Abstract
Tumour resistance to anticancer agents remains a challenge in oncological practice, because it results in exposure to toxicities, unnecessary costs and, most importantly, delay of a potentially more effective treatment. Drug uptake by tumours may be impaired by several resistance pathways. Reasons for primary resistance may be that the drug is not delivered to the tumour or that its uptake by the tumour is not sufficient. Drug delivery depends on its distribution within the body, its bioavailability in the circulation and its transport to the tumour. Binding of drugs to circulating cells and proteins, formation of inactive metabolites as well as a rapid drug clearance may limit bioavailability. Furthermore, drug delivery to tumours is regulated by tumour vascularisation. Finally, tumour targets such as hormone receptors and efflux pumps also influence drug uptake by tumours. The use of specific PET tracers such as radiolabelled anticancer drugs (e.g. [18F]fluoropaclitaxel and [18F]5-fluorouracil) provide a unique means for individualized treatment planning and drug development. Combining these specific tracers with other less specific tracers, such as tracers for blood flow (e.g. [15O]H2O) and efflux (e.g. [11C]verapamil), may provide additional information on drug resistance mechanisms. Furthermore, radiolabelled anticancer agents may be valuable to evaluate the optimal timing of combination therapies. This review will focus on how PET can reveal different mechanisms of tumour resistance and thus may play a role in drug development and prediction of tumour response.
Keywords: Radiolabelled Anticancer Drugs, Oncology, Tumour, PET, fluoropaclitaxel, fluorouracil
Current Pharmaceutical Design
Title: Individualized Treatment Planning in Oncology: Role of PET and Radiolabelled Anticancer Drugs in Predicting Tumour Resistance
Volume: 14 Issue: 28
Author(s): Astrid A.M. van der Veldt, Gert Luurtsema, Mark Lubberink, Adriaan A. Lammertsma and N. Harry Hendrikse
Affiliation:
Keywords: Radiolabelled Anticancer Drugs, Oncology, Tumour, PET, fluoropaclitaxel, fluorouracil
Abstract: Tumour resistance to anticancer agents remains a challenge in oncological practice, because it results in exposure to toxicities, unnecessary costs and, most importantly, delay of a potentially more effective treatment. Drug uptake by tumours may be impaired by several resistance pathways. Reasons for primary resistance may be that the drug is not delivered to the tumour or that its uptake by the tumour is not sufficient. Drug delivery depends on its distribution within the body, its bioavailability in the circulation and its transport to the tumour. Binding of drugs to circulating cells and proteins, formation of inactive metabolites as well as a rapid drug clearance may limit bioavailability. Furthermore, drug delivery to tumours is regulated by tumour vascularisation. Finally, tumour targets such as hormone receptors and efflux pumps also influence drug uptake by tumours. The use of specific PET tracers such as radiolabelled anticancer drugs (e.g. [18F]fluoropaclitaxel and [18F]5-fluorouracil) provide a unique means for individualized treatment planning and drug development. Combining these specific tracers with other less specific tracers, such as tracers for blood flow (e.g. [15O]H2O) and efflux (e.g. [11C]verapamil), may provide additional information on drug resistance mechanisms. Furthermore, radiolabelled anticancer agents may be valuable to evaluate the optimal timing of combination therapies. This review will focus on how PET can reveal different mechanisms of tumour resistance and thus may play a role in drug development and prediction of tumour response.
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Cite this article as:
van der Veldt A.M. Astrid, Luurtsema Gert, Lubberink Mark, Lammertsma A. Adriaan and Hendrikse Harry N., Individualized Treatment Planning in Oncology: Role of PET and Radiolabelled Anticancer Drugs in Predicting Tumour Resistance, Current Pharmaceutical Design 2008; 14 (28) . https://dx.doi.org/10.2174/138161208786404344
DOI https://dx.doi.org/10.2174/138161208786404344 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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