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No. of Patients Entered Completed and Withdrawals 34 28 Completed 1 round of low and high doses for each medication ; 6 Withdrawals not related to study drugs 1. Dighiero, G., Maloum, K., Desablens, B., Cazin, B., Navarro, M., Leblay, R., Leporrier, M., Jaubert, J., Lepeu, G., Dreyfus, B., Binet, J. L., and Travade, P. Chlorambucil in indolent chronic lymphocytic leukemia. French Cooperative Group on Chronic Lymphocytic Leukemia. N. Engl. J. Med., 338: 1506 1514, Keating, M. J., O'Brien, S., Lerner, S., Koller, C., Beran, M., Robertson, L. E., Freireich, E. J., Estey, E., and Kantarjian, H. Longterm follow-up of patients with chronic lymphocytic leukemia CLL ; receiving fludarabine regimens as initial therapy. Blood, 92: 1165 1171, Rai, K. R., Peterson, B. L., Appelbaum, F. R., Kolitz, J., Elias, L., Shepherd, L., Hines, J., Threatte, G. A., Larson, R. A., Cheson, B. D., and Schiffer, C. A. Fludarabine compared with chlorambucil as primary therapy for chronic lymphocytic leukemia. N. Engl. J. Med., 343: 1750 1757, Panasci, L., Paiement, J-P., Christodoulopoulos, G., Belenkov, A., Malapetsa, A., and Aloyz, R. Chlorambucil drug resistance in chronic lymphocytic leukemia: the emerging role of DNA repair. Clin. Cancer Res., 7: 454 461, Beigleiter, A., Mowat, M., Israels, L. G., and Johnston, J. B. Chlorambucil in chronic lymphocytic leukemia: mechanism of action. Leuk. Lymphoma, 23: 187201, 1996. Zinzani, P. L., Bendandi, M., Magagnoli, M., Albertini, P., Rondelli, D., Stefoni, V., Tani, M., and Tura, S. Long-term follow-up after fludarabine treatment in pretreated patients with chronic lymphocytic leukemia. Haematologica, 85: 11351139, 2000. McLaughlin, P., Hagemeister, F. B., Romaguera, J. E., Sarris, A. H., Pate, O., Younes, A., Swan, F., Keating, M., and Cabanillas, F. Fludarabine, mitoxantrone, and dexamethasone: an effective new regimen for indolent lymphoma. J. Clin. Oncol., 14: 12621268, 1996. Huang, P., Chubb, S., and Plunkett, W. Termination of DNA synthesis by 9- a mechanism for cytotoxicity. J. Biol. Chem., 265: 1661716625, 1990. Yang, S. W., Huang, P., Plunkett, W., Becker, F. F., and Chan, J. Y. Dual mode of inhibition of purified DNA ligase I from human cells by 9- triphosphate. J. Biol. Chem., 267: 23452349, 1992. Huang, P., and Plunkett, W. Fludarabine- and gemcitabine- induced apoptosis: incorporation of analogs into DNA is a critical event. Cancer Chemother. Pharmacol., 36: 181188, 1995. Huang, P., Robertson, L. E., Wright, S., and Plunkett, W. High molecular weight DNA fragmentation: a critical event in nucleoside analogue-induced apoptosis in leukemia cells. Clin. Cancer Res., 1: 10051013, 1995. Robertson, L. E., Chubb, S., Meyn, R. E., Story, M., Ford, R., Hittelman, W. N., and Plunkett, W. Induction of apoptotic cell death in chronic lymphocytic leukemia by 2-chloro-2 -deoxyadenosine and 9- D-arabinosyl-2-fluoroadenine. Blood, 81: 143150, 1993. Plunkett, W., Gandhi, V., Huang, P., Robertson, L. E., Yang, L-Y., Gregoire, V., Estey, E., and Keating, M. J. Fludarabine: pharmacokinetics, mechanism of action, and rationales for combination therapies. Semin. Oncol., 20: 212, 1993. Huang, P., Sandoval, A., van den Neste, E., Keating, M. J., and Plunkett, W. Inhibition of RNA transcription: a biochemical mechanism of action against chronic lymphocytic leukemia cells by fludarabine. Leukemia Baltimore ; , 14: 14051413, 2000. Sandoval, A., Consoli, U., and Plunkett, W. Fludarabine-mediated inhibition of nucleotide excision repair induces apoptosis in quiescent human lymphocytes. Clin. Cancer Res., 2: 17311741, 1996. Chaney, S. G., and Sancar, A. DNA repair: enzymatic mechanisms and relevance to drug response. J. Natl. Cancer Inst., 88: 1346 1360.

Entire nursing home system, the study minimizes the threats to external validity of observational studies restricted to a single institution or a limited period of time. Second, by permitting access to a complete population, comprehensive administrative data sources provide opportunities to select controls that are either representative of a sample population or closely comparable with cases 32 ; . In this study, we have emphasized the objective of maximizing the comparability of cases and controls. Controls were drawn from the sample population matched to cases on known potential confounding characteristics, and the method of measuring injurious falls and medication exposure was equivalent in cases and controls 33 ; . Conversely, there are potential limitations of these secondary data, primarily associated with the validity of measurement in three domains: the measurement of medication exposure, the ascertainment of injurious falls, and the measurement of chronic conditions. First, measurement of medication exposure in this study was based on the proxy indicator of a dispensed prescription. While this approach has been used by other studies 3-4, 10 ; , these data do not measure the actual administration of medication. Given the frequent use of "provide as needed" instructions in the administration of psychoactive medications, there is the potential for misclassification of drug exposure in this study. We would argue that the effect of this misclassification would be to bias odds ratio estimates toward the null and therefore suggest that the findings reported in this study represent conservative estimates of the magnitude of risk associated with the use of these agents.

Over 120 min at 37C. Rather than being completely conserved over 1 h, a large degree of isoform-dependent variability in remaining activity 39 110% at 120 min ; was observed. CYP2D6, which is responsible for catalyzing the majority of bufuralol metabolism, was the least stable of the enzymes studied. After a 120-min incubation, formation of 1 -hydroxybufuralol was at approximately 20 to 44% of control. This decrease in activity was observed whether the liver microsomes were preincubated with NADPH and no substrate protocol A ; or with substrate present and no NADPH protocol B ; . The initial increase in activity observed in HL-1057-2 with incubation time may be attributable to this lot containing a variant form of CYP2D6 not present in the other lots; however, this phenomenon was not probed further. We were able to block the lability observed in the presence of NADPH by including the ROS scavengers SOD and CAT in the incubation. These results would seem to indicate that although ROS play a role in the degradation of CYP2D6, as has been reported previously for P450 enzymes Goasduff and Cederbaum, 1999 ; , they cannot be the only contributors, as is evident in the loss of CYP2D6 activity in the absence of NADPH. Heme oxygenase has also been shown to play a role in CYP2D6 degradation, albeit in a whole cell system Ding et al., 2001 ; . However, the loss in CYP2D6 activity observed here in the absence of NADPH implicated a non-ROS and nonheme oxygenase mechanism of enzyme lability. This is in contrast to data observed in CYP2C19 incubations, where much less enzyme and chlorpheniramine.

M e g Offlc * In t h aiLata s f |terda " Whlta, deeellid, " Notlea ta crtdSteri to prsiaBt el a i against u t a first d a ? Picsm l ?r * 1SSS. o n t TCitk w U l fiftid d e e efk a d m Will s s n .as s f d paid a i t six f s e tha d a t aiofagald SF, d a r . wjli b i f lb!f actians t h e iiibseriheF, . B a t --" J O H N JHre * M, O r e. Professor Leigh Canham Chief Scientific Officer, pSivida, Australia R Saffie-Siebert, C H Lau, D Drage, N Torabi-Pour, M Totolici, and L T Canham pSiMedica Limited Z Kai, R Ng, and P Chow Singapore General Hospital T Morris and S Watson Unit of Cancer Studies, University of Nottingham, UK BioSiliconTM is a novel nanostructured, porous form of semiconductor silicon which is biocompatible and biodegradable. The clinical use of non-systemic intratumoural chemotherapy is still limited, even for those high mortality cancers which are characterized by well defined primary lesions, such as breast, colorectum, lung, prostate and skin. In recent years, much effort has been invested into developing `localized' therapeutic regimens. In particular, radioseeds radioactive rice-sized implants ; have been produced for injection directly into tumours brachytherapy ; . However, the delivery of anticancer drugs and drug carriers at concentrations required for effective tumour therapy and low systemic toxicity remains a challenge. Here we present evidence for the potential use of BioSiliconTM as a drug delivery system for intratumoural applications, which could open a new avenue for the use of BioSiliconTM in the medical field. We measured the effect of our formulation on the efficacy toxicity ratio of each treatment in tumour models. Cytotoxic agents, including Chlorambucil or Paclitaxel, delivered by BioSiliconTM and injected directly into the tumour significantly decreased the size of the tumour and increased the survival rate compared to the control mice, with 99% of the animals surviving long term. Based on the excellent efficacy and toxicology data, BioSiliconTM is being developed as a means of drug delivery in intratumoural therapy. BioSiliconTM can be designed so that it will slowly dissolve; thereby releasing the active cytotoxic material and allowing prolonged exposure to the tumour. This therapy has the potential to give better clinical results, increase patient compliance and have lower side effects than conventional cancer therapies and chlorpropamide.

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