural basis for this remains to be elucidated. In a previous study, which tested the functional properties of artificial mutants generated by systematically mutating residues containing CpG dinucleotides within the `cold' region of the TR gene, the R383H mutant was predicted not to cause RTH because, when tested with positively regulated reporter genes, its transcriptional impairment was less than that observed with even comparatively mild RTH mutants 15 ; , and another mutant R429Q ; was also predicted not to be involved in RTH on the same basis. However, both of these mutations have now been identified in association with RTH, and all affected individuals exhibited elevated serum thyroid hormones with nonsuppressed TSH levels 36, 46, 48 ; , suggesting that they might manifest by impairing negative feedback regulation at hypothalamic and pituitary levels. In the crystal structure of TR , the residue homologous to Arg 383 interacts with another arginine, which corresponds to Arg 429 in TR . Accordingly, it is intriguing that a naturally occurring RTH mutant involving this residue R429Q ; exhibits many functional similarities with R383H. Two groups have shown that the R429Q mutant exhibits greater functional impairment with negatively regulated than positively regulated promoters 36, 46 ; , as we have documented with the R383H mutant. However, our studies do not exclude the possibility that, in different promoter or cell type contexts, these mutants can exhibit slightly impaired transactivation as has been observed 8, 15 ; . We have also found that the R429Q mutant receptor is impaired for corepressor release in vitro and T3-dependent relief of silencing in vivo. Furthermore, with either mutant, these properties are not explicable on the basis of their T3 binding, as the R383H mutation results in a mild reduction in ligand-binding affinity, and the R429Q mutant binds ligand with wild-type affinity, and ligand and carmustine. Carboplatin chemotherapy for dogs Potassium citrate--to increase citrate excretion Struvite stones Treatment of infection is mandatory and may be needed in the long term Acetohydroxamic acid, a urease inhibitor, has been shown to reduce the urinary saturation of struvite but is associated with high frequency of side effects deep vein thrombosis, haemolytic anaemia ; , which limits its use Cystine stones Treatment must include increasing urine output to about 3 l day and adequate alkalinisation urine pH 7.0 ; with potassium citrate In addition, specific agents such as mercaptopropionylglycine or d-penicillamine that form soluble complexes with cystine are used.

The authors also studied the result of platinum and cyclophosphamide treatment according to the result of surgery. From 103 patients whose result of surgery was clearly recorded, 80 patients 77.7% ; had optimal surgery and 23 22.3% ; had suboptimal surgery. The overall RR, 5-year PFS, and 5-year SVR of the patients in whom optimal surgery was achieved were statistically significantly higher than those patients who had suboptimal surgery Table 3 ; . The PFS and SVR of patients who had optimal and suboptimal surgery are shown in Fig. 3 and 4 respectively. Discussion The benefit of platinum as a single agent or as combination chemotherapy for the treatment of EOC has long been recognized for decades. The Advanced Ovarian Cancer Trialists' Group by Aabo et al reported a meta-analysis study regarding the role of platinum in the treatment of advanced ovarian cancer 14 ; . The quantitative review using individual data of 5, 667 patients from 37 available randomized trials was performed. The authors made three conclusions. First of all, the results suggested that platinum based treatment was better than non-platinum regimens in terms of survival. Secondly, platinum in combination with other chemotherapeutic drug was better than single agent platinum when used at the same dose. Finally, cisplatin and carboplatin were equally effective. The combination of platinum and cyclophosphamide is one of the most common chemotherapy regimens used for EOC. Its efficacy is reported to be better than melphalan or intraperitoneal P-32 in terms of 5-year disease-free survival DFS ; and 5-year SVR 3 ; or single agent cyclo and carteolol. VEGF pathway to inhibit angiogenesis, combining either of these with chemotherapy regimens may increase the vascular toxicity profile. The TSP-1 mimetic ABT-510 is an endogenous angiogenesis inhibitor that, when combined with a chemotherapeutic schedule, does not appear to increase vascular and thromboembolic toxicity. Of interest is the question of whether endogenous angiogenesis inhibitors such as TSP-1 and angiostatin added to chemotherapy result in less frequent adverse vascular and thromboembolic events when compared with combinations in which the VEGF pathway is inhibited. There are preliminary data from a small phase II study in patients with NSCLC in which angiostatin was added to carboplatin and paclitaxel [24]. This combination was active in NSCLC patients and was well tolerated; only three of the 24 patients enrolled developed thromboembolic complications. More combination studies with endogenous angiogenesis inhibitors are needed to investigate their antitumor potential and define the toxicity profile. In the present study, pharmacokinetics of ABT-510, gemcitabine and cisplatin as single agents were similar to those reported in previous studies. The lack of pharmacokinetic interaction observed in this study is consistent with the different disposition pathways involved in the elimination of ABT-510, gemcitabine and cisplatin. Three of 12 assessable patients with various tumor types experienced PRs. Based on previous phase I data, several phase II trials have already been initiated in NSCLC, lymphoma, sarcoma and renal cell cancer patients with single-agent ABT-510 regimens or ABT-510 in combination with a cytostatic regimen. Any antitumor activity of combination treatment with ABT-510 needs to be explored in randomized phase II and III studies. In conclusion, a regimen of SC twice daily doses of 50 or 100 mg ABT-510 in combination with 1250 mg m2 gemcitabine on days 1 and 8 and 80 mg m2 cisplatin on day 1 can be given i.v. in a 3-week cycle with acceptable toxicity. No significant pharmacokinetic interactions were observed. Further phase II and III studies are warranted to evaluate the safety and efficacy of this combination in the treatment of advanced solid tumors.

91; 12] similarly, when carboplatin 450 mg m² was administered on day 1, the incidence of grade 3 and grade 4 leukopenia and thrombocytopenia was 8% and 11%, respectively and cefazolin. Non-resectable localized non-small cell lung cancer NSCLC ; . Lung Cancer 2000; 27: 145157. Lokich J, Anderson N. Paclitaxel hypersensitivity reactions: a role for docetaxel substitution. Ann Oncol 1998; 9: 573. Moon C, Verschraegen CF, Bevers M et al. Use of docetaxel Taxotere ; in patients with paclitaxel Taxol ; hypersensitivity. Anticancer Drugs 2000; 11: 565568. Mattson KV, ten Velde G, Krofta K et al. Taxotere as neoadjuvant therapy for radically treatable stage III NSCLC. Preliminary results of an international phase III study. Proc Soc Clin Oncol 2000; 19: 483a Abstr 1890 ; . Mattson K, Abratt R, ten Velde G et al. Docetaxel as neo-adjuvant therapy for radically treatable stage III non-small cell lung cancer: early results of an international phase III study. Lung Cancer 2001; 34 Suppl 4 ; : 2123. Moussa MA. Planning the size of survival time clinical trials with allowance for stratification. Stat Med 1988; 7: 559569. Amat S, Bougnoux P, Penault-Llorca F et al. Primary chemotherapy for operable breast cancer: high pathological response rate induced by docetaxel. Proc Soc Clin Oncol 2000; 19: 128a Abstr 500 ; . Gradishar WJ, Loh K, Erban J et al. Docetaxel as neoadjuvant chemotherapy in patients with stage III breast cancer. Oncology 1997; 11 Suppl 8 ; : 1518. Hutcheon AW, Ogston KN, Heys SD et al. Primary chemotherapy in the treatment of breast cancer: significantly enhanced clinical and pathological response with docetaxel. Proc Soc Clin Oncol 2000; 19: 83a Abstr 317 ; . Komaki R, Scott CB, Sause WT et al. Induction cisplatin vinblastine and irradiation vs. irradiation in unresectable squamous cell lung cancer: failure patterns by cell type in RTOG 88-08 ECOG 4588. Radiation Therapy Oncology Group. Eastern Cooperative Oncology Group. Int J Radiat Oncol Biol Phys 1997; 39: 537544. Sause W, Kolesar P, Taylor S et al. A. Five-year results; phase III trial of regionally advanced unresectable non-small cell lung cancer, RTOG 8808, ECOG 4588, SWOG 8992. Proc Soc Clin Oncol 1998; 17: 453a Abstr 1743 ; . Le Chevalier T, Arriagada R, Quoix E et al. Radiotherapy alone versus combined chemotherapy and radiotherapy in nonresectable non-smallcell lung cancer: first analysis of a randomized trial in 353 patients. J Natl Cancer Inst 1991; 83: 417423. Griesinger F, Baum RP, Paul J et al. Correlation of metabolic and morphometric tumor response after induction chemotherapy with docetaxel D ; and carboplatin C ; in stage III NSCLC. Proc Soc Clin Oncol 2000; 19: 548a Abstr 2160 ; . Betticher DC, Hsu Schmitz SF, Gauthier Y et al. Neoadjuvant chemotherapy with docetaxel DOC, Taxotere ; and cisplatin CIS ; in patients pts ; with non-small cell lung cancer NSCLC ; , Stage IIIA, N2 is highly active with few toxicities. Proc Soc Clin Oncol 1999; 18: 473a Abstr 1824 ; . Katakami N, Okazaki M, Nishimura T et al. Phase II trial of induction carboplatin CAR ; and docetaxel DOC ; with concurrent radiation RT ; in early-stage non-small cell lung cancer NSCLC ; . Proc Soc Clin Oncol 2000; 19: 524a Abstr 2060 ; . Nishimura T, Ikeda A, Katakami N et al. Phase II study of induction carboplatin CAR ; and docetaxel DOC ; with concurrent thoracic radiation CTRT ; followed by surgical resection in stage IB, IIA and IIB non-small cell lung cancer NSCLC ; . Proc Soc Clin Oncol 2001; 20: 254b Abstr 2767.

University of Chicago Hospitals 5841 S. Maryland Avenue, MC 4076 Chicago, IL 60637 Ph: 773.702.2394 University of Illinois at Chicago Medical Center 840 S. Wood Street, MC 787 Chicago, IL 60612-7323 Ph: 312.996.3800 Treatment with a compound that promises to extend the life span will start at an age of less than 65, because it may take more than 30 years to begin having a beneficial effect. Because our and ceftriaxone. Carey LA et al. Race, breast cancer subtypes, and survival in the Carolina Breast Cancer Study. JAMA 2006; 295 21 ; : 2492-502. Abstract Geyer CE et al. A phase III randomized, open-label, international study comparing lapatinib and capecitabine vs capecitabine in women with refractory advanced metastatic breast cancer EGF100151 ; . Proc ASCO 2006. No abstract available Kim C et al. Trastuzumab sensitivity of breast cancer with co-amplification of HER2 and cMYC suggests pro-apoptotic function of dysregulated cMYC in vivo. Presentation. San Antonio Breast Cancer Symposium 2005; Abstract 46. Perou CM et al. Molecular portraits of human breast tumours. Nature 2000; 406 6797 ; : 74752. Abstract Slamon D et al, on behalf of the BCIRG 006 Investigators. Phase III randomized trial comparing doxorubicin and cyclophosphamide followed by docetaxel AC T ; with doxorubicin and cyclophosphamide followed by docetaxel and trastuzumab AC TH ; with docetaxel, carboplatin and trastuzumab TCH ; in HER2 positive early breast cancer patients: BCIRG 006 study. Presentation. San Antonio Breast Cancer Symposium 2005; Abstract 1. Srlie T et al. Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proc Natl Acad Sci USA 2001; 98 19 ; : 10869-74. Abstract and carboplatin.

Figure 1. Treatment plan double high-dose protocol. anumber of patients; bno carboplatin in five patients and celestone.

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