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Modulation of Paclitaxel Antitumor Effects by Calcitriol: Preclinical and Clinical Studies of Mechanisms, Toxicity, and Efficacy in Prostate Cancer Calcitriol vitamin D ; has been shown to inhibit the growth of normal and cancerous cells in a variety of solid tumor model systems. It has also been shown to inhibit prostate cancer growth in the laboratory. However, administration of calcitriol for the treatment of cancer has been shown to increase blood calcium, which is very toxic. In an effort to develop a new treatment approach for prostate cancer, Dr. Donald Trump and his team formerly at the University of Pittsburgh and now at Roswell Park Cancer Institute RPCI ; , tested the combination of calcitriol and paclitaxel Taxol ; in a dose escalation phase 1 CT in patients with advanced prostate cancer. Paclitaxel is a chemotherapeutic agent that has been shown to be effective against ovarian and advanced breast cancers and shows great potential for the treatment of prostate cancer. While an MTD was not reached, escalation was completed through 38 g calcitriol daily for 3 days weekly + 80 mg sqm paclitaxel weekly. While myelosuppression was observed, no serum calcium levels greater than 11 mg dL were observed. The synergism of this combined therapy in preclinical models is important as it offers the potential for the enhancement of a potent antitumor agent paclitaxel ; with what appears to be a very safe regimen of calcitriol. The CT suggests that paclitaxel may reduce the potential for calcitriol-induced hypercalcemia, as the weekly total dose of calcitriol in this trial is almost 12x the usual weekly dose of oral calcitriol. The addition of paclitaxel enhances cell killing by calcitriol, while limiting calcium levels in the blood. The FDA has now approved docetaxel Taxotere ; , which like paclitaxel is a taxoid drug, for the treatment of men with androgenindependent prostate cancer. Additionally, Dr. Trump and colleagues at RPCI with the National Cancer Institute NCI ; sponsorship are conducting a phase 2 study of calcitriol and dexamethasone in patients with early, recurrent prostate cancer after prior radical prostatectomy or radiotherapy as well as studies of calcitriol administered intravenously either with docetaxel or gefitinib Iressa ; . Part of this research was made possible with funding from an FY97 PCRP Idea Development Award. Daily 1 alpha ; -OH-D 2 ; in Hormone Refractory Prostate Cancer Assessment of Clinical and Biochemical Effects 1 alpha ; -OH-D 2 ; doxercalciferol ; is a synthetic derivative of vitamin D that has been shown to inhibit the growth of cancer but with less of an effect on increasing calcium levels in the blood. Dr. Howard Bailey and researchers at the University of Wisconsin have been testing doses of doxercalciferol in prostate cancer patients. In Phase 1 of this trial, the safe dose of doxercalciferol in patients with hormone refractory prostate cancer was determined to be 12.5 g per day. Using this dose, the Phase 2 study showed that 6 of 26 patients with hormone refractory prostate cancer had stable disease for longer than 6 months. Toxicity was minimal except for a few cases of hypercalcemia and increased creatinine levels. Currently, an NCI Phase 2 randomized study comparing docetaxel alone versus docetaxel plus doxercalciferol in patients with localized prostate cancer is ongoing at the University of Wisconsin. Part of this research was made possible with funding from an FY97 PCRP Idea Development Award.
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Motion of an air bubble rising through water as it interacts with a wall of variable inclination. The bubble diameter varies about O 1 ; mm. We use lubrication theory to determine the modification of the bubble interface and compute the hydrodynamic force exerted by the wall. The present work is an extension of Moraga et al's model [Computers and Fluids 2006], which was devised for a horizontal wall. The predictions of the model are checked against experimental visualizations. The influence of the Weber number, Reynolds number and wall inclination is examined.
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[1] Struber M, Cremer J, Gohrbandt B, Hagl C, Jankowski M, Volker B, Ruckoldt H, Martin M, Haverich A. Human cytokine responses to coronary artery bypass grafting with and without cardiopulmonary bypass. Ann Thorac Surg 1999; 68 4 ; : 13301335. [2] Gu YJ, Mariani MA, van Oeveren W, Grandjaen JG, Boonstra PW. Reduction of the inflammatory response in patients undergoing minimally invasive coronary artery bypass grafting. Ann Thorac Surg 1998; 65: 420424. [3] Behnke H, Cornelissen J, Kahl M, Moller F, Cremer J, Wulf H. Postoperative pain therapy in minimally invasive direct coronary arterial and irinotecan.
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Response to Ang II challenge of Rho kinase and plasminogen activator inhibitor-1 PAI-1 ; [17], and by the reduced gene and protein expression of the upstream regulator of RhoA, p115RhoGEF [18]. The down-regulation of Rho Rho kinase pathway occurred in a context of the increased level of the endothelial subunit of NO synthase eNOS ; mRNA alongside elevated urinary NO metabolites and cGMP levels [19, 20]. Therefore, the reduced peripheral resistance, vascular hyporeactivity and normohypotension typical of BS GS patients and their collection of biochemical characteristics present a mirror image of those found in hypertension. In addition, the BS GS patients' unchanged level of CRP and other inflammatory mediators included VCAM, ICAM, IL-6 and TNF-a [9], whose expression is known to be dependent of NFkB activity, also provide, in a human model of altered vascular tone regulation, confirmatory data in support of a relationship between inflammation and hypertension. In fact, evidence has been recently provided for the involvement of Rho Rho-kinase signalling in CRP-induced atherothrombogenesis. CRP has been shown to activate Rho Rho-kinase signalling, which through activation of NFkB activity results in PAI-1 expression, a known atherothrombogenic factor [21]. One possible mechanism for the CRP-mediated activation of NFkB is through the RhoA-induced phosphorylation of the inhibitory subunit of NFkB IkB ; [22] and the activation of IkB kinase by Rho kinase [23]. Relevant to this mechanism, we have preliminary data that show, in BS GS patients compared with normotensive healthy subjects, an increased expression of IkB, while NFkB is unchanged; this is in keeping with a ` reduced activity of NFkB L.A. Calo and E. Pagnin, personal observation ; . In conclusion, the overall clinical, biochemical and molecular picture of BS GS may contribute to an understanding in humans of the pathophysiological mechanisms linking inflammation, hypertension and longterm complication such as cardiovascular remodelling and atherogenesis.
Biochemical characteristics of the joint fluid. Separation culture of for histologically Gynther, 1998 ; . The immunohistochemical staining was the disc cells was established in rabbit model and the preriminarypefreusnatiboesorI1 adTN-t.nrsls, herhocpc and In report presented in JADR meeting in 1998. The separation culture of perormed scor 2. as42.Teewsnihr the disc cells are effective method for evaluation of correlation each other nor with the concentration levels of cytokines of TMJ disc. The differences of matrix synthesis between superficial significant in synovial fluid. Histologically, there were several degrees of increased blood and deep layers of the disc were clarified. The disc cells in vessels and redundancy of the synovial layer. The majority of immunohistosuperficial layer were characterized as fibrous tissues and deep as cartilagenous expressions. The authors will present the results of chemical stainings demonstrated the strong expression in the superficial synovial metabolic characteristics of the cells in each layer of the disc teicrsd discuss with the relationships between hetrogeneity of the disc and of vsuaiysest lyasaiiatrl nptoeei fTJsnvts synovial fluid function and isdn.
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Specific references to the Plan provisions on which the decision is based. Docket Entry No. 65, Ex. A-1 at 66 ; . In the October 25, 2004 EOB, Acordia did not finally deny the claim. Instead, the EOB stated that the denial was only until information from "doctor to determine preexisting conditions" had been received. Id. ; . Galvan did not receive notice when additional information was received, when a further review was conducted, or when the claim was denied. In November 2004, Acordia asked Terry Mace, R.N., an internal medical reviewer, to determine whether Galvan's condition was preexisting and excluded from coverage. Docket Entry No. 65, Ex. D at 1 ; Mace reviewed the claim and information that Acordia had received in response to the requests it had sent. In addition to the admitting diagnosis code and the principal diagnosis code that were on the St. Luke's claim documents, Mace also reviewed information about Galvan from Cardio Vascular Care, from Dr. Sartori, and from Dr. Susan Burgert. Their responses to Acordia's requests for information showed the following: Galvan had been seen by Dr. Susan Burgert at St. Luke's hospital on November 27, 2003. Dr. Burgert's consultation notes described Galvan as a "diabetic patient with severe vascular disease." According to Dr. Burgert, Galvan suffered from diabetes, peripheral vascular disease, and coronary heart disease. She had had "bilateral lower.
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Balana ME, Labriola L, Salatino M, Movischoff F, Peters G, Charreau E & Elizalde PV 2001 Activation of ErbB-2 via a hierarchical interaction between ErbB-2 and type I insulin-like growth factor receptor in mammary tumour cells. Oncogene 20 3447. Baselga J, Albanell, Ruiz A, Gascon P & Guillen V 2003 Phase II and tumour pharmacodynamic study of gefitinib `Iressa' ZD1839 ; in patients with advanced breast cancer. Proceedings of the American Society for Clinical Oncology. 37 Abs 24. Biscardi JS, Maa M-C, Tice DA, Cox ME, Leu T-H & Parsons SJ 1999 C-Src-mediated phosphorylation of the epidermal growth factor receptor on Tyr845 and Tyr1101 is associated with modulation of receptor function. Journal of Biological Chemistry 274 83358343. Camirand A, Zakikhani M, Young F & Pollak M 2005 Inhibition of insulin-like growth factor-1 receptor signalling enhances growth-inhibitory and proapoptotic effects of gefitinib Iressa ; in human breast cancer cells. Breast Cancer Research 7 R570R579. Cappuzzo F, Toschi L, Tallini G, Ceresoli GL, Domenichini I, Bartolini S, Finocchiaro G, Magrini E, Metro G, Canecellieri A et al. 2006 Insulin-like growth factor 1 IGFR-1 ; is significantly associated with longer survival in non-small cell lung cancer patients treated with gefitinib. Annals of Oncology 17 11201127. Chakravati A, Loeffler JS & Dyson NJ 2002 Insulin-like growth factor receptor I mediates resistance to antiepidermal growth factor receptor therapy in primary human glioblastome cells through continued activation of phosphoinositide 3-kinase signalling. Cancer Research 62 200207. Chan KC, Knox WF, Gee JM, Morris J, Nicholson RI, Potten C & Bundred NJ 2002 Effect of epidermal growth factor receptor tyrosine kinase inhibition on epithelial proliferation in normal and pre-malignant breast. Cancer Research 62 122128. Ciardiello F & Tortora G 2001 A novel approach in the treatment of cancer: targeting the epidermal growth factor receptor. Clinical Cancer Research 7 29582970. Ciardiello F, Caputo R, Bianco R, Damiano V, Pomatico G, De Placido S, Bianco AR & Tortora G 2000 Antitumour effect and potentiation of cytotoxic drugs activity in human cancer cells by ZD1839 Iressa ; , an epidermal growth factor receptor-selective tyrosine kinase inhibitor. Clinical Cancer Research 6 20532063. Coppola D, Ferber A, Miura M, Sell C, D'Ambrosio C, Rubin R & Baserga R 1994 A functional insulin-like growth factor I receptor is required for the mitogenic and transforming activities of the epidermal growth factor receptor. Molecular and Cellular Biology 14 45884595. Gee JMW, Gutteridge E, Robertson JF, Wakeling AE, Jones HE & Nicholson RI 2004 Biological markers during early treatment of tamoxifen-resistant breast cancer with gefitinib `Iressa' ; . Breast Cancer Research and Treatment 88 Suppl 1 ; S32. Abs 307. Gee JMW, Robertson JF, Gutteridge E, Ellis IO, Pinder SE, Rubini M & Nicholson RI 2005 Epidermal growth factor receptor HER2 insulin-like growth factor receptor signalling and oestrogen receptor activity in clinical breast cancer. Endocrine-Related Cancer 12 Suppl 1 ; S99S111. Gilmore AP, Valentijn AJ, Wang P, Ranger AM, Bundred N, O'Hare MJ, Wakeling A, Korsmeyer SJ & Streuli CH 2002 Activation of BAD by therapeutic inhibition of epidermal growth factor receptor and transactivation by insulin-like growth factor receptor. Journal of Biological Chemistry 277 2764327650. Goetsch L, Gonzalez A, Leger O, Beck A, Pauwels PJ, Haeuw JF & Corvaia N 2005 Recombinant humanized anti-insulin-like growth factor receptor type I antibody h7C10 ; enhances the antitumor activity of vinorelbine and anti-epidermal growth factor receptor therapy against human cancer xenografts. International Journal of Cancer 113 316328. Gullick WJ 2001 The type 1 growth factor receptors and their ligands considered as a complex system. EndocrineRelated Cancer 8 7582. Gutteridge E, Gee JMW, Nicholson RI & Robertson JFR 2004 Biological markers associated with response to gefitinib `IRESSA' ; in patients with breast cancer. Proceedings of the American Society of Clinical Oncology. 38 Abs 648. Hofmann F & Garcia-Echeverria C 2005 Blocking the insulin-like growth factor-I receptor as a strategy for targeting cancer. Drug Discovery Today 10 10411047. Hutcheson IR, Knowlden JM, Barrow D, Gee JMW, Wakeling AE & Nicholson RI 2003 Heregulin-induced AKT activation promotes growth of gefitinib `Iressa', ZD1839 ; -treated, tamoxifen-resistant breast cancer cells. Breast Cancer Research and Treatment 82 Suppl 1 ; S170. Abs 1008. Jones HE, Dutkowski CM, Barrow D, Harper ME, Wakeling AE & Nicholson RI 1997 New EGFR selective tyrosine kinase inhibitor reveals variable growth responses in prostate cancer cell lines PC-3 and DU145. International Journal of Cancer 71 10101018. Jones HE, Goddard L, Gee JMW, Hiscox S, Rubini M, Barrow D, Knowlden JM, Williams S, Wakeling AE & Nicholson RI 2004 Insulin-like growth factor-1 receptor signalling and acquired resistance to gefitinib ZD1839; Iressa ; in human breast and prostate cancer cells. Endocrine-Related Cancer 11 122. Jones HE, Gee JMW, Taylor KM, Barrow D, Williams HD, Wakeling AE, Holloway B, Tonge D, Rubini M & Nicholson RI 2005 Development of strategies for the use of anti-growth factor treatments. Endocrine-Related Cancer 12 Suppl 1 ; S173S182. Jones HE, Gee JMW, Barrow D, Holloway B, Tonge D & Nicholson RI 2006a Maintenance of EGFR phosphorylation by the IGF-1R in the presence of gefitinib in lung cancer cells: co-targeting the EGFR and IGF-1R maximises anti-tumour effects. Proceedings of the 4th.
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From the Amaurosis Fugax Study Group: Henry J. M. Bamett, MD, The John P. Roberts Research Institute, London, Canada; Eugene F. Bernstein, MD, PhD, Chairman, Amaurosis Fugax Study Group ; , Division of Vascular and Thoracic Surgery, Scripps Clinic and Research Foundation, La Jolla, California; Allan D. Callow, MD, PhD, Department of Surgery, Tufts University New England Medical Center, Boston, Massachusetts; Louis R. Caplan, MD, Department of Neurology, Tufts University, Boston, Massachusetts; John E. Carter, MD, Division of Neurology and Ophthalmology, The University of Texas Medical School, San Antonio, Texas; Donald J. Dalessio, MD, Department of Medicine, Scripps Clinic and Research Foundation, La Jolla, California; Ralph B. Dilley, MD, Division of Vascular and Thoracic Surgery, Scripps Clinic and Research Foundation, La Jolla, California; J. Donald Easton, MD, Department of Neurology, Brown University, Providence, Rhode Island; William K. Ehrenfeld, MD, Department of Surgery, University of California, San Francisco, San Francisco, California; William S. Fields, MD, Department of Neurooncology, The University of Texas System Cancer Center, Houston, Texas; Jean-Claude Gautier, Professor of Neurology, Service d'Urgences Cerebrovasculaires, Hopital de la Salpetriere, Paris, France; Laurence A. Harker, MD, Division of Hematology, Emory University School of Medicine, Atlanta, Georgia; Michael J. G. Harrison, DM, FRCP, The Reta Lila Weston Institute for Neurological Studies, University of London, London, United Kingdom; Sohan S. Hayreh, MD, PhD, Department of Ophthalmology.
Cause for the synergistic pro-apoptotic effect with no or only minimal involvement of the mitochondrial route of apoptosis. When cells were subsequently analyzed for expression of cFLIPL, an important regulator of caspase 8 processing, a marked down regulation in both Jurkat.EGFRvIII and A431 cells was observed within 3 h of combination treatment with scFv425: sTRAIL and Iressa. Down-regulation of cFLIPL coincides with caspase 8 activation and was preceded by inactivation of the PI3K pathway in Jurkat.EGFRvIII cells. In A431 cells, combination treatment significantly inhibited MAPK-signaling but only to the level observed for treatment with Iressa alone. Based on these results, it can be concluded that the synergistic pro-apoptotic effect largely depends on the specific down-regulation of cFLIPL. For EGFRvIII positive Jurkat cells, down-regulation of cFLIPL is a consequence of PI3K inhibition. In A431 cells, MAPK dephosphorylation may play a role but the exact mechanism remains to be further elucidated. In conclusion, we report for the first time on a recombinant fusion protein that combines the tumoricidal effect of EGFR-signal inhibition with target cell-restricted apoptosis induction. The unique characteristics of scFv425: sTRAIL described here indicate its potential therapeutic value, alone and in combination with EGFR tyrosine kinase inhibitor Iressa, for the treatment of EGFR and EGFRvIII expressing human cancers and kaon.
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| Iressa sideFunctional ABCG2 show only a low rate of increase in fluorescence. By applying the specific ABCG2 inhibitor, Ko143, the Hoechst 33342 dye extrusion activity of ABCG2 can be quantified 46 ; . This assay is very sensitive and allowed the detection of functional endogenous ABCG2 even in control A431 cells Fig. 1B, Ctrl A431 ; . However, in the ABCG2 G2 ; expressing cells, a much greater Hoechst 33342 extrusion activity was seen, which was further augmented after mitoxantrone selection of the transduced A431 G2MX ; cells. In contrast, the catalytic site mutant, ABCG2K86M, possessed even less Hoechst 33342 transport activity than the A431 control cells. This is likely due to the overexpressed mutant protein, which may form a dominant-negative heterodimeric complex with endogenous ABCG2. In conclusion, we have created A431 cell lines expressing differing levels of transportcompetent ABCG2 as well as its inactive mutant form, ABCG2K86M. In the following experiments, we studied if the overexpression of ABCG2 conferred a survival advantage to A431 cells exposed to Iressa. As shown in Fig. 2A, we compared the effects of Iressa on cell survival of A431 cells over a 48-hour period of exposure to various concentrations of Iressa 50-500 nmol L ; . Cells were treated with Iressa and then plated for following cell growth in the surface-attached cell populations. As shown, low concentrations and iressa.
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